Type 2 Diabetes Present in Jamaican Youth

March 30, 2007 (Newswise) — New research indicates that a significant number of Jamaican adolescents and young adults are being diagnosed with type 2 diabetes, a disease once seen almost exclusively in middle aged and elderly adults. These findings will be presented at the American Association of Clinical Endocrinologists (AACE) Sixteenth Annual Meeting and Clinical Congress which will be held April 11-15 at the Washington State Convention & Trade Center in Seattle.

“Type 2 diabetes at this age can be considered an indicator of obesity in a society. This research helps confirm that the ‘obesity epidemic’ is not just an American problem,” Marshall Tulloch-Reid, MBBS, DSc, FACE, the study’s author said. “It is becoming a significant public health challenge in the developing world.”

In America, adolescents diagnosed with type 2 diabetes are generally between ten and 19 years old, obese, have a family history of type 2 diabetes, and are insulin resistant. Because there is no golden rule to differentiate the types of childhood diabetes, Dr. Tulloch-Reid’s research is significant as he presents criteria that can be used to identify patients who may have type 2 diabetes. It is the first profile of youth onset type 2 diabetes from the English Speaking Caribbean.

As more adolescents become obese at an earlier age, they are at an increased risk of developing type 2 diabetes. According to Tulloch-Reid, “Surveys in Jamaica show that nearly 19 percent of adolescents are considered obese. One in five diabetic youth in this study was diagnosed with type 2 diabetes.”

This original research is being presented by Dr. Tulloch-Reid, along with colleagues from The University of the West Indies and the Kingston Public Hospital.

This study will be featured as part of a poster session held during the Sixteenth Annual Meeting and Clinical Congress. Members of the press are invited to attend on Thursday, April 12 and Friday, April 13 from 9:00 a.m. to 9:45 a.m. The preview session will be located at the Convention Center Exhibit Hall 4E in Seattle. Dr. Tulloch-Reid will be available in the media room to discuss his findings on Friday, April 13, from 10:00 a.m. to 11:00 a.m.

Posted by dlife at 03:03 PM | Comments (0)

Aspirin Resistance Is Higher in Diabetics

March 30, 2007 (Newswise) — Aspirin has long been the industry standard for the prevention and treatment of heart attacks. However, for the more than 20 million Americans living with diabetes, the standard dose of aspirin might not provide adequate protection against future heart attacks. Researchers at Sinai Hospital of Baltimore recently demonstrated that aspirin resistance is higher in diabetics with coronary artery disease (CAD) than in non-diabetics at the standard 81mg dose of aspirin. The study (#1019-179) will be presented in its entirety at the 56th Annual Scientific Session of the American College of Cardiology (ACC) in New Orleans on March 26.

Most CAD deaths are caused by platelets sticking together and forming blood clots (thrombosis) that block blood flow within arteries, resulting in a heart attack. Aspirin inhibits clotting by specifically blocking an important enzyme, COX-1, which keeps platelets from sticking together. However, some diabetic patients may require a higher aspirin dose to achieve sufficient COX-1 blockade.

“The occurrence of clotting in patients on aspirin therapy is of major interest within the cardiovascular community. The effect of aspirin dosing in diabetic patients on the prevalence of aspirin resistance remains unclear,” said Paul A. Gurbel, M.D., director of the Center for Thrombosis Research at Sinai Hospital of Baltimore and lead author on this study. “Our data suggest that there may be a higher risk of thrombosis in diabetic patients during low dose aspirin therapy.”

The team at the Sinai Center for Thrombosis Research studied 120 aspirin treated patients (30 patients with diabetes) with stable coronary artery disease. Participants were randomly assigned to receive 81mg, 162mg, or 325mg of aspirin daily for four weeks each, for a total of 12 weeks. The response to aspirin was then tested by multiple laboratory methods. It was found that diabetic patients exhibited a higher prevalence of aspirin resistance than non-diabetic patients with 81mg of aspirin.

“The results of our findings may help to determine the best aspirin dose for diabetic patients, moving physicians away from the one-size-fits-all approach to aspirin therapy,” said Gurbel.

Sinai Hospital of Baltimore is a member of LifeBridge Health, a regional health organization, which also includes Northwest Hospital Center, Levindale Hebrew Geriatric Center and Hospital, Jewish Convalescent & Nursing Home, and related subsidiaries and affiliates.

Posted by dlife at 02:58 PM | Comments (1)

Weight-Loss Surgery Reduces Insulin Resistance, Improves Beta Cell

March 28, 2007 (PR Newswire) - Bariatric surgery -- any of several procedures designed to reduce how much a person eats or how many calories their bodies absorb -- can reduce insulin resistance and improve beta cell function in severely obese people, regardless of whether they lose any weight, according to a study by researchers in Italy.

With the number of obese people rising rapidly in the U.S. and around the world, bariatric surgery has been growing in popularity. Previous research has shown this surgery can restore glucose tolerance in the majority of severely obese people. But this study found it could also improve beta cell function, regardless of how much weight a person does or doesn't lose after surgery.

Obesity greatly increases a person's risk of developing type 2 diabetes, which is characterized by insulin resistance and impaired beta cell function.

"Why these surgeries would improve beta cell function and glucose tolerance, independent of weight loss, remains unclear," said lead researcher Dr. Ele Ferrannini, Department of Internal Medicine and CNR Institute of Clinical Physiology, University of Pisa School of Medicine, Italy. "But obviously the fact that it does improve beta-cell function could make bariatric surgery a useful tool in the prevention of diabetes in the severely obese patient."

Posted by dlife at 09:24 AM | Comments (2)

Soy Nut Consumption Reduces Markers of Inflammation

March 28, 2007 (PRNewswire) Eating soy nuts instead of red meat decreases some markers of inflammation and improves endothelial function in postmenopausal women with a collection of cardiometabolic risk factors, a new study by researchers at Isfahan University of Medical Sciences in Iran and the Harvard School of Public Health found. In previous studies by the same group, subjects who ate soy nuts also showed improvements in their lipid profiles, suggesting that soy may improve cardiac health among a subgroup of women.

Previous research has looked at the effect of soy on inflammatory markers and endothelial function in the general population, but this was the first study to look more narrowly at how eating soy nuts (versus soy protein) would specifically affect postmenopausal women who already had a number of metabolic abnormalities. Consuming soy protein did not produce the same benefits, the researchers found.

Women (and men) who have certain cardiometabolic risk factors (abdominal obesity, high blood pressure, high cholesterol and insulin resistance) are at high risk for type 2 diabetes and for heart disease, the number one killer of people with diabetes. Studies have shown that lifestyle changes, such as losing moderate amounts of weight and increasing physical activity, can substantially reduce the chances of developing diabetes for people who already have these risk factors.

"A well-balanced meal plan should be part of any program designed to lose weight or improve overall health. This study shows that adding soy nuts to your diet -- and eating less red meat -- could be an important part of that meal plan," said lead researcher Dr. Leila Azadbakht, at the Isfahan University of Medical Sciences Department of Nutrition in Iran.

Soy is also often used as an alternative or adjunct to hormone replacement therapy in postmenopausal women. The researchers note that the mechanisms by which soy affects the inflammatory state may be related to the effects of soy phytoestrogens, which mimic hormone replacement therapy. However, more research needs to be done to understand the mechanisms through which soy affects inflammation and endothelial function. It is also unclear whether other groups of postmenopausal women would benefit as much as those participating in this study who had a number of high risk factors for diabetes and heart disease.

Posted by dlife at 09:18 AM | Comments (0)

Diabetes Linked to Higher Parkinson's Risk

March 28, 2007 (PRNewswire) -- People who have type 2 diabetes are more likely to develop Parkinson's disease as they age, though researchers are uncertain what accounts for the link between the two diseases, according to a new study being published in the April issue of Diabetes Care.

The study, by researchers in Finland, is the first large prospective study to find type 2 diabetes to be a risk factor for Parkinson's disease, a movement disorder characterized by muscle rigidity and tremors.

According to the authors, people with type 2 diabetes are 83 percent more likely to be diagnosed with Parkinson's than people in the general population. The study found the association between the two diseases existed for both men and women, independently of other confounding factors.

"Diabetes might increase the risk of Parkinson's disease partly through excess body weight," the researchers hypothesized, since their work showed that excess body weight was also associated with an elevated risk of Parkinson's disease. However, they concluded that more research needed to be done to fully understand the mechanisms behind this link.

Posted by dlife at 09:15 AM | Comments (2)

Who Gets Heart Failure? Race Takes Back Seat to Diabetes and High Blood Pressure

Study limits role of race in explaining high rates of disease among African-Americans

March 28, 2007 (EurekAlert) - Diabetes and high blood pressure, two conditions rooted in genetics and environmental surroundings, play a much greater role than race alone in determining who is mostly likely to develop heart failure, according to the latest study from cardiologists at Johns Hopkins. Each year, nearly 300,000 Americans die from heart failure.

Experts say that racial disparities have long been known to exist in who actually develops risk factors for the condition, with African Americans nearly twice as likely to be diagnosed with diabetes and more than a third as likely to have high blood pressure than Caucasian Americans. But researchers have only now determined the precise role played by race in comparison to other risk factors, including socio-economic factors, age, gender, smoking, family history, and other health problems, as well as diabetes and hypertension.

The Hopkins team will present its findings March 27 in New Orleans at the American College of Cardiology’s annual Scientific Sessions in New Orleans.

In the study, researchers monitored nearly 7,000 men and women, age 45 to 84, of different ethnic backgrounds and with no existing symptoms of heart disease. African Americans developed heart failure at significantly higher rates (4.6 cases per 1,000 per year) than all other races, including Hispanics and Caucasians. Their rate was almost five times that of Chinese Americans (1 case per 1,000 per year) and almost twice that of Caucasians (2.4 cases per 1,000 per year).

However, these apparent risk differences among races almost disappeared (dropping from twice as likely, a significant difference, to no more than one-and-a-half times as likely, an insignificant difference) when researchers used statistical techniques to exclude the two traditional risk factors for heart disease.
“When all major factors are taken into account, the differences between races for heart failure largely evaporate in the absence of diabetes and hypertension among African Americans,” says senior study investigator João Lima, M.D.

According to Lima, an associate professor of medicine and radiology at The Johns Hopkins University School of Medicine and its Heart Institute, these early results add to other interesting findings from the so-called Multiethnic Study of Atherosclerosis (MESA).

The study, started in 2001, is monitoring its ethnically diverse participants for six to eight years to see who develops heart failure and who does not. It is the first large-scale analysis of racial or ethnic differences in heart function. So far, 79 study participants have developed congestive heart failure.
Other results presented at the meeting showed differences among races in heart strain, or contraction, which may contribute to disparities in heart failure, albeit to a lesser extent. Indeed, African American hearts were found to contract less strongly than those of Hispanic, Caucasian or Chinese American backgrounds.

Lima cautions, however, that much remains to be understood about the root causes of racial disparities and how to fix them.

He points out that while African Americans are at much higher risk of heart failure, there is no similarly higher number for risk of suffering heart attack, which, like diabetes and hypertension, often leads to heart failure.

In MESA, researchers found a reverse relationship, with African Americans having the lowest rates of heart failure due to myocardial infarct (at 25 percent), while other races had a much higher proportion:

Caucasians (40 percent), Hispanics (42 percent), and Chinese Americans (100 percent.)

Lima says the difference could be due to successful disease prevention efforts among all racial groups, except for African Americans, at controlling hypertension.

“A lot of public health attention has already been paid to getting high blood pressure under control, so it may be just that this risk factor is under tighter control in some ethnic groups than in others,” he says. “African Americans are clearly getting heart failure from causes other than heart attack.”

According to lead researcher Hossein Bahrami, M.D., M.P.H., the message to physicians is clear, “warding off heart failure in African Americans requires aggressive treatment of diabetes and hypertension.

Whether through increased screening or greater emphasis on drug therapies, these are two risk factors that must be brought under control.”

Bahrami, a senior cardiology research fellow at Hopkins, says removing barriers for African Americans to controlling their diabetes and hypertension could be critical to reducing new cases of heart failure.

Across all ethnic groups, an estimated 550,000 Americans are diagnosed each year.

Bahrami says the team’s next steps are to determine why different rates exist for these risk factors and the role played by biological and environmental factors.

Posted by dlife at 09:09 AM | Comments (0)

Clinical Trial for Diabetic Macular Edema

Phoenix-based retinal consultants of Arizona to serve as local clinical trial center

March 26, 2007 (EurekAlert) – New York, NY -- The Juvenile Diabetes Research Foundation, the world’s largest charitable funder of type 1 diabetes research, announced that the Ranibizumab for Edema of the mAcula in Diabetes Phase 2 Study (READ 2) is now enrolling patients.

The READ 2 Study will test the long-term safety and effectiveness of intraocular injections of ranibizumab in patients with diabetic macular edema (DME), a condition characterized by swelling of the retina due to leaking of fluid from blood vessels within the macula. DME is the leading cause of vision loss among working-age Americans.
The READ2 study is supported by Genentech and JDRF. The Phoenix-based Retinal Consultants of Arizona will serve as a clinical center for the trial.

This Phase 2 clinical trial builds on the results of a phase 1 trial (which was supported by an Innovative Grant Award from JDRF), which showed the ability of ranibizumab to improve visual acuity in patients with diabetic macular edema. Visual acuity was assessed using a reading chart, and median and mean visual acuity improved by 11 and 12.3 letters respectively at 7 months. This corresponds to the ability to read two additional lines on a reading chart. In the phase 1 study, there were no adverse events that were judged by the investigators to be related to the drug. Some patients experienced redness on the surface of the eye at the site of injection that lasted up to 72 hours. The redness was thought to be due to the injection itself, however, and not the drug.

The READ 2 study will look specifically for additional dosing and safety information, as well as combination therapy of ranibizumab and laser photocoagulation (which has been the standard therapy for DME). The study consists of a two-week screening period, a six-month active treatment period, and an 18-month follow-up and treatment period.

Posted by dlife at 02:55 PM | Comments (2)

Crestor Effective at Halting Early Atherosclerosis

March 25, 2007 (EurekAlert) – An international study using ultrasound technology has found that the most potent cholesterol-lowering drug is also effective at halting early changes in the blood vessels that can lead to atherosclerosis.

"Rosuvastatin arrested the progression of thickened carotid arteries compared to a placebo," said John R. Crouse, M.D., lead researcher and a professor of endocrinology at Wake Forest University School of Medicine. "The findings show that the benefits of cholesterol management on arteries can be extended to low-risk patients."

Results from the study were reported today at the annual meeting of the American College of Cardiology in New Orleans and were published on-line by the Journal of the American Medical Association. The research involved people with moderately elevated cholesterol levels who didn't qualify for treatment under national guidelines.

Participants all had minimal thickening of their carotid arteries, which supply blood to the brain, and were considered at low risk for having a heart attack or dying from a heart-related event based on their age and other risk factors.

Over a two-year period, the therapy lowered low-density lipoprotein, or "bad" cholesterol, by 49 percent and increased high density lipoprotein, or "good" cholesterol, by 8 percent. Triglycerides were reduced by 16 percent and the progression of artery thickness was halted.

Rosuvastatin (sold under the trade name Crestor®) is the newest member of a family of drugs known as statins that work to lower levels of cholesterol and other fats in the blood. Other statins have been tested – with similar results – in patients who've already had a heart attack or who had high cholesterol levels. This was the first study to evaluate Crestor in a group of people at low risk for heart attacks.

"Atherosclerosis is often advanced before symptoms appear and it hasn't been clear whether treatment of low-risk individuals is beneficial," said Crouse. "This study shows that aggressive cholesterol management arrests the progress of even small changes in the arteries."

The study used ultrasound to assess whether Crestor was effective at halting progressive thickening of the carotid arteries. Vessel thickening is an early sign of atherosclerosis, the deposit of fatty material in blood vessels that can lead to heart attacks and strokes.

There were 984 study participants: 702 were randomly assigned to receive 40 mg of Crestor daily and 282 were randomly assigned to receive a placebo, or inactive tablet. Male participants were between 45 and 70 years old and females were between 55 and 70.

Crestor arrested the development of artery thickening overall and in all 12 sites of the carotid artery that were measured. Drug safety was assessed by vital signs, adverse events, laboratory tests and electrocardiograms. The frequency of adverse events was similar between the two groups and included muscle pain and gastrointestinal disorders.

"The drug was well tolerated during the two-year period and showed a similar safety profile to the placebo," said Crouse.

The study included 61 primary care practices in the United States and Europe and was conducted between August 2002 and May 2006. Each participant was followed for two years and received an ultrasound exam at the beginning and end of the study and every six months during the study period.

Participants were considered at low risk of a heart attack or death from a heart-related-event based on a formula developed by the National Cholesterol Education Program from the long-running Framingham Heart Study, which takes such factors as age, sex, blood pressure and cholesterol levels into account. Low risk was considered a heart disease risk of less than 10 percent over a 10-year period.

The study is known as METEOR (Measuring Effects on intima media Thickness: an Evaluation of Rosuvastatin).

Crouse said additional studies should be conducted to determine if the drug also affects the number of clinical events.

Posted by dlife at 12:27 PM | Comments (0)

Joslin Diabetes Center Reminds People with Diabetes to Schedule Annual Eye Exams to Preserve Vision

March 23, 2007 (Joslin) -- Did you know that diabetes is the number one cause of preventable vision loss and blindness? Did you also know that an annual eye exam can lead to early detection of diabetic retinopathy and other eye disease, a frequent complication of diabetes?

On Diabetes Alert Day, March 27 -- a day set aside by the American Diabetes Association to raise public awareness of the rampant incidence of diabetes in our nation -- the care team at the world renowned Joslin Diabetes Center's Beetham Eye Institute reminds the 20.8 million Americans with diabetes to schedule an annual eye exam. Joslin's Beetham Eye Institute clinicians have shown that an annual exam can provide early detection and help prevent or delay 90 percent of cases of vision loss due to diabetic retinopathy. According to the Centers for Disease Control and Prevention, diabetic retinopathy is a leading cause of blindness in adults, resulting in 12,000 to 24,000 new cases of blindness each year.

Diabetic retinopathy, the most common eye disease in people with diabetes, occurs when the small blood vessels in the eye are damaged by high levels of glucose in the blood. Because diabetic retinopathy can progress to advanced stages without the patient knowing it, it is crucial to have annual eye exams to help preserve vision.

Joslin clinicians recommend a three-prong approach to preserving vision:

- Maintain excellent A1C levels. (The A1C is a test that measures average blood glucose levels over the 2 to 3 month period before the test.)
- Keep blood pressure, blood lipids and other health factors in check.
- Have an annual eye exam.

To watch a video on Joslin's Web site about the importance of annual eye exams, click here: http://www.joslin.org/754_871.asp

For more information about eye research and clinical trials at Joslin, click here: http://www.joslin.org/755_3819.asp

Posted by dlife at 12:22 PM | Comments (0)

Dramatic Increase of Type 1 Diabetes in Under-Fives

March 16, 2007 (Diabetes UK) - Researchers are calling for more work into the reasons behind a big increase of young children with type 1 diabetes.

A new study, announced today at Diabetes UK’s Annual Professional Conference, has discovered that the number of under-fives with type 1 diabetes has increased five-fold over 20 years.

While the largest rise of the condition was seen in children under five years old, type 1 diabetes in under-15s almost doubled during the study. There was a 2.3 per cent increase in the number of children diagnosed with type 1 diabetes each year.

“This project has produced some very interesting results," said Simon O’Neill, Director of Care, Information and Advocacy Services at Diabetes UK.

“The evidence of a steep rise of type 1 diabetes found in the under-fives indicates that the peak age for diagnosis of the condition in the UK is becoming younger. While 10- to 14-year-olds remain the largest group for diagnosis, the rise in cases found in children under five is worrying.”

Professor Polly Bingley from Bristol University added: “The incidence of childhood Type 1 diabetes has been shown to be increasing all over Europe, particularly in the very young.

“The increase is too steep to be put down to genetic factors, so it must be due to changes in our environment. This could either mean that we are being exposed to something new, or that we now have reduced exposure to something that was previously controlling our immune responses. We now need to work to identify what these changes might be.”

The results come from researchers at the University of Bristol who were funded by Diabetes UK. The study looked at Oxford’s population of 2.6m people between 1985 and 2004.

Posted by dlife at 08:27 AM | Comments (1)

Erectile Dysfunction in Diabetes is Due to Selective Defect in the Brain

March 15, 2007 (Eurekalert) BETHESDA, MD -- A new study sheds additional light on how erectile dysfunction (ED) interacts with diabetes. The study is another step in uncovering the link between the two disorders, and may lead to improved efficacy in treatments.

The study, "Lack of Central Nitric Oxide Triggers Erectile Dysfunction in Diabetes," was conducted by Hong Zheng, William G. Mayhan, and Kaushik P. Patel, Departments of Cellular and Integrative Physiology; and Keshore R. Bidasee, Department of Pharmacology, University of Nebraska Medical Center, Omaha, NE. The results appear in the March 2007 edition of the American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, one of 11 peer-reviewed scientific publications issued monthly by The American Physiological Society (APS) (www.The-APS.org).

Background

Sexual dysfunction is a well-recognized consequence of diabetes mellitus in men. Erectile dysfunction, retrograde ejaculation and the loss of seminal emission have all been described by such patients. This study examined induced penile erection, yawning and stretch in diabetic rats. Male Sprague-Dawley rats treated with streptozotocin (STZ) to induce diabetes were used as they exhibit sexual and behavioral symptoms similar to those found in diabetic men with sexual dysfunction.

The researchers focused on the paraventricular nucleus (PVN) of the hypothalamus, located in the brain, an integration center between the central and peripheral nervous systems. The site is involved in numerous functions, including erectile function and sexual behavior, and is a primary site within the forebrain that has been implicated in penile erection. The investigators also examined central nitric oxide (NO within the PVN) which plays an important role in the neurotransmission of normal penile erection.

Penile erection is a behavioral response that occurs in response to the administration of N-methyl-D-aspartic acid (NMDA) within the PVN. At the same time, inhibition of NO synthase with NG-monomethly-L-argining (L-NMMA) prevents NMDA-induced erection. The researchers hypothesized that the blunted NMDA mediated responses in diabetes reflects an impaired NO mechanism within the PVN. The involvement of an NO mechanism in the NMDA mediated behavioral response was also explored.

Methodology

The rats were exposed to a light/dark cycle, with standard temperature and humidity levels. The animals were randomly selected to receive chemical injection of the streptozotocin (STZ) to induce diabetes. Those rats that did not receive STZ (vehicle injected) served as controls. The experiments began on each of the rats four weeks after the injections.

Four experiments were conducted. Experiment one examined the effect of L-NMMA on NMDA mediated behavioral responses in normal rats; experiment two measured behavioral responses to NMDA or sodium nitroprusside (SNP), an NO donor in both control and diabetic rats; the third experiment observed the effect of diabetes on nNOS protein in the PVN; the fourth experiment measured NMDA mediated behavioral responses in diabetic rats after restoring the nNOS protein in the PVN using viral gene transfer.

Results

The researchers found that:

* when L-NMMA was used to block NO production in the PVN, NMDA mediated penile erectile responses were blunted

* NMDA-induced erections were significantly blunted in diabetic rats compared with control rats

* the nNOS protein levels in the PVN were decreased in rats with diabetes and

* restoring nNOS protein within the PVN of diabetic rats with viral gene transfer could alleviate the blunted NMDA induced erectile responses.

Conclusion

The researchers conclude that erectile dysfunction in diabetes is due to a selective defect in the NO mechanisms within the PVN. This defect is a loss in the synthetic enzyme for the production of NO within the neurons of the PVN. Restoring this synthetic enzyme may have a significant therapeutic value for diabetic patients with ED.

Posted by dlife at 11:53 AM | Comments (8)

Belly Fat May Drive Inflammatory Processes Associated with Disease

March 14, 2007 (Eurekalert) - As scientists learn more about the key role of inflammation in diabetes, heart disease and other disorders, new research from Washington University School of Medicine in St. Louis suggests that fat in the belly may be an important promoter of that inflammation.

Excess fat is known to be associated with disease, but now the researchers have confirmed that fat cells inside the abdomen are secreting molecules that increase inflammation. It's the first evidence of a potential mechanistic link between abdominal fat and systemic inflammation.

For years, scientists have been aware of a relationship between disease risk and excess belly fat. "Apple-shaped" people, who carry fat in the abdomen, have a higher risk of heart disease, diabetes and other problems than "pear-shaped" people, who tend to store fat in the hips and thighs. Too much abdominal fat is associated with a defect in the body's response to insulin. During medical exams, some physicians measure waist circumference to identify patients at increased risk for these problems.

Not just any belly fat will cause inflammation, however. Back in 2004, Washington University investigators found that removing abdominal fat with liposuction did not provide the metabolic benefits normally associated with similar amounts of fat loss induced by dieting or exercising.

"Despite removing large amounts of subcutaneous fat from beneath the skin — about 20 percent of a person's total body fat mass — there were no beneficial medical effects," says Samuel Klein, M.D., the Danforth Professor of Medicine and Nutritional Science and the senior investigator on both studies.

"These results demonstrated that decreasing fat mass by surgery, which removes billions of fat cells, does not provide the metabolic benefits seen when fat mass is reduced by lowering calorie intake, which shrinks the size of fat cells and decreases the amount of fat inside the abdomen and other tissues."

In this new study, researchers looked instead at visceral fat — the fat that surrounds the organs in the gut. Unlike subcutaneous fat, visceral fat is not easy to remove surgically because it is very close to the intestines and other internal organs. Since they couldn't just take out the fat, the research team decided to analyze the blood that ran through it to determine whether visceral fat was involved in inflammation or whether, like subcutaneous fat, it was merely a marker of potential problems.

Reporting in the journal Diabetes, the research team says visceral fat likely contributes to increases in systemic inflammation and insulin resistance. They sampled blood from the portal vein in obese patients undergoing gastric bypass surgery and found that visceral fat in the abdomen was secreting high levels of an important inflammatory molecule called interleukin-6 (IL-6) into portal vein blood.

"The portal vein is filled with blood that drains visceral fat," says first author Luigi Fontana, M.D., Ph.D., assistant professor of medicine at Washington University in St. Louis and an investigator at the Istituto Superiore di Sanita, Rome, Italy. "Portal vein blood had levels of IL-6 that were 50 percent higher than blood from the periphery."

Increased IL-6 levels in the portal vein correlated with concentrations of an inflammatory substance called C-reactive protein (CRP) in the body. High CRP levels are related to inflammation, and chronic inflammation is associated with insulin resistance, hypertension, type 2 diabetes and atherosclerosis, among other things.

"These data support the notion that visceral fat produces inflammatory cytokines that contribute to insulin resistance and cardiovascular disease," says Klein.

Klein, Fontana and J. Christopher Eagon, M.D., assistant professor of surgery, looked at blood samples from 25 patients. All were extremely obese, and all were undergoing gastric bypass surgery. They took blood from the portal vein and from the radial artery in the arm and found differences in levels of IL-6 between the samples.

Fontana believes the findings help explain how visceral fat can lead to inflammation, insulin resistance and other metabolic problems. And he says by contributing to inflammation, visceral fat cells in the abdomen may be doing even more than that.

"Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries," Fontana says. "Nowadays, it's clear that atherosclerosis is an inflammatory disease. There also is evidence that inflammation plays a role in cancer, and there is even evidence that it plays a role in aging. Someday we may learn that visceral fat is involved in those things, too."

Posted by dlife at 10:45 AM | Comments (4)

Periodontal Diseases May Aggravate Pre-Diabetic Characteristics

March 14, 2007 (EurekAlert) - Periodontal diseases may contribute to the progression to pre-diabetes, according to a new study that appears in the March issue of the Journal of Periodontology.

Pre-diabetes is a condition in which blood glucose levels are higher than normal, but not high enough to be diagnosed as diabetes. The American Diabetes Association estimates 54 million people in the United States have pre-diabetes, and a significant portion of those people will develop Type 2 diabetes within 10 years.

Researchers from Denmark investigated if having periodontal diseases can influence pre-diabetes and contribute to the progression of diabetes. They found that having periodontal disease can cause someone to develop pre-diabetic characteristics, and probably disturb the glucose regulation of a non-diabetic who has pre-diabetic characteristics, contributing to the progression of Type 2 diabetes. The study, conducted with rat models known to exhibit pre-diabetes characteristics, is believed to be the first to evaluate the relationship between periodontitis and pre-diabetes.

"This study found that having periodontal diseases can alter the metabolic conditions which would probably lead to the progression to pre-diabetic characteristics and Type 2 diabetes," said Dr. Carla Pontes Andersen, Department of Periodontology at the University of Copenhagen.

"We have known that people with diabetes are more susceptible to periodontal diseases and have more severe disease," said Dr. Preston D. Miller, Jr., President of the American Academy of Periodontology.

"This breakthrough research shows having periodontal disease may aggravate pre-diabetes which is a precursor for diabetes. These findings underscore the importance of taking good care of your teeth and gums: it may be a simple way to prevent diabetes, or to prevent the progression of diabetes."

Posted by dlife at 10:39 AM | Comments (0)

World Decision-Makers Confront Diabetes Pandemic at Novo Nordisk Global Changing Diabetes Leadership Forum

March 13, 2007 (Newswire) -- Former President Bill Clinton joined global diabetes leaders today in New York City to discuss ways to break the curve of the diabetes pandemic at a forum hosted by Novo Nordisk and supported by the International Diabetes Federation (IDF).

At the first meeting of policymakers, patient organizations, healthcare professionals, and media since the United Nations passed a resolution to address diabetes in December 2006, the discussion explored ways to make diabetes a global health priority and ultimately, improve the way the disease is treated.

Today, 20.8 million Americans -- or seven percent of the population -- have diabetes, at least 10 million of whom are not in control of the condition. It is estimated that one in three American children born in 2000 and beyond will develop type 2 diabetes. Worldwide, an estimated 246 million people have diabetes, a number that is expected to grow to 380 million within the next 20 years if no urgent action is taken. Diabetes accounts for 3.8 million deaths per year globally, similar in magnitude to HIV/AIDS.

The Global Changing Diabetes Leadership Forum hopes to redefine healthcare around the needs of people with diabetes.

"Recognizing that there is not a single answer to the diabetes pandemic, Novo Nordisk hopes to provide a forum for identifying multiple actions at all stages to combat diabetes -- from prevention to the treatment of serious complications," said Lars Rebien Sorensen, president and CEO of Novo Nordisk. "Only by placing the person with diabetes at the center of care and changing how healthcare systems around the world approach the disease can this silent killer be defeated."

Martin Silink, president of the IDF, emphasized that "the reality is that there will not be an automatic increase in funds for diabetes for either prevention or treatment in the short term. In developing countries, which bear 70% of the global burden of diabetes, the solutions will involve increasing access to proven but low-cost therapies."

During the two day Forum, attendees from around the world will participate in a series of workshops and dialogues designed to evoke a provocative debate about how to chart a course for changing diabetes management globally.

Posted by dlife at 05:16 PM | Comments (0)

FDA Approves New Medtronic Continuous Glucose Monitoring Devices for Children and Teenagers

March 12, 2007 (BUSINESS WIRE)--Medtronic, Inc. (NYSE:MDT) today announced that the U.S. Food and Drug Administration (FDA) has approved new REAL-Time Continuous Glucose Monitoring (CGM) devices for children and teenagers ages 7-17. Previously approved for only adult patients, Medtronic’s REAL-Time CGM will soon be available in specifically designed pediatric models of the MiniMed Paradigm® REAL-Time System and Guardian® REAL-Time System.

“This indication reinforces Medtronic’s commitment to developing and marketing novel therapies for the millions of Americans with diabetes,” says Chris O’Connell, President of Medtronic’s diabetes business. “We are particularly excited that children and their families will sleep better at night knowing that REAL-Time CGM is providing a new level of protection against dangerous glucose levels.”

Medtronic REAL-Time CGM therapy is clinically proven to help patients monitor and better control their diabetes. Clinical studies have shown that Medtronic REAL-Time CGM therapy can reduce the duration of hypoglycemic events, and lower HbA1c levels by as much as two percentage points. This is significant because as much as 60 percent of hypoglycemic events go undetected by current glucose monitoring standards, and for every one percentage point drop in HbA1c, there is a 35 percent reduction in diabetes-related complications like blindness, amputation and organ failure.

“Diabetes management is especially difficult for pediatric patients, and Medtronic REAL-Time CGM therapy could benefit thousands of children and their families who struggle to maintain control of their disease,” says Dr. Bruce Buckingham, director of Pediatric Endocrinology at Lucille Packard Children's Hospital, Stanford University. “By providing real-time glucose values and alarms, patients can now recognize previously undetected glucose fluctuations.”

Medtronic REAL-Time CGM technology displays REAL-Time glucose values, trend graphs and directional arrows, allowing patients to discover how diet, exercise, medication and lifestyle affect their glucose levels. With this information, patients can gain valuable insights and intervene earlier to reduce the frequency and severity of high and low glucose levels. The technology alerts patients if their glucose levels fall below—or rise above—preset values. Values are not intended to be used directly for making therapy adjustments, but rather to provide an indication of when a meter blood glucose measurement may be required. All therapy adjustments should be based on measurements obtained using a home glucose meter and not on Medtronic REAL-Time CGM System values.

Medtronic currently markets the MiniMed Paradigm REAL-Time Insulin Pump and Continuous Glucose Monitoring System – the world's first insulin pump with REAL-Time continuous glucose monitoring. The MiniMed Paradigm REAL-Time System has all of the benefits of CGM plus the added value of precise insulin delivery through the use of insulin pump therapy. The Guardian REAL-Time System, a stand-alone CGM device, will be available later this year.

Posted by dlife at 12:04 PM | Comments (0)

18 Diabetic Patients Implanted With VeriMed RFID Microchip at Atlanta Diabetes EXPO

March 12, 2007 (PR Newswire) -- VeriChip Corporation (Nasdaq: CHIP), a provider of RFID systems for healthcare and patient-related needs, announced today it added 18 diabetic patients to its VeriMed Patient Identification System at an Atlanta Diabetes EXPO sponsored by the American Diabetes Association (ADA).

At the Diabetes EXPO, physicians implanted VeriMed RFID microchips in conference attendees who signed up for the voluntary procedure. The VeriMed Patient Identification System, which utilizes an implantable RFID microchip in combination with a handheld RFID scanner and a secure patient database, provides immediate access to important health information for patients who arrive at an emergency department unable to communicate.

Scott R. Silverman, Chairman and CEO of VeriChip, commented, "We believe the VeriMed Patient Identification System is an essential health care solution for at-risk patients, including diabetics, who tend to present with various co-morbidities and medications, and are more frequently admitted to emergency departments. Since the inception of the VeriMed System, we always knew that the diabetic community was in need of a way to communicate their medical information better and more frequently. We will continue to focus on diabetics and to enhance our relationship further with the American Diabetes Association. The Atlanta Diabetes EXPO provides us direct access so we can continue to educate an important target audience."

The Diabetes EXPO is a patient-driven tradeshow, including professional speakers and a variety of ADA program/event information, where exhibitors from pharmaceutical and medical device companies display beneficial products for diabetics. The Diabetes EXPO began in 1995 in Phoenix, Arizona, and has grown to 18, metro, major and mid-size cities around the U.S. The next event will be held in Boston on March 17, 2007. of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934, and as that term is defined in the Private Litigation Reform Act of 1995. Such forward-looking statements involve risks and uncertainties and are subject to change at any time, and the Company's actual results could differ materially from expected results. The Company undertakes no obligation to update forward-looking statements to reflect subsequently occurring events or circumstances.

Posted by dlife at 11:59 AM | Comments (1)

Diabetes, Depression Together Increase Risk for Heart Patients

March 9, 2007 (EurekAlert) -- Having both depression and type 2 diabetes increases the risk of death for heart patients. Each factor had been known to increase the risk of heart disease deaths by itself, but together they’re even more deadly.

In an analysis of more than 900 patients with established coronary artery disease, Duke University Medical Center psychologists found that those with both type 2 diabetes and symptoms of depression were more likely to die than heart patients without those conditions.

The study showed that among type 2 diabetes patients, having high depression scores increased the risk of dying by 20 to 30 percent compared to patients with similar depression scores but no type 2 diabetes.

"We found a trend showing that the probability of death increases as the level of depression increases in diabetic patients with coronary artery disease," said Duke researcher Anastasia Georgiades, Ph.D. She presented the results of the Duke analysis on Friday, March 9, 2007, at the annual meeting of the American Psychosomatic Society, in Budapest, Hungary. "Our data appear to show an important interaction between type 2 diabetes and depression, meaning that physicians should closely monitor their heart patients who have both of these disorders.

"There is some sort of synergistic effect between type 2 diabetes and depression that we don’t fully understand," Georgiades said. "In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association."

The research was supported by the National Heart, Lung, Blood Institute.

The researchers followed 933 heart patients for more than four years and correlated the 135 deaths that occurred during that period with the presence of type 2 diabetes and depression alone and together.

Georgiades said there are some possible explanations for the link between depression and diabetes.

"Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise and numerous appointments with their doctor," she said. "It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk."

Depression has also been linked to other cardiovascular risk factors such as insulin resistance, hypertension, obesity, increased cigarette smoking, alcohol abuse and physical inactivity.

Posted by dlife at 02:50 PM | Comments (1)

Strong Evidence Links Soft Drink Consumption to Obesity, Diabetes

March 8, 2007 (Newswise) — The case against swigging soda just got stronger. A large systematic review reveals clear associations between consumption of nondiet soft drinks and increased calorie intake and body weight.

Full-calorie soft drinks are also linked with reduced intake of milk and fruit and increased risk of type 2 diabetes. “Recommendations to reduce population soft drink consumption are strongly supported by the available science,” concludes the review of 88 studies.

The American Beverage Association, however, presents a different view on its Web site. “It is not feasible to blame any one food product or beverage as being a sole contributor to obesity …. No science supports such a claim.”
Carbonated soft drinks are the single largest source of calories in the American diet, according to a 2005 report called “Liquid Candy,” produced by the nonprofit Center for Science in the Public Interest (CSPI). Companies annually manufacture enough soda pop to provide more than 52 gallons to every man, woman and child in the United States.

“Nobody claims there is a single cause to the obesity problem, but the existing science certainly puts soft drinks in the list of leading contributors,” said review co-author Kelly Brownell, Ph.D. He is director of the Rudd Center for Food Policy and Obesity at Yale University.

The systematic review appears in the April issue of the American Journal of Public Health. The work was supported in part by the Rudd Foundation, a private philanthropic organization focusing on obesity and education.
The authors say that a “true test” of links between a consumer product such as soft drinks and health outcomes requires a critical mass of large studies employing strong methods.

“These conditions now exist, and several clear conclusions are apparent,” they say. One of the most “powerful” findings is the link between soft drink intake and increased calorie consumption.

Of 21 studies, 19 showed that as people drink more soda pop, the number of calories they consume rises. Moreover, the studies using the most reliable statistical methods showed the largest effects.

Instead of satisfying a sweet tooth, soft drinks may do just the opposite. Several studies found that the caloric increase is actually greater than that contained in the soda, raising “the possibility that soft drinks increase hunger, decrease satiety or simply calibrate people to a high level of sweetness that generalizes to preferences in other foods,” the authors say.

“These results, taken together, provide clear and consistent evidence that people do not compensate for the added calories they consume in soft drinks by reducing their intake of other foods,” the reviewers say.

The authors anticipated a weaker relationship between soft drink consumption and body weight, because there are many other calorie sources in the diet. Yet in the highest-quality studies, which controlled for a number of unrelated variables, a moderate relationship existed. The review also showed a slight correlation between soft drink consumption and lower intakes of milk, calcium, fruit and fiber.

The “most striking link” was between soft drink consumption and the incidence of type 2 diabetes, according to the reviewers. In a study of 91,249 women followed for eight years, those who consumed one or more soft drinks per day were twice as likely as those who consumed less than one per month to develop diabetes

“This result alone warrants serious concern about soft drink intake, particularly in light of the unprecedented rise in type 2 diabetes among children,” the review says.

The authors acknowledge that there is a great deal of variability among the studies included in this review, which incorporate differing methods, populations, beverage types and measurements of key factors such as body weight. Future research with more uniform approaches “would help clarify the impact of soft drink consumption on nutrition and health outcomes,” they say.

CSPI, on the other hand, is satisfied with the research to date. “There’s so much damning evidence,” says Michael F. Jacobson, Ph.D., executive director. “This is just sugar water. The real need is for laws and regulations that would help rein in soft drink consumption.”

The consumer advocacy group calls for clearly presented calorie information at vending machines, convenience stores and restaurants. The group urges schools to stop selling full-calorie soft drinks. CSPI has also petitioned the federal government to require health notices on all nondiet sodas warning that they may promote obesity, diabetes, tooth decay, osteoporosis and other health problems.

The soft drink industry, for its part, has developed voluntary school beverage guidelines designed to limit the availability of sugary sodas and offer more water, milk, juice, energy drinks and diet soft drinks to students.

“All foods and beverages can play an important role in a healthy diet if they’re consumed in moderation and also with regular exercise,” said Tracey Halliday, a spokesperson for the American Beverage Association.

Posted by dlife at 10:12 AM | Comments (0)

Even 'High Normal' Glucose Levels May Increase the Risk of Hospitalization for Heart Failure

March 6, 2007 (EurekAlert) - Fasting glucose levels may independently predict the risk of being hospitalized with congestive heart failure in heart attack survivors and others who are at high risk of developing the disorder, researchers reported in Circulation: Journal of the American Heart Association.

Drawing on data from 31,546 high-risk patients participating in two international trials, researchers found that even small increases in fasting glucose raised the risk of congestive heart failure in both diabetes patients and those whose blood sugar fell within the normal range.

"This illustrates that blood glucose by itself is a continuous risk factor for developing heart failure because all of these patients were free of heart failure when they enrolled in the trials," said Claes Held, M.D., Ph.D., lead author of the study.

"However, these are only associations," said Held, an associate professor of cardiology at the Karolinska Institutet in Stockholm, Sweden. "They do not prove that elevated blood glucose causes heart failure. To demonstrate a causal relationship, you would have to do a study that showed lowering blood glucose levels would reduce the incidence of heart failure."

About 5.2 million Americans evenly divided between males and females suffer from heart failure, according to the American Heart Association. Each year about 550,000 new cases are diagnosed and about 57,700 people die from it. Heart failure is a debilitating condition in which the heart fails to pump an adequate supply of blood throughout the body. Established heart failure risks include uncontrolled high blood pressure, diabetes and heart attack.

To examine the relationship between blood glucose levels and congestive heart failure, Held and colleagues performed an interim analysis on the blinded data from the ONgoing Telmisartan Alone and in combination with the Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomized AssessmeNt Study in aCE iNtolerant subjects with cardiovascular Disease (TRANSCEND) trials. Both were randomized, controlled, parallel clinical studies testing drug regimens aimed at reducing fatal and nonfatal cardiovascular events. ONTARGET had 25,620 patients enrolled and TRANSCEND had 5,926, and both included patients with and without diabetes. Researchers obtained fasting blood glucose levels for patients when they entered the trials and periodically thereafter.

"We know that diabetes is a strong risk factor for cardiovascular disease including heart failure, but these studies included patients with and without diabetes," Held said. "This was a great opportunity to evaluate a broad population of high-risk individuals and study the association between blood glucose and cardiovascular disease, regardless of the diabetic state."

Patients in the two trials were average age 67 at entry, and 69 percent were men. Thirty-seven percent had been previously diagnosed with diabetes and 3.2 percent were diagnosed with the disease at the time of entry.

Patients were assigned to five groups based on their entry fasting blood glucose levels, measured in millimoles per liter of blood, or mmol/L. The lowest group had an average fasting blood glucose of 4.6 mmol/L and the highest had an average reading of 8.5 mmol/L.

The mmol/L is the international standard unit for measuring blood glucose. In the United States, blood glucose levels are usually reported in milligrams per deciliter, mg/dL. Multiplying the number of mmol/L by 18 converts the number to mg/dl.

Researchers analyzed data from patients with an average follow-up of 2.4 years. During this time there were:

• 1,067 cardiovascular deaths
• 926 heart attacks
• 823 strokes
• 668 hospitalizations for congestive heart failure

When the researchers examined fasting blood glucose levels alone as a risk factor by adjusting for other known risk factors, they found that, for all patients, an increase of 1 mmol/L above a patient's entry glucose level increased the risk of hospitalization for congestive heart failure by 5 percent.

Similarly, a 1 mmol/L rise increased the risk of congestive heart failure hospitalization or cardiovascular death by 9 percent for all patients, by 3 percent for patients without diabetes and by 5 percent for patients with diabetes.

"Even in the normal range, our results indicate that elevated blood glucose is associated with the risk of heart failure," Held said. "You can look at blood glucose much like blood pressure or cholesterol. Even if you have normal blood glucose, there is a gradual increase in risk wherever you start on the scale. If the blood sugar is "high normal" there is a higher risk than those with "low normal fasting blood glucose levels."

He and colleagues suggested several potential mechanisms for rising glucose levels which increase the risk of developing congestive heart failure.

"Individuals with disturbances in their glucose regulation usually have more coronary artery disease, which is a well known underlying risk factor for heart failure," Held said. "That is a strong explanation for our findings but the others are more speculative and hypothetical."

Posted by dlife at 01:40 PM | Comments (2)

Joslin Researchers Discover a Surprising Culprit in the Search for Causes of Diabetic Birth Defects

Protein Makes It Possible for High Blood Glucose to Enter Embryonic Cells

March 5, 2007 (EurekAlert) - Over the past several years, Joslin Investigator Mary R. Loeken, Ph.D., and her colleagues at Joslin Diabetes Center have unlocked several mysteries behind what puts women with diabetes more at risk of having a child with birth defects. Even though those risks have decreased significantly over the years, thanks in part to advancements at Joslin, women with diabetes still are two to five times more likely than the general population to have a baby with birth defects, especially of the heart and spinal cord, organs that form within the first few weeks of pregnancy.

In past work, Dr. Loeken and her research team were able to establish through their studies in mice that the mother's high blood glucose levels are the cause of these defects. This is one of the reasons why women with diabetes who are planning a pregnancy are encouraged to have their blood glucose levels under good control prior to conception. The Joslin researchers also have shown that the damage occurs because the extra glucose in the mother's blood inhibits the expression of embryonic genes that control essential developmental processes.

Now, in this latest study done in mice, Dr. Loeken and her colleagues have discovered that the protein called glucose transporter 2 (Glut2) makes it possible for the high concentrations of glucose to get into the embryonic cells efficiently when the mother's blood glucose concentrations are high. Also involved in the study was Rulin Li, Ph.D., a former postdoctoral fellow at Joslin. The study, supported by the National Institutes of Health, will appear in the March print edition of Diabetologia and was published online by the journal on Jan. 18.

"Glut2 is a gene that we wouldn't have expected to be switched on in early embryonic development," said Dr. Loeken, Investigator in the Section on Developmental and Stem Cell Biology and Associate Professor of Medicine at Harvard Medical School. "Yet our research in mice shows that the expression of this gene in the early embryo enables the cells to absorb glucose about two to three times faster when the mother's glucose levels are elevated, while other glucose transporters would be saturated at normal glucose concentrations. This makes the embryo very susceptible to the malformations that high glucose levels cause, such as neural tube defects."

Researchers so far have identified 14 different glucose transporters, a class of proteins that sit on the membranes of cells and enable the cells to absorb glucose. Each type plays a different role in glucose uptake and is found in different cell types. "We knew that the embryo expresses a variety of glucose transporters that bring necessary glucose into the developing cells," said Dr. Loeken, "but what caught my eye was that one of them was Glut2." This protein, Dr. Loeken explained, is what is known as a high-Km glucose transporter, that is, it works efficiently only when glucose levels are high. Low-Km glucose transporters, on the other hand, become saturated at these higher levels and no longer work efficiently to get glucose into the cells.

Low Km transporters can be thought of like a narrow doorway into a room that will only allow one person to pass at a time, whereas a high Km transporter is like a wide-open door that will allow several people to pass at a time, explained Dr. Loeken. When very few people need to get through the doors at a time, the narrow doors will work just as well as the wide-open doors, but if a crowd needs to get through the doors, the narrow doors will be saturated, the wide open doors will allow the people to go through at a high rate, and the concentration of people in the room will be very high.

"After birth, the Glut2 transporter is expressed on insulin-producing beta cells of the pancreas and in the liver, the tissues that receive blood carrying high concentrations of glucose absorbed from the intestine after a meal," said Dr. Loeken. "It makes sense that Glut2 would be expressed in the pancreas where the high glucose level signals the beta cells to release insulin, and in the liver, where it signals the liver to store the glucose. In a normal pregnancy, the glucose in the mother's blood that circulates to the uterus would never be as high as the blood that flows by the pancreas and the liver, and the embryo would not be exposed to high concentrations of glucose. Therefore, Glut2 won't work any better than the other glucose transporters to absorb glucose. But glucose concentrations can be very high during a diabetic pregnancy, and if this highly efficient glucose transport is functioning, the embryo cells act like a glucose sponge, absorbing glucose at a much higher rate than normal."

Using mice that lacked Glut2 genes, which were developed by one of the study's co-authors, Bernard Thorens, Ph.D., of the Center for Integrated Genomics at the University of Lausanne in Switzerland, Joslin researchers found that only embryos carrying normal Glut2 genes developed malformations when the mothers were diabetic, whereas embryos that lacked Glut2 genes were protected from malformations during diabetic pregnancy. "This shows that the high-transport Glut2 transporter was responsible for getting higher concentrations of glucose in the cell and causing the malformations." The embryos were examined on the 10th day of gestation. The time span in the mice, Dr. Loeken explained, is comparable to about the fourth or fifth weeks of a human pregnancy, which is about the time a woman may discover that she is pregnant.

The Joslin researchers were also surprised to find that there were fewer embryos recovered on day 10 of gestation if they lacked the Glut2 genes, whether or not the mothers were diabetic, suggesting that there is a survival advantage in having the Glut2 transporter. "Recent research by our collaborator, Dr. Thorens, has shown that Glut2 is also a transporter for glucosamine, an amino sugar that serves important functions in the synthesis of proteins," said Dr. Loeken. "Since glucosamine is synthesized in the liver, which the early embryo still lacks, it must get it from its mother's circulation. Although we don't know for sure, Glut2 could be needed by the embryo for glucosamine transport."

Putting these findings together, Dr. Loeken said, "The early embryo must express Glut2 for some reason, because fewer embryos survived early development if they lacked this transporter. Perhaps it is because it is needed to transport glucosamine. However, because this transporter, which works so well after birth to allow the pancreas to produce insulin and the liver to store glucose, also makes the early embryo take up glucose very efficiently when glucose concentrations are high, as can occur during diabetic pregnancy, this explains why the embryo is so sensitive to the mother's hyperglycemia.

"While it is too early yet to give any clinical recommendations to patients based on these new findings, the research does suggest that once the glucose reaches the concentration where the Glut2 transporter functions efficiently, that is probably sufficient to cause malformations," said Dr. Loeken. "The best we can do now to prevent malformations in diabetic pregnancy is to help a woman establish good blood glucose control before she becomes pregnant, so that she will be better able make sure her glucose levels are as close to normal during pregnancy," she added.

Posted by dlife at 01:51 PM | Comments (0)

Diabetes will be a Bigger Burden than Predicted

March 2, 2005 (EurekAlert) - By 2005, prevalence of diabetes in Ontario, Canada, had already exceeded the global rate that was predicted for 2030, according to an Article published in this week's issue of The Lancet. Thus WHO's predicted 39% rise in the global rate of diabetes from 2000 to 2030 might be a gross underestimate.

The number of people with diabetes has increased substantially during the past 20 years, making it one of the most costly and burdensome chronic diseases of our time. WHO predicts that the global diabetes prevalence in adults will reach 6.4% by 2030—a 60% increase since 1995, and a 39% rise from 2000 to 2030.

Lorraine Lipscombe (Institute for Clinical Evaluative Sciences, Toronto, Canada) and colleagues used population-based data from Ontario, Canada, to examine trends in diabetes prevalence, incidence and mortality from 1995 to 2005, to determine whether diabetes prevalence rates rose beyond predicted levels during that period. The authors found a 69% increase in diabetes prevalence between 1995 and 2005. This rise has already exceeded the 60% global increase, and the 65% Canadian increase that was projected to occur in the 35 years from 1995 to 2030. They acknowledge that Ontario might have a higher diabetes rate than other developed countries because of a high rate of immigration from regions, with more susceptible populations, such as south Asia. However, they argue that if similar trends are occurring throughout the developed world, than the size of the emerging diabetes epidemic will be far greater than anticipated.

The authors conclude: "Our data are important to enable policymakers to adequately prepare for the increasing burden of diabetes on health-care resources…[accordingly] effective public-health interventions to manage and prevent obesity are sorely needed. Future research should also focus on identification of high-risk sociodemographic groups for whom specific interventions might be required."

Posted by dlife at 03:26 PM | Comments (0)

New Joslin Study Reveals How a Specific Fat Type Can Protect Against Weight Gain and Diabetes

March 1, 2007 (Joslin) - A new study from Joslin Diabetes Center may shed light on why some people can eat excessive amounts of food and not gain weight or develop type 2 diabetes, while others are more likely to develop obesity and this most common form of diabetes on any diet. The study, which used two strains of mice with differing tendencies to gain weight and develop diabetes on a high-fat diet, identified genetic and cellular mechanisms that may prevent certain mice on a calorie-dense diet from gaining weight and developing metabolic syndrome.

"Although this study was done with mice, it points out new mechanisms that may underlie the ability of genetically different mice -- and perhaps genetically different people -- to not gain much weight on high caloric diets," said lead investigator C. Ronald Kahn, M.D., an internationally recognized researcher who is Head of Joslin's Section on Obesity and Hormone Action and the Mary K. Iacocca Professor of Medicine at Harvard Medical School.

The study, published in the online edition of the Proceedings of the National Academy of Sciences on Feb. 5-9, builds upon years of research at Joslin and elsewhere on energy metabolism and the genetics of fat cells.

It has long been known that people significantly differ in their tendency to gain weight and develop metabolic syndrome, a group of conditions including hypertension, abdominal obesity, high triglycerides and glucose intolerance that can lead to type 2 diabetes. More than 60 million Americans either are obese or have metabolic syndrome, putting them at risk for type 2 diabetes and its frequent complications, including cardiovascular disease and other serious conditions. Currently 21 million Americans have diabetes and approximately one-third of them do not even know they have the disease. Formerly known as adult-onset diabetes, type 2 diabetes is occurring more frequently in young adults and even children.

Previous studies at Joslin and elsewhere have uncovered the differing functions of the two types of body fat -- white and brown. White fat, the more familiar form of fat that accumulates in the abdomen, thighs, buttocks and under the skin, stores energy for future needs, whereas brown fat or brown adipose tissue (BAT) burns energy and generates heat.

White fat, which is packed with large lipid droplets, is deposited under the skin, around internal organs and as visceral fat -- one of the most harmful forms of abdominal fat. Brown fat, on the other hand, contains small lipid droplets tucked behind tiny energy factories called mitochondria. These cells are most prevalent in the necks of infants and between the shoulder blades in mice to help their bodies generate heat, but tend to mostly disappear by adulthood. A 2005 Joslin study by Dr. Kahn and his colleagues discovered genes that control the creation of the precursor cells that give rise to brown fat cells. This latest study shows that brown fat may not disappear in all adult animals and that little collections of brown fat may account for why some mice are protected from obesity and diabetes and others are not.

This study began by exploring differences in basal energy expenditure (the amount of energy required to maintain the body's normal metabolic activity, such as respiration and maintenance of body temperature) and its role in the development of obesity and metabolic syndrome in two different genetic strains of mice: the B6 mouse and the 129 mouse. The B6 mouse is one of the most commonly used strains in metabolic research and an established model for diet-induced obesity.

When placed on a high-fat diet, the B6 mouse develops severe obesity, high blood glucose and insulin resistance with extremely high insulin levels. By contrast, the 129 mouse gains on average 30 to 50 percent less weight on either a high or low-fat diet than the B6 mouse and has been considered resistant to dietary induced obesity and glucose intolerance. In the new study, Dr. Kahn and his colleagues showed that this difference is due to the higher basal energy expenditure in the 129 mouse. When searching for the source of the energy expenditure, the researchers found unexpected clusters of brown fat cells stuck between bundles of muscle fibers in the leg of the mouse. In this case, the 129 mouse had over 100 times more brown fat in muscle than the B6 mouse.

"This site of brown fat was previously unrecognized and is certainly one of the reasons for the differences in energy expenditure between strains of mice. Now we need to see if the same is true for humans and if this could account for why some people gain weight easily and others seem to be protected against weight gain and metabolic syndrome that can lead to type 2 diabetes," Dr. Kahn said. "Finding drugs that stimulate the amount or activity of this brown fat could also lead to a new therapy for obesity and prevention of diabetes."

Other researchers participating in the study include: lead author Katrine Almind, Ph.D., formerly of Joslin and now of Novo Nordisk, Denmark; Monia Manieri and Saverio Cinti, M.D., Institute of Normal Human Morphology-Anatomy, University of Ancona, Italy; and William I. Sivitz, Ph.D., Department of Internal Medicine, University of Iowa, Iowa City.

Posted by dlife at 04:10 PM | Comments (0)