Research
October 8, 2009 (EurekAlert) - Attention weekend warriors: the simple act of exercise and not fitness itself can convince you that you look better, a new University of Florida study finds.People who don't achieve workout milestones such as losing fat, gaining strength or boosting cardiovascular fitness feel just as good about their bodies as their more athletic counterparts, said Heather Hausenblas, a UF exercise psychologist. Her study is published in the September issue of the Journal of Health Psychology.
"You would think that if you become more fit that you would experience greater improvements in terms of body image, but that's not what we found," she said. "It may be that the requirements to receive the psychological benefits of exercise, including those relating to body image, differ substantially from the physical benefits."
The study by Hausenblas and graduate student Anna Campbell is the first to systematically analyze the wide-ranging effects of exercise on body image by examining all intervention studies on the subject until June 2008. From the 57 publications, the researchers found conclusively that exercise buffed up the way people see their bodies regardless of the actual benefits, but the results varied.
Negative body image has grown to almost epidemic proportions in the past 20 years, with as many as 60 percent of adults in national studies saying they don't like the way their bodies look, Hausenblas said.
Americans spend billions of dollars a year for products designed to change their body size and shape, including diet pills and various cosmetic procedures, she said.
"Body dissatisfaction is a huge problem in our society and is related to all sorts of negative behavior including yo-yo dieting, smoking, taking steroids and undergoing cosmetic surgery," she said. "It affects men and women and all ages, starting with kids who are as young as five years old saying they don't like how their bodies look."
The psychological advantages of exercise have been less explored, including the reduction of depression or confidence in body image, compared with the well-researched and understood physical benefits, she said.
The study found no difference in body image improvement between people who met the American College of Sports Medicine guidelines by exercising at least 30 minutes a day five days a week and those who did not, Hausenblas said. The guidelines are considered the minimum amount of exercise needed to receive the health related benefits of physical activity, she said.
"We would have thought that people exercising this amount would have felt better about their bodies than those who did not work out as much," she said.
In other results, the study showed slightly larger benefits from exercise in terms of improving body image for women than men, Hausenblas said.
"We believed the gap would be much bigger, but what could be coming into play is the rise of body image issues among men," she said. "We're seeing more media portrayals of the ideal physique for men rather than the overriding emphasis on women we did in the past."
Age presented another difference, with older people most likely to report enhanced body images from exercise, Hausenblas said. The gap may be explained by the older generation having more concerns about their body image than young people, who tend to exercise more, she said.
While the frequency of exercise mattered for boosting body perceptions, there were no differences for the duration, intensity, length or type of exercise, the study found.
"People who say they have high body dissatisfaction tend to exercise the least, so we wanted to take it a step further and see whether exercise causes people's body image to improve," she said.
Kathleen Martin Ginis, a kinesiology professor at McMaster University in Ontario, Canada, and exercise expert, praised the research. "This is an important study because it shows that doing virtually any type of exercise, on a regular basis, can help people feel better about their bodies," she said. "With such a large segment of the population dissatisfied with their physiques, it's encouraging to know that even short, frequent bouts of lower intensity exercise can improve body image."
October 7, 2009 (EurekAlert) - One of the biggest mysteries about diabetes is why specialized cells in the pancreas stop secreting insulin, which the body needs in order to store glucose from food. A team from the Children's Hospital of Eastern Ontario (CHEO) Research Institute has identified a protein that inhibits insulin production in mice - work that offers a new way of understanding, and perhaps of one day treating, both Type 1 and Type 2 diabetes.A study to be published today in the leading international journal Cell Metabolism describes how a research group led by Dr. Robert Screaton, who holds the Canada Research Chair in Apoptotic Signaling at the University of Ottawa, used sophisticated genetic engineering to remove or 'knock out' the Lkb1 gene from beta cells of laboratory mice. The result was an increase in both the size and number of beta cells, as well as greater amounts of insulin stored and released by the cells.
Importantly, the improved beta cell function lasted for at least five months, even in mice fed a high-fat diet designed to mimic the high caloric intake associated with Metabolic Syndrome and Type 2 diabetes in humans.
"We were surprised by the impressive accumulation of Lkb1 in beta cells of diabetic mice, which suggested that Lkb1 might contribute to their impaired function. After removal of the Lkb1 gene, the beta cells grow larger, proliferate more, and secrete more insulin. It's a one-stop shop for the much needed insulin", said Dr. Screaton.
"The knockout mice on a high-fat diet have lower blood glucose. If this observation is confirmed in humans, it may give us another clue into the development of Type 2 diabetes, and perhaps new treatment options".
"Type 1 and 2 diabetes, already common diseases, are showing disturbingly steady growth in incidence. The two conditions are among Canada's, and indeed the globe's, greatest health challenges," said Dr. Alex MacKenzie, CEO of the CHEO Research Institute and a physician who treats children with diabetes at CHEO. "The findings of Dr. Screaton's team introduce a novel and unanticipated potential therapeutic avenue for this costly and serious condition. It is some of the most important work to come out of our institute."
October 6, 2009 (EurekAlert) - Restrictions on fast-food chain restaurants in South Los Angeles are not addressing the main differences between neighborhood food environments and are unlikely to improve the diet of residents or reduce obesity, according to a new RAND Corporation study.
Researchers from RAND Health found that the South Los Angeles region has no more fast-food chain establishments on a per capita basis than other parts of the city, but rather many more small food stores and other food outlets.
Those outlets are more likely to be the source of high-calorie snacks and soda consumed substantially more often by residents of South Los Angeles as compared to other parts of the city, according to the study published online by the journal Health Affairs.
"The Los Angeles ordinance may have been an important first by being concerned with health outcomes, but it is not the most promising approach to lowering the high rate of obesity in South Los Angeles," said Roland Sturm, the study's lead author and a senior economist at RAND, a nonprofit research organization. "It does not address the main differences we see in the food environment between Los Angeles neighborhoods nor in the diet of residents."
The Los Angeles City Council in August 2008 approved a ban on opening or expanding fast-food restaurants in an area of the city known as South Los Angeles. The ordinance focused on fast food restaurants characterized by "excessive signage, little or no landscaping, large expanses of surface parking, drive-through windows, multiple driveways, parking lots fronting the street" and argued that the low-income region had a higher concentration of fast-food establishments than more-affluent sections of the city.
But an analysis by Sturm and study co-author Dr. Deborah Cohen found that South Los Angeles actually has a lower concentration of fast-food chain restaurants than other parts of the city.
Researchers found there were about 19 fast-food chain restaurants per 100,000 residents in South Los Angeles, while there were 29 per 100,000 people in affluent West Los Angeles and 30 per 100,000 residents for all of Los Angeles County. There are significantly fewer restaurants of any type per person in South Los Angeles compared to Los Angeles County overall, according to the study.
In contrast, the density of small food stores was about double that of the county average and more than three times the number in West Los Angeles. This was partially offset by a lower density of large supermarkets in South Los Angeles.
Researchers also analyzed information from a survey of 1,480 adults from across Los Angeles County that asked residents about their food purchases and habits of eating out. The results showed that adults in South Los Angeles consumed significantly more "discretionary" calories from sugary or salty snacks and soft drinks compared with residents of wealthier neighborhoods.
Residents of South Los Angeles and residents of more-affluent areas reported eating similar amounts of fruits and vegetables each day and had fairly similar levels of physical activity, although residents of South Los Angeles did report watching more television.
Researchers say their work suggests that focusing on the sources of snack calories would address the differences between South Los Angeles and other parts of Los Angeles better than the current ban on new fast-food establishments.
"The ubiquitous availability of food can be overwhelming and stimulate hunger and cravings for food, regardless of whether an individual has a physiological need for nutrition," Cohen said. "Research has made it clear that frequency and saliency of food cues in the environment, the type of foods available, and the portion sizes served, are key issues that effective policies need to address."
One of the goals of the Los Angeles regulation is the creation of more sit-down restaurants, but in terms of diet, this is not necessarily an improvement, according to researchers.
"There is a misconception that sit-down restaurants provide 'healthier' food and are less likely to lead to obesity," Sturm says. "However, when we looked at some common offerings, an average lunch sandwich in a sit-down restaurant had more than the combined calories of three Big Mac hamburgers; many dinner choices have over 2,000 calories and cover the energy needs for a full day. And that does not even include possible appetizers or desserts."
The study also found that residents of South Los Angeles and those from wealthier areas reported eating out in restaurants at about the same frequency, although South Los Angeles residents are more likely to purchase items from a food cart or mobile vender and less likely to eat in a sit-down restaurant.
While residents of South Los Angeles and those from more-affluent areas seem to shop at similar types of stores, there was one dramatic difference -- many South Los Angeles residents walk or take public transit to the market, something seldom done in higher-income areas.
October 6, 2009 (
Sirtuins are expressed virtually everywhere throughout the body and until now, little has been known about what tissues mediate resveratrol's beneficial effects. Knowing where in the body the beneficial effects of activated sirtuins are mediated could help in the development of more effective targeted diabetes medications.
"We know that sirtuins are expressed in parts of the brain known to govern glucose metabolism, so we hypothesized that the brain could be mediating resveratrol's anti-diabetic actions," said Roberto Coppari, PhD, of the University of Texas Southwestern Medical Center and co-author of the study. "To test the hypothesis, we assessed the metabolic consequences of delivering resveratrol directly into the brain of diabetic mice. We found that resveratrol did activate sirtuins in the brain of these mice which resulted in improving their high levels of blood sugar and insulin."
"These findings may lead to new strategies in the fight against type 2 diabetes," said Coppari. "By knowing that the brain mediates resveratrol's anti-diabetic actions, industry can now focus on developing sirtuin activators that directly target the brain. When orally-delivered, these drugs will likely improve diabetes without affecting the other organs in which activation of sirtuins may not always be beneficial."
Other researchers working on the study include Giorgio Ramadori, Laurent Gautron, Teppei Fujikawa, Claudia Vianna and Joel Elmquist of the University of Texas Southwestern Medical Center in Dallas, Tex.
The article, "Central administration of resveratrol improves diet-induced diabetes," will appear in the December 2009 issue of Endocrinology.
October 2, 2009 (Newswise) - Obesity and type 2 diabetes are inextricably linked, but Cornell biochemist and geneticist Ling Qi is working to break that connection. Finding just the right gene could do it, says Qi, an assistant professor of nutritional sciences in Cornell's College of Human Ecology.In his Cornell laboratory, Qi is looking at two mechanisms that could potentially impact obesity and diabetes: the endoplasmic-reticulum (ER) stress response, which affects the expression of proteins, and the inflammation status of fat tissues. As a postdoctoral fellow at the Salk Institute for Biological Studies in La Jolla, Calif., before he joined the Cornell faculty last summer, Qi found that some of the mice in his lab became obese on a Western-diet regimen while others did not. In other cases, some developed diabetes after gaining weight on a Western diet but some didn't. The question is: Why?
Qi is trying to find out. In his Cornell laboratory, he is looking at two mechanisms that could potentially impact obesity and diabetes: the endoplasmic-reticulum (ER) stress response, which affects the expression of proteins, and the inflammation status of fat tissues.
Diabetes occurs when certain molecules malfunction in the signaling pathway, an event Qi finds fascinating.
"In the case of ER stress response, there's a DNA-binding protein that drives gene expression in cells; it's a key element for cells to respond to environmental cues -- in this case to glucose changes," explains Qi, who just won the 2008 Rosalinde and Arthur Gilbert Foundation/American Federation for Aging Research (AFAR) New Investigator Awards in Alzheimer's Disease as well as a Junior Faculty Award from the American Diabetes Association..
Little is known about this protein, so Qi and his research associate, postdoctoral fellow, graduate student, technician and an undergraduate student in his lab are seeking to learn more. Their studies in inflammation status also are proving to be promising, because it is now recognized that fat is a lot more than a storage depot for energy; it is an active organ that secretes hormones, many of which affect obesity and insulin sensitivity.
In a 2006 Science paper he published and in a manuscript he recently submitted, Qi describes how he demonstrated that altering fat-cell function changes obesity and insulin.
"Fat tissue has become the center of the metabolic control. If you change the fat mass, you will likely see the changes in insulin sensitivity of the whole system," says Qi, who has also published in the journal Nature.
When fat cells become bigger, immune cells infiltrate into the fat tissues. Qi wants to know what the functions of these macrophages are and what signals the recruitment of these macrophages. Such studies are so fundamental that they could one day reveal the origins of obesity and diabetes.
"It is crucial to understand the mechanism underlying the etiology of obesity and diabetes to develop well-targeted, efficient pharmacological interventions," Qi explains. "Working on genetic control of obesity and diabetes is very challenging but quite rewarding."
October 2, 2009 (Newswise) - Nutrition scientists led by Young-Cheul Kim at the University of Massachusetts Amherst have identified the molecular pathway that allows foods rich in soy bioactive compounds called isoflavones to lower diabetes and heart disease risk. Eating soy foods has been shown to lower cholesterol, decrease blood glucose levels and improve glucose tolerance in people with diabetes.According to Kim, the study shows that "what we eat can have tremendous impact on health outcomes by interacting with certain genes. Recent research also suggests that diet can even change the copy number of a certain gene, leading to biological changes."
Soy is the most common source of isoflavones in food. In experiments with mouse cells, Kim, a molecular nutrition researcher who studies how fat cells develop in the body, and colleagues, focused on daidzein, one of the two main isoflavones found in soy. Many epidemiological observations and human clinical studies have shown that adding soy to one's diet is associated with lower diabetes risk and improved insulin sensitivity, as well as lower cardiovascular disease risk, Kim notes. However, until now the direct target tissue and molecular pathways by which soy exerts its anti-diabetic effects was not clearly understood.
Kim and colleagues at Southern Illinois University, with others at the universities of Tennessee and Florida, had earlier found that dietary isoflavones reduced the severity of diabetes in an animal model of the disease by increasing the activity of certain transcription regulators in the fat tissue. For the current study, they hypothesized that daidzein and its metabolite, equol, are part of this activation process.
They found that daidzein and equol enhanced adipocyte differentiation, or the formation of fat cells, through activation of a key transcription regulator, the same receptor that mediates the insulin-sensitizing effects of anti-diabetes drugs. Thus, daidzein and equol daidzein and equol seem to work in a similar manner as anti-diabetic drugs currently in the market. Their findings are reported in a September online version of the Journal of Nutritional Biochemistry.
"Our results suggest that soy isoflavones exert anti-diabetic effects by targeting fat cell-specific transcription factors and the downstream signaling molecules that are important for glucose uptake and thus insulin sensitivity," Kim notes. "The new findings help us to understand the cellular mechanisms." That is, how these biologically active compounds in soy interact to regulate and initiate metabolic and biological functions.
Results demonstrate that daidzein and equol enhance adipocyte differentiation by activating a specific receptor. The downstream responses include increased expression of three proteins, resulting in enhanced glucose uptake and insulin sensitivity.
"Although some details remain to be worked out, our data provide an additional molecular basis for the mechanism of insulin-sensitizing action by soy isoflavones," says Kim. "These new findings help fill a critical gap between epidemiological observations and clinical studies on the anti-diabetic benefits of dietary soy."
Future studies will extend the work to primary cultures of human cells through collaboration with researchers at Pioneer Valley Life Science Institute and Baystate Medical Center in Springfield. If replicated, studies can move on to further work in whole body systems.
October 2, 2009 (Newswise) - In a study of adults who survived cancer as children, St. Jude Children's Research Hospital investigators found that many survivors lead sedentary lifestyles and are more likely to be less physically active than their siblings. Childhood cancer survivors are at greater risk of diabetes, obesity and heart disease than the rest of the population.Cancer treatments such as cranial radiation can damage the hypothalamus and pituitary; the result is an abnormal metabolism, which increases the risk of obesity and diabetes. Also, chemotherapy with the drug anthracycline increases the risk of heart disease; and radiation to the body can cause blood vessels to become less pliant.
"Physical activity is a key step that survivors can take to reduce the health risk of these effects," said Kiri Ness, Ph.D., of the Epidemiology and Cancer Control department at St. Jude. "Medical center programs to encourage physical activity in adult survivors could help significantly. However, one problem is that researchers have not firmly established the factors that affect cancer survivors' participation in physical activity."
To understand those factors, Ness and her colleagues drew data from the Childhood Cancer Survivor Study (CCSS), a St. Jude-led consortium of 30 centers in the United States and Canada. The study gathers extensive data from the participating centers on more than 20,000 childhood cancer survivors who received diagnoses between 1970 and 1986.
The researchers analyzed 9,301 CCSS participants' answers to questions about their physical activity; as a comparison, the scientists also analyzed the same answers given by 2,886 siblings. The investigators compared those answers with information on physical activity obtained from a massive health survey database maintained by the Centers for Disease Control and Prevention.
Because of the cohort's large size, the researchers explored the relationships between health and exercise in all the different types of cancer. Also, because the cohort is older, Ness and her colleagues were able to investigate adult behaviors and relate them back to the data on their childhood cancers.
"Thus, we could identify who has the highest risk of having an inactive lifestyle," Ness said. "Knowing this makes it possible to begin to design interventions that will address the problems that put survivors at most risk."
The researchers found that the cancer survivors showed significant deficits in physical activity compared to their siblings. Survivors were less likely than their siblings to meet physical activity guidelines and more likely to report inactive lifestyles.
"It was particularly striking that 23 percent of the survivors reported that they were completely inactive over the previous month, compared with 14 percent of their siblings," Ness said.
The researchers' analysis revealed that survivors of medulloblastoma, a type of brain tumor, and osteosarcoma, a type of bone cancer, reported the most inactive lifestyles. Also associated with inactivity were treatments with cranial irradiation or amputation as well as other factors, including gender, race, age and education level. If survivors smoked, were underweight or obese or had suffered from depression, they were also prone to inactivity.
Ness hopes the findings will spark more research on the role of fitness in cancer survivors' quality of life, as well as the design of facilities and programs to encourage good fitness in survivors.
"For instance, if we know that patients with medulloblastoma who received cranial irradiation are at a high risk for having inactive lifestyles as adults, we might design a rehabilitation program they can undergo while they are still children to encourage physical activity as they age," she said.
Ness and her colleagues plan to investigate whether programs to encourage exercise in both children and adult childhood cancer survivors can help them avoid obesity, diabetes and other health problems.
October 2, 2009 (Newswise) - Mathematicians at Michigan Technological University have developed powerful new tools for winnowing out the genes behind some of humanity's most intractable diseases.With one, they can cast back through generations to pinpoint the genes behind inherited illness. With another, they have isolated 11 variations within genes-called single nucleotide polymorphisms, SNPs or "snips"-associated with type 2 diabetes.
"With chronic, complex diseases like Parkinson's, diabetes and ALS [Lou Gehrig's disease], multiple genes are involved," said Qiuying Sha, an assistant professor of mathematical sciences. "You need a powerful test."
That test is the Ensemble Learning Approach (ELA), software that can detect a set of SNPs that jointly have a significant effect on a disease.
With complex inherited conditions, including type 2 diabetes, single genes may precipitate the disease on their own, while other genes cause disease when they act together. In the past, finding these gene-gene combinations has been especially unwieldy, because the calculations needed to match up suspect genes among the 500,000 or so in the human genome have been virtually impossible.
ELA sidesteps this problem, first by drastically narrowing the field of potentially dangerous genes, and second, by applying statistical methods to determine which SNPs act on their own and which act in combination. "We thought it was pretty cool," Sha said.
To test their model on real data, Sha's team analyzed genes from over 1,000 people in the United Kingdom, half with type 2 diabetes and half without. They identified 11 SNPs that, singly or in pairs, are linked to the disease with a high degree of probability. Their work was published in the journal Genetic Epidemiology available online at http://www3.interscience.wiley.com/journal/117890704/abstract?CRETRY=1&S... .
ELA is used to compare the genetic makeup of unrelated individuals to sort out disease-related genes. The team has also developed another approach, which uses a two-stage association test that incorporates founders' phenotypes, called TTFP, that can examine the genomes of family members going back generations.
"In the past, researchers have dealt with the nuclear family, parents and children, but this could go back to grandparents, great-grandparents . . . as far back as you want."
The team has published their findings in the European Journal of Human Genetics. An abstract is available at www.nature.com/ejhg/journal/v15/n11/abs/5201902a.html .
Now that they've developed the software, the analysis is relatively simple, says Sha. But getting the genetic data to work on is not. "We don't have the data sets yet to work with," she says, clearly frustrated. "That's the problem with having no medical school."
Those who do have data sets, however, can use the team's software to help find the genes associated with a panoply of illnesses. ELA is available in Windows and Linux versions at www.math.mtu.edu/~shuzhang/software.html, and TTFP is available by request.
September 28, 2009 (EurekAlert) - Richard Feinman, PhD, professor of biochemistry and of family medicine at SUNY Downstate Medical Center in Brooklyn, New York, will speak at the annual conference of the European Association for the Study of Diabetes (EASD) on October 2, 2009. EASD is holding its annual conference September 28 - October 2 in Vienna, Austria.Dr. Feinman will be one of four speakers covering the topic, Controversies in Dietary Strategies in the Treatment of Diabetes.
According to Dr. Feinman, it has been scientifically documented that carbohydrate consumption raises blood glucose and there is no disagreement that diabetes is a disease of carbohydrate intolerance. "There really is no controversy about the science," Dr. Feinman explains. "It's as simple as this: An increase in dietary carbohydrate will raise HbA1c, which in turn will raise the risk of microvascular complications, and this is science we all agree on."
"That being said," he adds, "the controversy may indeed be whether or not we are getting good advice from our healthcare professionals, but that is out of my area - I will be at the conference in Vienna to explain the science."
Dr. Feinman's presentation will take place at the Messe Wien in van Swieten Hall on October 2, 2009.
September 28, 2009 (Newswise) - Dr. Pinchas Cohen, professor of pediatrics at the David Geffen School of Medicine at UCLA, has won a $2 million Transformative R01 (T-R01) award from the National Institutes of Health (NIH) to fund his innovative research on mitochondrial dysfunction.Considered the power generators of the cell, mitochondria convert oxygen and nutrients into chemical energy for the cell that fuels metabolic activities.
Mitochondrial dysfunction has been associated with many diseases, including Alzheimer's, cancer and diabetes, although its exact role in the development of these diseases remains controversial.
The new T-R01 program was specifically created under the NIH Roadmap for Medical Research to support exceptionally innovative, high risk, original or unconventional research projects that have the potential to transform a field of science. The selected projects tend to be inherently risky, but if successful, can profoundly impact a broad area of biomedical research.
Cohen's bold proposal will test the paradigm-shifting hypothesis that previously unrecognized molecules, he dubbed "mitochondrial-derived peptides" (MDPs), play an earlier unappreciated role in the regulation of cellular and organismal function, and that disregulation of MDPs is important in disease development.
Likewise, understanding the role of MDPs may lead to development of new therapeutic and diagnostic targets. Since Alzheimer's, cancer and diabetes particularly affect the elderly, these findings could have a significant impact as the world's aging population continues to grow. The first of these agents, which Cohen named "small humanin-like peptides," have already demonstrated promise in animal models of diabetes and cancer.
Cohen was one of only 42 researchers nationwide chosen for the T-R01 award. He also serves as chief of endocrinology at the Mattel Children's Hospital UCLA, as well as co-director of the UCSD/UCLA Diabetes and Endocrinology Research Center.