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Archive - 04 - 2009

Popular Diabetes Treatment Could Trigger Pancreatitis, Pancreatic Cancer

Posted by dlife on Thu, Apr 30, 09, 12:23 PM 0 Comment

April 30, 2009 (EurekAlert) - A drug widely used to treat Type 2 diabetes may have unintended effects on the pancreas that could lead to a form of low-grade pancreatitis in some patients and a greater risk of pancreatic cancer in long-term users, UCLA researchers have found.In a study published in the online edition of the journal Diabetes, researchers from the Larry L. Hillblom Islet Research Center at UCLA found that sitagliptin, sold in pill form as Januvia, caused abnormalities in the pancreas that are recognized as risk factors for pancreatitis and, with time, pancreatic cancer in humans. Januvia is marketed by Merck & Co. Inc. Sitagliptin is a member of a new class of drugs that enhance the actions of the gut hormone known as glucagon-like peptide 1 (GLP-1), which has been shown to be effective in lowering blood sugar in people with Type 2 diabetes. The study is available at http://diabetes.diabetesjournals.org/cgi/content/abstract/db09-0058v1."Type 2 diabetes is a lifelong disease people often take the same drugs for many years, so any adverse effect that could over time increase the risk for pancreatic cancer would be a concern," said Dr. Peter Butler, director of the Hillblom Center and the study's lead investigator. "A concern here is that the unwanted effects of this drug on the pancreas would likely not be detected in humans unless the pancreas was removed and examined."An observed connection between Byetta, a drug used to treat Type 2 diabetes that is related to Januvia in its intended actions, and pancreatitis has already been reported, prompting a Food and Drug Administration warning. Amylin Corp., which markets Byetta, has suggested that since there is no known mechanism linking the cases of pancreatitis with Byetta, the association might be chance. The UCLA study suggests that there may indeed be a link between drugs that enhance the actions of GLP-1 and pancreatitis by increasing the rate of formation of cells that line the pancreatic ducts.In the study, researchers used human IAPP transgenic (HIP) rats to test both sitagliptin and metformin; metformin, a member of an older, different class of diabetes drugs in use since the 1950s, has recently been found to have anti-tumor properties. The researchers sought to determine how the drugs, both singly and in combination, affected islet disease progression in the pancreas particularly how they affected beta cells in the pancreas's Islets of Langerhans. Beta cells are responsible for releasing insulin in people with normal metabolism, but they don't produce insulin in sufficient amounts in diabetes patients. HIP rats approximate both the islets and metabolism of people with Type 2 diabetes. The drugs were tested in 40 rats for 12 weeks.The researchers found that the two drugs in combination had a synergistic effect that helped preserve beta cells, improved their function and enhanced insulin sensitivity in the test rats. With the sitagliptin alone, however, the rats had abnormally high rates of cell production in their pancreatic ducts; a few developed an abnormality known as ductal metaplasia, and one developed pancreatitis.But the metformin, trade name Glucophage, seems to counteract sitagliptin's adverse effect."The apparent protection against the unwanted actions of sitagliptin in the exocrine pancreas are intriguing and may offer a potential way of using the GLP-1 class of drugs safely," Butler said. "The protective effect may have been either by the actions of metformin to decrease blood glucose values or its recently appreciated properties as a tumor suppressive agent."Butler noted that the present study was undertaken in rats and that it is possible the adverse effects observed would not occur in humans."Given these findings, it is probably sensible to use the GLP-1 class of drugs only with metformin until other data is forthcoming," he said.

Cancer-Obesity Link Discovery by MSU Researchers Could Aid Prevention Efforts

Posted by dlife on Thu, Apr 30, 09, 12:21 PM 0 Comment

April 30, 2009 (EurekAlert) - A new link between body fat and cancer identified by a Michigan State University researcher underscores obesity's health risk and could lead to new cancer treatment and prevention strategies.Jenifer Fenton, an MSU food science and human nutrition researcher with the Michigan Agricultural Experiment Station, identified the connection between obesity and colon cancer, the third-leading killer of Americans, in part by examining tissue hormones.Working with MSU/MAES physiologist Julia Busik and biologist Fay Hansen-Smith of Oakland University in Rochester, Mich., Fenton examined a key hormone found in fat tissue and thought to promote cancer. Her conclusions are published in a study today in the journal Carcinogenesis.Leptin a fat cell-derived hormone regulating body energy is higher in obese individuals. Fenton's study is the first to demonstrate that, at higher levels, leptin induces precancerous colon cells to produce more of a growth factor that can increase blood supply to early cancer cells promoting tumor growth and cancer progression."Adipose tissue, or fat, is recognized as a significant risk factor for diabetes and heart disease, but the role of adipose tissue in cancer risk is less understood," Fenton said. "Abdominal fat in particular seems to be associated with the greatest risk for cancer. As your waist-to-hip ratio increases, so does your risk for cancer, especially breast, colon and endometrial cancers."Some 149,000 Americans will be diagnosed with colon cancer and 50,000 will die from it this year, according to the American Cancer Society. More than a million have been diagnosed with colon or rectal cancer in the U.S. as of 2006, the National Cancer Institute reported.Fenton and her team focused on colon cancer because, unlike breast or prostate cancer, colon cancer affects both genders equally, allowing them broader reach and a larger impact on cancer prevention."Trying to address the problem when someone already has a late-stage tumor is not primary prevention," Fenton said. "Our goal is to understand the active signals and mechanisms involved so we can create opportunities to prevent or interrupt cancer progression early in the process."The impact of obesity and cancer are a priority for the health of the nation," Fenton added. "Although weight loss is the ideal prevention strategy for reducing obesity as a risk factor for colon cancer, 95 percent of all people who lose weight will gain it back and often more within a year, so behavior modification as a prevention strategy is difficult and challenging. For this reason, continuing research also will include the identification of dietary compounds that may prevent or reduce colon cancer risk associated with obesity in the absence of weight loss."

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