redOrbit Staff & Wire Reports – Your Universe Online
A fat recycling system contained within pancreatic beta cells helps regulate the amount of insulin they secrete, making them a potential target for new and novel ways to treat diabetes, according to new research appearing online in the journal Diabetologia.
The pancreas is the organ that produces the precise amount of insulin needed by our bodies when we eat, but when a person develops diabetes, the production of the hormone begins to slow down, the study authors explain.
A small structure inside the pancreatic beta cells, known as the lysosome, helps break down unwanted fats and proteins so that they can be re-used. The study authors call it “an intracellular recycling unit,” but when lysosomes are prevented from breaking down fat, the beta cells actually secreted more insulin.
According to study authors Gemma Pearson and Trevor Biden of the Garvan Institute of Medical Research in Australia, their work is in its earliest stages. However, thus far, the results appear promising, and could provide the medical community with a new approach for treating diabetes.
“There are many different ways fats can be used within the beta cell – so if you stop them being recycled, you force them to be used in a different way,” Pearson, a doctoral student, said in a statement Tuesday. “When you shift fats from the lysosome, you store them in other parts of the cell, and they become available to participate in various signaling pathways. One of these pathways clearly increases insulin secretion.”
“Fat molecules… can bind to proteins and activate them, causing a range of downstream events to occur,” she added. “The good thing about this particular pathway is that it is only stimulated by glucose. That limits the beta cell to producing excess insulin only to deal with food, rather than around the clock. Too much insulin circulating in the blood, or hyperinsulinaemia, can be very detrimental to health in many respects”.
Should a drug ultimately be developed in order to block fat degradation from occurring in the lysosome, Pearson explained that it would have to be fine-tuned so that it only had an effect on beta cells.
Earlier this month, researchers from the Tufts Medical Center announced that they had received a $40 million grant from the National Institutes of Health (NIH) in order to settle the ongoing debate as to whether or not vitamin D can be beneficial in treating diabetes.
According to Dr. Anastassios Pittas, who is leading the new study, there is currently little clinical evidence suggesting that the supplement could help prevent or delay type 2 diabetes. He hopes that his study, which will span several years’ time and feature 2,500 participants, will finally put an end to the debate.
“Past observational studies have suggested that higher levels of vitamin D may be beneficial in preventing type 2 diabetes, but until this large, randomized and controlled clinical trial is complete, we won’t know if taking vitamin D supplements lowers the risk of diabetes,” Dr. Pittas said in a statement.
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