High Fat Diet Compromises Pancreatic Beta Cell Function

A study published online on August 14 in Nature Medicine has identified a pathway that links high-fat diets to a series of molecular events responsible for the onset and severity of Type 2 diabetes. The team discovered that Type 2 diabetes may begin with pancreatic beta cells.The study was led by Jamey D. Marth, Ph.D., director of the Center for Nanomedicine, which is a collaboration between the University of California, Santa Barbara, and Sanford-Burnham Medical Research Institute (Sanford-Burnham). This work was primarily funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH). Co-authors include Kazuaki Ohtsubo at Sanford-Burnham and Mark Z. Chen and Jerrold M. Olefsky from the University of California, San Diego.In general, diabetes is a malfunction of the body’s ability to manage glucose, a “simple” sugar.  Glucose is the body’s main source of fuel, primarily provided by eating carbohydrate-containing food.In healthy people, pancreatic beta cells monitor the level of glucose in the blood and produce insulin to closely match rising blood sugar levels. This system to monitor and control blood sugar results in relatively stable and “normal” blood glucose levels. Type 1 diabetes results when these cells are attacked and destroyed by the bodies’ immune system. People with Type 1 diabetes must take insulin by injection to control the levels of the sugar glucose in the bloodstream.In Type 2 diabetes, beta cells are not destroyed, but this system does not function efficiently to keep blood sugar levels “normal.” High blood glucose over the long term contributes to serious increases in risk for heart disease and other so-called “complications.”  Because overweight/ obesity is the strongest risk factor for developing Type 2 diabetes, much research has focused on a potential connection between Type 2 diabetes, obesity, and diet.This study found that high levels of fat interfered with the ability of beta cells to sense and respond to blood glucose levels. Fat levels interrupted the production of a critical enzyme called GnT-4a glycosyltransferase, and in normal mice fed a high-fat diet beta-cell function was dysfunctional. Conversely, when researchers preserved the function of GnT-4a in obese mice, the onset of diabetes was prevented.Researchers hope these findings may lead to alternative treatments for Type 2 diabetes. A study published online on August 14 in Nature Medicine has identified a pathway that links high-fat diets to a series of molecular events responsible for the onset and severity of Type 2 diabetes. The team discovered that Type 2 diabetes may begin with pancreatic beta cells.The study was led by Jamey D. Marth, Ph.D., director of the Center for Nanomedicine, which is a collaboration between the University of California, Santa Barbara, and Sanford-Burnham Medical Research Institute (Sanford-Burnham). This work was primarily funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH). Co-authors include Kazuaki Ohtsubo at Sanford-Burnham and Mark Z. Chen and Jerrold M. Olefsky from the University of California, San Diego.In general, diabetes is a malfunction of the body’s ability to manage glucose, a “simple” sugar.  Glucose is the body’s main source of fuel, primarily provided by eating carbohydrate-containing food.In healthy people, pancreatic beta cells monitor the level of glucose in the blood and produce insulin to closely match rising blood sugar levels. This system to monitor and control blood sugar results in relatively stable and “normal” blood glucose levels. Type 1 diabetes results when these cells are attacked and destroyed by the bodies’ immune system. People with Type 1 diabetes must take insulin by injection to control the levels of the sugar glucose in the bloodstream.In Type 2 diabetes, beta cells are not destroyed, but this system does not function efficiently to keep blood sugar levels “normal.” High blood glucose over the long term contributes to serious increases in risk for heart disease and other so-called “complications.”  Because overweight/ obesity is the strongest risk factor for developing Type 2 diabetes, much research has focused on a potential connection between Type 2 diabetes, obesity, and diet.This study found that high levels of fat interfered with the ability of beta cells to sense and respond to blood glucose levels. Fat levels interrupted the production of a critical enzyme called GnT-4a glycosyltransferase, and in normal mice fed a high-fat diet beta-cell function was dysfunctional. Conversely, when researchers preserved the function of GnT-4a in obese mice, the onset of diabetes was prevented.Researchers hope these findings may lead to alternative treatments for Type 2 diabetes.