Excess fat diet causes type 2 diabetes

Researchers at the University of California, Santa Barbara, USA and the Sanford-Burnham Medical Research Institute, have discovered a link between a high-fat diet and a series of molecular events responsible for start and severity of diabetes.

Pancreatic beta cells from a mouse with a normal diet (left) and a mouse with a high-fat diet (right).

The results of this study were published online in the Journal of Natural Medicine, August 14, 2011.

Initial diagnosis always confirms that type 2 diabetics always have one thing in common is obesity . The need to understand exactly how the mechanism and diet and obesity cause type 2 diabetes, which has long been the subject of intensive medical research.

In a long-term study of mice and humans, a team of researchers, led by Jamey D. Marth, director of the Nanomedicine Center, discovered the mechanism by which type 2 diabetes is triggered by cells. Pancreatic cells, and then lead to defects, metabolism in organs and other tissues, including muscle, liver and fat (fat). Together, all of these factors have exacerbated type 2 diabetes.

" In the beginning, we were surprised to discover that the role of pancreatic beta cells contributes to the onset and severity of diabetes ," Marth said. " Observations of beta cells have contributed significantly to many signs of disease, including the expected insulin resistance. We noted the results of this study, though, laboratory studies. Other published in the past few decades alluded to this possibility . "

In healthy people, pancreatic beta cells help monitor the use and transport of glucose in the blood stream. When high blood sugar levels, such as after a meal, beta cells are supplemented with glucose and respond by secreting insulin during selection and response measurement. In turn, insulin stimulates other cells in the body to take glucose, and nutrients needed to regenerate energy.

In turn, insulin stimulates other cells in the body to take glucose, an essential nutrient for energy production.

The results of the new study intervened in two major transcription factors that turned on genes that turned on genes and turned off genes. These transcription factors, FOXA2 and HNF1A , which are necessary for the production of an enzyme called GNT-4a glycosyltransferase, modify proteins with the structure of a specific polysaccharide (polysaccharide or sugar). The storage of glucose transport in the cell membrane depends on this change, but when FOXA2 and HNF1A are not working properly, the enzyme function GNT-4a greatly reduces.

So when the researchers gave normal mice a high-fat diet, they found that the animal's beta cells could not sense and respond to blood sugar. The function of the enzyme GNT-4a can prevent the onset of diabetes, even in obese animals. Reducing glucose perception of beta cells is considered an important determinant of the onset and severity of type 2 diabetes.

" Now, we know that obesity can lead to type 2 diabetes, we can find clear interventions ," Marth said. Marth and colleagues are considering various methods to further increase the activity of beta cells and GNT-4a enzymes in humans, as a means to prevent and possibly treat type 2 diabetes.

" Identifying elements at the molecular level indicates new therapeutic goals and approaches towards developing a preventive or possibly effective treatment for type 2 diabetes, " Marth continue. " This can be done with beta cell gene therapy or with drugs that help maintain normal beta cell function ."

In the United States, more than 24 million children and adults, accounting for nearly 8% of the population, have diabetes. In adults, type 2 diabetes accounts for about 90 to 95% of all cases of diabetes diagnosis. This study is funded primarily by the National Institute of Diabetes, Digestive and Kidney Disease (NIDDK), part of the National Institutes of Health (NIH). Co-authors of this study include Kazuaki Ohtsubo working at Sanford-Burnham Medical Research Institute and Mark Z. Chen and Jerrold M. Olefsky from University of California, San Diego, USA.