Researchers at Mount Sinai School of Medicine have identified a common compound in the modern diet that could play a major role in the development of abdominal obesity, insulin resistance, and type 2 diabetes. The findings are published in the August 20, 2012 issue of the Proceedings of the National Academy of Sciences.
The research team, led by Helen Vlassara, MD, Professor and Director of the Division of Experimental Diabetes and Aging, found that mice with sustained exposure to the compound, methyl-glyoxal (MG), developed significant abdominal weight gain, early insulin resistance, and type 2 diabetes. MG is a type of advanced glycation endproduct (AGEs), which is produced when food is cooked with dry heat. AGEs have been found to lower the body's protective mechanisms that control inflammation.
In the study, one group of mice was fed a diet high in MG over four generations, while the control group was fed a diet without MG. Both diets had normal calories and fat. Over four generations, the mice that ate the MG started to develop early insulin resistance and increased body fat, whereas the control group did not have either of these conditions. The researchers found that MG caused a marked deficiency in protective mechanisms, such as the survival factor SIRT1 that is present in fat and controls inflammation, while enhancing the metabolism of glucose and insulin. The ingestion of MG also adversely affected the activity of an important anti-AGE receptor called AGER1, which protects SIRT1 and fights insulin resistance.
"This was a prolonged but rewarding study showing that a specific AGE compound abundant in foods, within only a few generations in mouse terms, contributes to the increase in weight gain, insulin resistance, and, diabetes, reproducing the pattern seen increasingly in humans over the last decades ," said Dr. Vlassara. "These key findings should inform how we understand and prevent the human epidemic of obesity a
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