New research on belly fat/diabetes connection

Abdominal fat, the spare tire that many of us carry, has long been implicated as a primary suspect in causing the metabolic syndrome, a cluster of conditions that includes the most dangerous heart attack risk factors: prediabetes, diabetes, high blood pressure, and changes in cholesterol. But with the help of powerful new imaging technologies, a team of Howard Hughes Medical Institute (HHMI) researchers at Yale University School of Medicine has found that insulin resistance in skeletal muscle leads to alterations in energy storage that set the stage for the metabolic syndrome.

The new study, published July 16, 2007, in the Proceedings of the National Academy of Sciences (PNAS), demonstrates that insulin resistance in skeletal muscle -- caused by decreased ability of muscle to make glycogen, the stored form of carbohydrate from food energy -- can promote an elevated pattern of lipids or fats in the bloodstream that underpins the metabolic syndrome. Coauthors of the paper were from Yale and Harvard Medical School.

The subjects for the study were all young, lean, non-smoking, healthy individuals who were sedentary and matched for physical activity. Aside from insulin resistance in one cohort, these volunteers had none of the other confounding factors typically associated with obesity and type 2 diabetes, which have been thought to play a key role in the pathogenesis of the metabolic syndrome. After providing the study's subjects with two meals high in carbohydrates, magnetic resonance spectroscopy measured the production of liver and muscle triglyceride, the storage form of fat, and of glycogen, the storage form of carbohydrate. "What we found is that (insulin) sensitive individuals took the energy from carbohydrate in the meals and stored it away as glycogen in both liver and muscle," said rersearchers. In the insulin resistant subjects, the energy obtained from their carbohydrate rich meals was rerouted to liver triglyceride production, elevating triglycerides in the blood by as much as 60 percent and lowering HDL cholesterol (the “good cholesterol”) by 20 percent. "What we see," they noted, "is alterations in patterns of energy storage. An additional key point is that the insulin resistance, in these young, lean, insulin resistant individuals, was independent of abdominal obesity and circulating plasma adipocytokines, suggesting that these abnormalities develop later in the development of the metabolic syndrome."

Another key observation was that skeletal muscle insulin resistance precedes the development of insulin resistance in liver cells, and that fat production in the liver is increased. “These findings also have important implications for understanding the pathogenesis of nonalcoholic fatty liver disease, one of the most prevalent liver diseases in both adults and children” The good news, according to Shulman, is that insulin resistance in skeletal muscle can be countered through a simple intervention: diet exercise.

Bonnie - I see this pattern routinely with people who have large amounts of belly fat. These people should always be on a low glycemic load diet (meaning most of their carbs should come from fruits and vegetables). Also, because cow's milk affects insulin (skim more than 2%), they should also avoid milk (but not necessarily, plain yogurt or lowfat cheese).