Central obesity is associated with insulin resistance through factors that are not fully understood. Researchers studied the effects of three different diets on body fat distribution, insulin sensitivity and peripheral adiponectin gene expression.

Adiponectin is secreted from fat tissue into the blood. The presence of adiponectin can result in improved insulin sensitivity and glucose tolerance, and can assist in mobilizing sugar out of the blood The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis and non-alcoholic fatty liver disease.

The study involved 11 volunteers who were the offspring of obese type 2 diabetic patients with noticeable abdominal fat deposits. The volunteers were considered insulin resistant and they maintained average hemoglobin A1c levels of greater than 6.5% without medication. All subjects underwent three dietary periods of 28 days each in a crossover design: a) diet enriched in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrates (CHO). Weight, body composition and resting energy expenditure remained unchanged during the three dietary periods. However, when patients were fed a CHO-enriched diet their fat mass was redistributed towards their abdominal region and their periphery fat accumulation decreased compared with a diet MUFA-rich and high SAT diets. Changes in fat deposition were associated with decreased levels of adiponectin after meals and lower insulin sensitivity.

The results of this study conclude a diet rich in monounsaturated fat prevents central fat redistribution and a decrease in after meal adiponectin levels. These findings support the belief that a carbohydrate-rich diet in insulin-resistant subjects exacerbates the insulin resistance. The moral of the story is: to enhance insulin sensitivity - look for a diet rich in monounsaturated fats and less dense in carbohydrates. Chances are if you've tinkered around with your food pyramid - you already knew the results of this study.

An enzyme named eIF2alpha kinase (GCN2) was shown to profoundly regulate fat metabolism in mice.

Scientists provoked the mice into starvation mode by removing a single amino acid named leucine from their diets. By doing this, the body represses fat synthesis and consumes virtually all of its stored fat. After 17 days of a leucine-deficient diet, the mice with GCN2 lost 48% of their liver mass and 97% of the fat from their abdomens. In contrast, the mice without GCN2 kept a steady liver mass and lost only 69% of abdominal body fat.

The mice without GCN2 did not lose as much fat as the mice with GCN2. Furthermore, they developed symptoms that could lead to fatty liver disease. In most events of rapid weight loss, the liver tends to take a beating. However, the fastidious weight loss in the mice with GCN2 occurred because of the repressed synthesis of new fats coupled with the depletion of stored fats. This says a lot for safe handling when it comes to teamwork.

According to research conducted by Ohio State University, conjugated linoleic acid (CLA) may help reduce body fat, but it also increases your risk for nonalcoholic fatty liver disease.

In 2003, a study showed that a 2 month supplementation of CLA lowered body mass and blood sugars in diabetics. The recent studies conducted on mice fed a CLA supplemented diet lost weight very fast, but also accumulated excessive amounts of fat in their livers - a side effect of rapid weight loss. In addition, excessive accumulation of fat in the liver is associated with insulin resistance, a factor exacerbating type 2 diabetes.

Although the recent findings were conducted on mice, CLA may or may not have a similar effect on humans. CLA has been a hot selling item in supplement stores for years. I wonder what the results would be if people who have taken CLA (the t10c12 variety) for years were to discontinue use for 4 weeks. I would be curious to see the baseline and follow-up tests for body mass, insulin sensitivity and fat accumulation in the liver. Any med students out there interested in setting-up a lab profiling hepatic function in CLA poppers?

According to a new study published in the New England Journalism of Medicine, the diabetes drug Actos may help prevent serious complications from nonalcoholic fatty liver disease. The disorder is primarily caused by being overweight. Insulin resistance, diabetes and high levels of cholesterol all contribute to the development of nonalcoholic fatty liver disease and its complications.

The study included candidates with either insulin resistance or type 2 diabetes. About half of the group took 45 milligrams of pioglitazone (brand name Actos, manufactured by Takeda Pharmaceuticals) daily for six months, while the other half took a placebo. Both groups were asked to maintain a lower calorie diet. The group taking pioglitazone saw a decrease in their levels of abnormal liver enzymes and a 54 percent reduction in liver fat, compared to the placebo group. Insulin sensitivity in the liver improved by 48 percent in the pioglitazone group, as compared to only 14 percent in the placebo group.

Current treatment for nonalcoholic fatty liver disease is aimed at lifestyle changes, such as losing weight and exercising regularly. Pioglitazone offers a resolution to improve the metabolism of blood glucose, and decreases cholesterol. Researchers were especially excited by the findings of this study because there is now a pharmacological option that might help prevent end-stage liver disease.