Abdominal fat may increase heart disease risk by promoting inflammation
A study published in the April 2005 issue of the American Journal of Physiology – Endocrinology and Metabolism (http://ajpendo.physiology.org ) reports the findings of researchers from Wake Forest University Baptist Medical Center that inflammation may explain how extra abdominal fat becomes a risk factor for cardiovascular disease.

Barbara Nicklas, PhD and colleagues studied obese postmenopausal women over the age of 50 whose waist measurements were greater than 35 inches. Postmenopausal women are at risk of developing metabolic syndrome, a cluster of factors that increase heart disease risk, that include increased abdominal obesity and elevated triglycerides and glucose. Five of the 20 participants were diabetic.

The team found that abdominal fat volume was inversely related to the expression of leptin, a protein that regulates energy metabolism. Abdominal fat volume was also inversely correlated with expression of the anti-inflammatory protein adiponectin. When abdominal subcutaneous fat tissue samples were analyzed, greater expression of the inflammation-promoting proteins interleukin 6 and tumor necrosis factor alpha, which are involved in atherosclerosis, was related to a diminished ability to respond to insulin and utilize glucose in the nondiabetic women. However, when expression of the anti-inflammatory protein adiponectin was measured, an increase was associated with an improved ability to use glucose. In the e ight participants diagnosed with metabolic syndrome, adiponectin levels were 32 percent lower than those of the remainder of the women in the study. Lead author and Wake Forest Baptist instructor in geriatric medicine Tongjian You, PhD observed, “This suggests that low production of adiponectin in subcutaneous fat is linked with an elevated risk of heart disease."

"It is well known that obesity affects nearly one-third of adults in the United States and is closely linked with heart disease, “ Dr You explained. “While we don't fully understand the link between obesity and heart disease, our study suggests that inflammatory proteins produced by fat itself may play a role."

Dr Nicklas is conducting another study to determine whether diet and exercise can modify levels of the proteins studied in the current investigation. “We need to understand more about the mechanism," she said.

Obesity
As people age, they often accumulate excess body fat. Weight gain not only creates cosmetic problems, but it also contributes to disorders such as Type II diabetes, cardiovascular disease, cartilage breakdown, sexual dysfunction, and even cancer.

A surprising number of studies report that excess serum insulin (hyperinsulinemia) is a major health problem. It appears that excess insulin promotes hypertension by impairing sodium balance. Too much insulin harms the kidneys. The vascular system is severely damaged by prolonged exposure to excess insulin. By acting as a catalyst in promoting cell growth, excess insulin increases the risk and progression of certain cancers. Excess insulin is a contributory factor to benign prostate enlargement because it promotes overgrowth of prostate cells.

For people trying to reduce body fat, excess insulin suppresses the release of growth hormone and prevents fat from being released from fat cells. High serum insulin is associated with the development of abdominal obesity and a number of health problems, including atherosclerosis and impotence. Obesity is associated with excess insulin and reduced insulin sensitivity, both risk factors for Type II diabetes.

Prior to the 1950s, scientists believed that stored fat was relatively inert and that once adipose (body fat) tissue was formed, very little metabolic activity took place in fat cells; however, it was then learned that the triglyceride stores of fat tissue are constantly turning over (Bjorntorp 1996). An enzyme called lipoprotein lipase controls the passage of fat precursors into the fat cell. The breakdown of stored fat and the passage of these breakdown products out of the fat cell are controlled by a different enzyme, hormone sensitive lipase. Insulin prevents the action of the second enzyme (hormone sensitive lipase).

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