Insulin Resistance in Muscle, Liver May Be Triggered by Fat Cell Defect
This is a rather complex article looking at the commonly held belief that fat cells do not have an influence on insulin resistance; rather, they are believed to suffer the effects of insulin resistance occurring in muscle and liver. This may not be so. This study used mice to initiate insulin resistance only in fat cells. Soon, changes in insulin sensitivity were also seen in the liver and muscle cells. In English, this means that the fat cells send out some (currently called “resistin”) hormone that leads to insulin resistance in other cells. And remember that insulin resistance is a major contributor to diabetes. So much for calories in, calories out being the only thing you need to worry about for weight loss!!
Nature. 2001;409(6820) Fat cells that can’t take up blood sugar normally appear to trigger the same problem in muscle and a related problem in liver, say researchers from Beth Israel Deaconess Medical Center in Boston, Massachusetts. Using a sophisticated genetic approach, the researchers wiped out the key protein in mouse fat cells that insulin tells to move glucose from the blood into the cells. Soon, muscle also ignored insulin’s orders to take up glucose, and liver disregarded insulin’s instructions to shut down the organ’s glucose production. “This paper clearly shows that fat also is important for whole-body insulin action. We think fat releases a molecule that circulates to muscle and liver and impairs insulin signaling in those cells, ” says senior author Barbara Kahn, MD, chief of the division of endocrinology and metabolism at Beth Israel Deaconess Medical Center. “For years, people have thought — and data have shown — that glucose uptake in muscle is very important for normal insulin action and to prevent diabetes. researchers thought the decreased glucose uptake into fat of obese and diabetic people was not important in causing insulin resistance,” says Kahn, also a professor of medicine at Harvard Medical School. The new study reinforces a new appreciation of fat as an endocrine organ that influences other tissues. In January, for example, other researchers identified a hormone produced by fat cells, dubbed resistin, that prompts other tissues to resist insulin. Resistin is the latest in the list of active factors known to be secreted by fat that can affect insulin action. The list includes tumor necrosis factor-alpha, fatty acids and leptin, which works through the brain to regulate feeding and metabolism. Kahn’s research group excludes all of these as likely culprits in the new paper.