Obese individuals often have excessive fatty tissue in and around their abdomen, high cholesterol, elevated blood pressure, and an inability to utilize insulin or blood sugar (insulin resistance). These symptoms that put them at high risk for coronary
heart disease and stroke. The molecular mechanisms linking obesity and insulin resistance are the subject of intense investigation and are not completely understood.
In a study conducted in Kobe University, Japan, the concentration of monocyte chemoattractant protein-1 (MCP-1) in fat cells and blood plasma was increased both in genetically obese diabetic mice as well as healthy mice in which obesity had been induced by feeding them a
high-fat food diet. Mice expressing an MCP-1 transgene in fat cells manifested insulin resistance, increased infiltration of macrophages into fatty tissue, and high cholesterol levels.
The said effects were not observed in mice lacking MCP-1 even when fed with the high-fat diet. The results suggest that MCP-1 links obesity and
insulin resistance by the induction of an inflammatory response (macrophage infiltration) in fatty tissue. The authors also suggest that blocking the interaction of MCP-1 and its receptor, known as CCR2, might provide the basis for development of new therapies for this syndrome.
