This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Type 2 diabetes is increasing in the US, in part, because rates of obesity have climbed 30% over the last 3 decades. The precise ways in which obesity causes type 2 diabetes and its complications are not known. Recent research indicates that fat cells secrete a large number of hormones and molecules that may directly or indirectly cause diabetes and its complications. In this project, we will examine 2 of these factors, MCP-1 and MIF. We will measure MCP-1 and MIF in fat tissue (obtained by needle biopsy under local anesthesia from underneath the skin of the abdomen) and in blood in 50 men and women with a wide range of obesity (measured by DEXA scanning) and glucose tolerance. MCP-1 and MIF will be related to glucose and insulin levels during the oral glucose tolerance test, measures of insulin secretion and action (from the intravenous glucose tolerance test) and the reactivity of blood vessels in the forearm. Overweight subjects will be studied before and after a 6-month weight loss intervention. We will also assess the effect of diabetes control on MCP-1 and MIF by studying patients with type 2 diabetes before and after 6 months of treatment with either pioglitazone (Actos) or glimepiride (Amaryl). This research will help us understand how obesity leads to type 2 diabetes and its complications and may suggest new approaches to diagnosis, prevention and treatment.
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