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. The Insulin Resistant Syndrome provides the 'common soil' for the development of Type 2 Diabetes & Cardiovascular Disease. Insulin stimulates glucose transport via translocation of intracellular GLUT4 glucose transporters to the cell surface. IR in NIDDM is caused by profound depletion of GLUT4 in fat, but normal in muscle, suggesting that GLUT4 translocation to plasma membrane may be defective.
Aim of this hypothesis is that IR is due to defects in GLUT4 trafficking which impair insulin-mediated GLUT4 translocation in skeletal muscle. To accomplish this multiple sub-groups will be studied: healthy subjects before and during intralipid infusion, type 2 diabetics before and after intensive insulin therapy, subjects before and after short-term dexamethasone administration, and subjects before and during treatment with insulin sensitizing medications (pioglitazone/rosiglitazone). Subjects will be admitted to GCRC for medical history, physical examnation, KEG, blood pressure, laboratory blood/urine tests to determine eligibility. Qualified persons will undergo metabolic studies to characterize body compositon, energy expenditure, glucose tolerance, in vivo insulin sensitivity and glucose metabolism, insulin secretion, & lipid metabolism. Studies include OGTT, 24 hr urine, V02MAX, indirect and room calorimetry, DEXA, Leg NMR, muscle biopsy of thigh, subcutaneous fat biopsy of lower abdominal wall, and intravenous glucose tolerance test or hyperinsulinemic euglycemic infusion (clamp).
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