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. It is apparent that an insulin mediated increment in skeletal muscle could be a significant determinant of in vivo rates of IMGU and therefore a defect(s) in this insulin effect could be an important cause of in vivo insulin resistance. Subjects in this study are comprised of 5 groups: 1. Non-obese, non-diabetic, non-hypertensive controls, 2. Obese non-diabetic, non hypertensive subjects 3. Obese non-hypertensive Type II diabetics (DMII) 4. Non-obese, non-hypertensive Type 1 diabetics (DMI), and 5. Non-obese, non-diabetic essential hypertensive (EH) subjects. The ability of insulin to generate increases in skeletal muscle blood flow will be assessed; the changes in cardiac output and skeletal muscle blood flow and their contribution to the disposal of an oral carbohydrate load will be characterized and quantitated; and the impact of intensive insulin therapy and weight reduction upon the above aspects of insulin induced hemodynamic changes in obese and Type II diabetics will be defined.
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