Trial Information

Official Title:

Summary

A. HYPOTHESES: In older men low testosterone levels, abdominal obesity and elevated fasting insulin who are at risk for the cardiovascular complications such as heart attack and stroke. 1. Supplemental testosterone will decrease abdominal fat (visceral adominal adipose tissues (VAT), subcutaneous abdominal adipose tissue (SAT), and hepatic fat) and intramyocellular lipid in peripheral muscles(IMCL). 2. Supplemental testosterone will improve insulin sensitivity by: 1. Decreasing hepatic glucose output (HGO), a measure of central insulin resistance 2. Decreasing VAT 3. Decreasing SAT 4. Increasing adiponectin production 5. Improving peripheral glucose disposal (Rd) by reducing IMCL 6. Increasing appendicular skeletal muscle mass and basal metabolic rate B. OBJECTIVES: 1. Primary Objective: To determine the effects of supplemental testosterone to achieve testosterone levels in the upper normal physiologic range on central adipose tissue (abdominal VAT, SAT, and hepatic fat) and peripheral skeletal muscle fat (IMCL and intermyocellular fat). 2. Secondary Objectives: To determine the effects of supplemental testosterone to achieve testosterone levels in the upper normal physiologic range: 1. on hepatic glucose output (HGO) and peripheral glucose disposal (Rd) 2. on hepatic glucose synthesis from glycogen, glycerol and the Krebs cycle using [1,6-13C2C] glucose, D2O, and [U-13C3] palmitate isotope dilution studies 3. on adiponectin and apoprotein B levels 4. on basal metabolic rate (REE, R/Q) as related to changes in skeletal muscle mass Results of this study will provide greater understanding whether androgen therapy enhances insulin sensitivity by decreasing HGO, decreasing adiponectin production, improving peripheral Rd and if these desired effects are achieved, whether they are due to reductions in VAT, SAT, liver fat, IMCL or effects of augmenting muscle mass per se. Results will generate hypotheses to investigate cellular and molecular mechanisms of androgen effects in persons at risk for the Metabolic Syndrome.

Phase: Phase 2

Sponsor: University of Southern California

Overall Contacts:

Yolanda Stewart
323-226-7571 ext. 7571
cerda@usc.edu