During aging, there is an increase in body fat, especially in upper body sites, al aerobic capacity (VO2max) declines; these changes cause glucose insulin sensitivity and lipoprotein lipid profiles to deteriorate. examines the mechanisms responsible for upper body distribution of fat and its relationship to lipoprotein lipid profiles and insulin sensitivity in obese older men. Metabolic testing revealed hyperinsulinemia with normal glucose tolerance, and reduced glucose disposal rates (euglycemic clamp), indicative of an insulin resistant state. HDL-C levels were also low. Adipose tissue biopsies at abdominal and gluteal sites demonstrated fasting adipose tissue lipoprotein lipase (LPL) activity correlated directly with % body fat and inversely with insulin sensitivity. LPL activity increased in abdominal fat during euglycemic clamps but did not change in buttock fat. Basal lipolysis correlated negatively with V02Max in abdominal and directly with % body fat in buttock fat. There were significant declines in WHR, adipose tissue LPL activity, fat cell size and basal lipolysis in abdominal fat, no change in buttock fat metabolism and increases in HDL-C levels and insulin sensitivity with weight loss (WL). In men with an upper body fat distribution, there was less of an increase in beta stimulated lipolysis in abdominal fat after WL than in gluteal fat; similar results occurred in men with a lower body fat distribution. Thus there are regional differences in adipose tissue responses to beta agonists which appear specific to fat distributed in upper or lower body sites suggesting that selective differences in mobilization of triglyceride from adipose depots may be one mechanism by which body fat is deposited preferentially in a body site with age and increasing obesity. This is important since upper body fat distribution increases morbidity and mortality from cardiovascular events.