ADIPOSE TISSUE METABOLISM AND LIPOPROTEIN LIPIDS IN OBESE OLDER MEN

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.