Published studies have shown that overproduction of
very low density lipoproteins is a major factor leading to hypertiglyceridemia in
obesity. Few systematic studies of
triglyceride removal or
postheparin lipoprotein lipase activity (LPLA) in
obesity have appeared. We have examined
heparin-released
lipoprotein triglyceride hydrolase activities in 12 lean and 12 obese age- and sex-matched volunteers after overnight fasting.
Heparin doses were calculated to compensate for the disproportionality between body mass and plasma volume in
obesity.
Triglyceride hydrolase activities of hepatic (HTGLA) and extrahepatic (LPLA) origin were distinguished by in vitro inhibition of LPLA with
protamine sulfate. Incremental
heparin doses were given to each subject to determine
lipase activities under conditions of maximal release and to define sensitivity to
heparin-facilitated
lipase release. Maximal postheparin LPLA and HTGLA (u/ml plasma or u/total plasma vol) were similar in lean and obese individuals despite a nearly three-fold increase in calculated adipose tissue mass in the obese. Since adipose tissue LPLA has been reported to increase in proportion to adipocyte size, the lack of difference in maximal postheparin LPLA was expected. There was an inverse correlation between plasma
triglyceride concentration and LPLA/kg adipose tissue. These empirical observations may reflect relatively decreased
heparin-releaseable (functional) LPLA in relation to adipose organ mass in obese subjects. The mechanism of this relationship has not been established.