Ullrich N F, Purnell J Q, Brunzell J D
Department of Medicine, University of Washington School of Medicine, Seattle 30086, USA.
J Investig Med. 2001 May;49(3):273-5.
Lipid stores in human adipose tissue are maintained primarily by incorporating lipid from circulating chylomicrons and very low density lipoproteins. Adipose tissue lipoprotein lipase (LPL) hydrolyzes triglyceride from these lipoprotein particles to facilitate their entry into adipocytes for storage. Subjects deficient in LPL still have normal adiposity, and this may result from increased adipocyte lipogenesis or from uptake of circulating lipid through alternate mechanisms. The objective of this study was to determine whether fatty acid composition of adipose tissue from LPL-deficient subjects reflects maintenance of lipid stores through increased lipogenesis or through alternate mechanisms of lipoprotein uptake.
Adipose tissue samples from LPL-deficient subjects who consume fat-restricted diets and normal subjects were analyzed for fatty acid composition by gas-liquid chromatography.
Compared with that of normal subjects, adipose tissue from LPL-deficient subjects showed an increase in 16:1 and decreases in 18:0, 18:2, and 18:3 fatty acids, whereas other nonessential fatty acid levels were not statistically different.
The reduction in essential fatty acids and increase in nonessential fatty acids in adipose tissue of those with LPL deficiency, taken together with recent data from animal studies, suggest that lipid stores in these subjects are maintained primarily through enhanced adipocyte lipogenesis.
