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Papers In Press, published online ahead of print November 1, 2003
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Institute of Molecular Biology, Biochemistry and Microbiology, University of Graz, Graz, Graz 8010
Corresponding Author: rudolf.zechner{at}uni-graz.at
Lipoprotein lipase (LPL) is the only known enzyme in the capillary endothelium of peripheral tissues that hydrolizes plasma triglycerides and provides fatty acids (FA) for their subsequent tissue uptake. Previously, we demonstrated that in mice that express LPL exclusively in muscle, the absence of LPL in adipose tissue (AT) causes the deprivation of nutritionally derived FA and a drastic reduction of essential FA in stored fat. However, the animals develop essentially normal amounts of fat mass. Using this mouse model, we now investigated the nature and regulation of the metabolic response to LPL deficiency and the restricted FA import that enables maintenance of normal AT mass. We show that the rate of FA production was 1.8-fold higher in LPL-deficient AT than in control AT. The levels of mRNA and enzymatic activities of important enzymes involved in FA biosynthesis including acetyl-CoA carboxylase, fatty acid synthase, ATP-dependent citrate lyase, glucose-6-phosphate dehydrogenase and malic enzyme were induced concomitantly. Elevated plasma insulin levels, increased plasma glucose clearance and increased 14C-deoxyglucose uptake into LPL-deficient mouse fat pads indicated that glucose provided the carbon source for lipid synthesis. Leptin expression was decreased in LPL-deficient AT. The induction of de novo FA synthesis in LPL-deficient AT was associated with increased expression and processing of SREBP-1 together with an increase in INSIG-1 expression. These results suggest that in the absence of LPL in AT, lipogenesis is activated through increased SREBP-1 expression and processing triggered by decreased availability of nutrition-derived FA, elevated insulin and low leptin levels.
Revised on September 30, 2003
Accepted on October 17, 2003
Defective uptake of triglyceride-associated fatty acids in adipose tissue causes the SREBP-1c-mediated induction of lipogenesis
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