出版社：American Society for Biochemistry and Molecular Biology
摘要：Acylation-stimulating protein (ASP) increases triglyceride (TG) storage (fatty acid trapping) in adipose tissue and plays an important role in postprandial TG clearance. We examined the capacity of ASP and insulin to stimulate the activity of lipoprotein lipase (LPL) and the trapping of LPL-derived nonesterified fatty acid (NEFA) in 3T3-L1 adipocytes. Although insulin increased total LPL activity (secreted and cell-associated; P P = 0.04; 5% of total LPL activity). Neither hormone increased LPL translocation from adipocytes to endothelial cells in a coculture system. However, ASP and insulin increased the V max of in situ LPL activity ([3H]TG synthetic lipoprotein hydrolysis and [3H]NEFA incorporation into adipocytes) by 60% and 41%, respectively ( P ⩽ 0.01) without affecting K m. Tetrahydrolipstatin (LPL inhibitor) diminished baseline, ASP-, and insulin-stimulated in situ LPL activity, resulting in [3H]TG accumulation ( P P Therefore, 1 ) the clearance of TG-rich lipoproteins is enhanced by ASP through increasing TG storage and relieving NEFA inhibition of LPL; and 2 ) the effectiveness of adipose tissue trapping of LPL-derived NEFAs determines overall LPL activity, which in turn determines the efficiency of postprandial TG clearance.
