Evidence for a role of somatostatin in lipid metabolism of liver and adipose tissue

Abstract

We have studied the effects of somatostatin on lipid metabolism in liver and adipose tissue of fasted mice. The animals were injected subcutaneously with 8 μg somatostatin and killed 5 min after injection. In vivo incorporation of [ 14C]acetate into triglycerides in both tissues and into hepatic cholesterol was significantly enhanced by somatostatin. Concomitantly, a decrease of triglyceride lipase activity was observed, which corresponds well with the variation undergone by cyclic AMP-protein kinase system. In addition, a marked increase of serum cholesterol levels was observed. Additionally, in vitro experiments were also performed by employing 2.4 × 10 −6 M somatostatin. The results showed that the direct effect of somatostatin on liver seems to be a decrease in acetate uptake. The results obtained with the adipose tissue were similar to those obtained in in vivo conditions. On the other hand, when somatostatin was administered in vivo, the ability to incorporate ortho[ 32P]phosphate into phospholipids was enhanced in both tissues. Likewise in the in vitro experiments with [ 14C]acetate, the somatostatin seems to act by decreasing the ortho[ 32P]phosphate uptake in liver. While in adipose tissue the somatostatin only caused a strong increase in the specific activity of phosphatidylcholine. These data demonstrate in fasted mice that somatostatin is able to counteract the lipolytic manifestations of the fasted state.