Effects of somatostatin on the insulin- and gastric inhibitory polypeptide-stimulated fatty acid esterification in rat adipose tissue.

Relations exist between insulin, somatostatin (S) and gastric inhibitory polypeptide (GIP) for the reciprocal control of their secretion but also for their role in lipid metabolism. In the present experiment, we studied the effects of somatostatin on fatty acid incorporation into epididymal adipose tissue (FIAT) of Wistar rats when it was stimulated by insulin and GIP. Cyclic somatostatin-14 was used at physiological (S1 : 50 pg/ml, S2 : 200 pg/ml) and supraphysiological (S3 : 666 pg/ml) concentrations whereas insulin and GIP were used at postprandial levels (100 microU/ml and 2 ng/ml respectively). Results were expressed as percent of basal incorporation (without any hormones). Somatostatin inhibited basal FIAT at all concentrations and totally abolished the insulin-stimulated FIAT (from 106.4 +/- 2.3 per cent with insulin alone to 92.6 +/- 2.5 per cent with S3, P less than 0.001). GIP enhanced the insulin-stimulated FIAT from 106.4 +/- 2.3 per cent to 113 +/- 3.0 per cent (P less than 0.01). On the contrary, when somatostatin was added with GIP and insulin, FIAT decreased to 102.3 +/- 2.5 per cent for S1 (P less than 0.01) and to 98.2 +/- 2.6 per cent for S3 (P less than 0.001). These results indicate that somatostatin totally inhibits the fatty acid esterification induced by insulin and in the same proportions that induced by insulin associated with GIP. Somatostatin is not only an inhibitor of the secretion of these hormones but also a regulator of their biological action in adipose tissue.