Starvation-induced changes of palmitate metabolism and insulin secretion in isolated rat islets stimulated by glucose

• Published in: Biochemical journal Vol. 221; no. 2; pp. 317 - 324
• Main Authors: Tamarit-Rodriguez, J, Vara, E, Tamarit, J
• Format: Journal Article
• Language: English
• Published: England 15.07.1984
• Subjects: Animals; diet-related diseases; Glucose - metabolism; Glucose - pharmacology; human nutrition; In Vitro Techniques; Insulin - metabolism; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Oxidation-Reduction; Palmitic Acid; Palmitic Acids - metabolism; Perfusion; Phospholipids - metabolism; Rats; Rats, Inbred Strains; Starvation - metabolism; Stearic Acids - pharmacology; Triglycerides - metabolism
• ISSN: 0264-6021; 1470-8728
• DOI: 10.1042/bj2210317

The influence of 48 h starvation on glucose-induced changes of palmitate metabolism and insulin release in isolated rat islets was investigated. (1) Islet insulin response to 20 mM-glucose was abolished after 48 h starvation, and it was restored by 0.25 mM-2-bromostearate, an inhibitor of fatty acid oxidation. (2) The increase in glucose concentration from 3 to 20 mM was accompanied by a 50% decrease in the oxidation rate of 0.5 mM-[U-14C]palmitate in control (fed) islets, and a concomitant increase (100%) in its incorporation into triacylglycerol and phospholipid fractions. (3) Starvation induced a higher basal (3 mM-glucose) rate of palmitate oxidation, which was resistant to inhibition by 20 mM-glucose. The latter also failed to increase palmitate incorporation into islet triacylglycerols and phospholipids. (4) 2-Bromostearate (0.25 mM) strongly inhibited the high oxidation rate of palmitate in islets of starved rats, and allowed a normal stimulation of its incorporation rate into islet lipids by 20mM-glucose. (5) The results suggest that starvation restricts islet esterification of fatty acids by inducing a higher rate of their oxidative degradation that is insensitive to regulation by glucose.