Induction of Uncoupling Protein 2 mRNA in -Cells Is Stimulated by Oxidation of Fatty Acids But Not by Nutrient Oversupply

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Abstract
We tested for regulation of uncoupling protein 2 (UCP-2) in -cells in response to fatty acids and glucose. A 48-h culture with oleate (0.2 mM) at 5.5 or 11 mM glucose increased UCP-2 mRNA by 30 - 60% in INS-1 cells and in rat pancreatic islets. In contrast, oleate was ineffective after coculture at 27 mM glu- cose, P < 0.05 for difference 5.5 vs. 27 mM glucose. Also, culture with palmitate (0.1 mM) stimulated UCP-2 expression at 5.5 and 11 mM, but not at 27 mM glucose. Glucose per se failed to affect UCP-2 mRNA. Oxidation of (1-14C) oleate was increased by culture with oleate; however, this increase was attenuated by glucose during coculture, P < 0.05 for coculture at 5.5 vs. 27 mM glucose. Culture with aminoimidazole-4-carboxamide-1- -D-ribofuranoside, an activator of AMP-activated protein ki- nase, decreased cellular triglycerides, increased postculture (1-14C) oleate oxidation, and increased UCP-2 mRNA. Eto- moxir, an inhibitor of carnitine palmitoyltransferase I, de- creased the oleate-induced increase in UCP-2 mRNA. Rosigli- tazone, a peroxisome proliferator-activated receptor ligand, affected neither UCP-2 mRNA nor (1-14C) oleate oxidation. Antioxidants (vitamin E and sodium selenite) did not affect oleate-induced UCP-2 mRNA. We conclude that: 1) UCP-2 mRNA is induced by fatty acid oxidation in -cells; and 2) glucose exerts a modulating effect that is coupled to inhibition of fatty acid oxidation (Endocrinology 143: 1371-1377, 2002)

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