The Composition of Dietary Fat Directly Influences Glucose-Stimulated Insulin Secretion in Rats

Abstract

Acute elevations of plasma free fatty acid (FFA) levels augment glucose-stimulated insulin secretion (GSIS). Prolonged elevations of FFA levels reportedly impair GSIS, but no one has previously compared GSIS after prolonged exposure to saturated or unsaturated fat. Because the GSIS of rats consuming Lard diets consistently exceeded that of the Soy group, we also assessed responses after 48-h infusions of lard or soy oil. Again, lard oil exhibited greater insulinotropic potency. These data indicate that prolonged exposure to saturated fat enhances GSIS (but this does not entirely compensate for insulin resistance), whereas unsaturated fat, given in the diet or by infusion, impairs GSIS. Inferences regarding the impact of fatty acids on GSIS that are based on models using unsaturated fat may not reflect the effects of saturated fat.

Soybean oil treatment impairs glucose-stimulated insulin secretion and changes fatty acid composition of normal and diabetic islets

“…The appearance of the long-chain C22:1 fatty acid and the impairment of insulin secretion were consistent with previous studies reporting that the increase of the number of carbons has a negative effect on insulin release by increasing β-cell KATP channel activity and inducing the uncoupling of β-cell oxidative phosphorylation [7,16]. Other studies show that saturated fatty acids are associated with a higher risk of type 2 diabetes [18,20,24]. In our study, the decrease in saturated fatty acids observed in islets isolated from treated W rats may represent an attempt of animals to circumvent the β-cell secretory deficiency.…”

“…Accumulating evidence suggests that chain length, spatial conformation and degree of saturation of FFAs profoundly influence the insulinotropic potency and the stimulation of KATP channel activity [7,16,[18][19][20]. Studies focussed on fatty acids chain length reported that the increase of the number of carbons has a negative effect on insulin release by increasing β-cell KATP channel activity and induces uncoupling of β-cell oxidative phosphorylation [7,16,18].…”

“…Studies focussed on fatty acids chain length reported that the increase of the number of carbons has a negative effect on insulin release by increasing β-cell KATP channel activity and induces uncoupling of β-cell oxidative phosphorylation [7,16,18]. Concerning the spatial conformation, trans fatty acids induce better results in insulin release than the corresponding cis isoforms [21].…”

“…Previous studies suggested that a MUFA-enriched diet may be useful in the treatment of patients with glucose intolerance or type 2 diabetes [23]. However, studies showing a positive association between saturated fatty acids and a higher risk of type 2 diabetes are more consistent [18,20,24]. It has been shown that palmitic acid (C16:0) is toxic to β-cells, even at moderate levels [19,25].…”

Interaction between specific fatty acids, GLP-1 and insulin secretion in humans

“…In humans, no differences in insulin responses were found after meals [39,40] or longterm diets [41], which were high in monounsaturated or saturated fatty acids. Some studies have reported greater stimulation of insulin secretion after diets high in saturated fatty acids in subjects with Type II diabetes [42] and normal rats [43] but others have reported a more pronounced effect with polyunsaturated fatty acids [44]. A comparable pattern of glucose-stimulated insulin response to that observed in our study was seen when similar oils were given as a mixed test meal followed by a glucose drink [45].…”