Palatinose and oleic acid act together to prevent pancreatic islet disruption in nondiabetic obese Zucker rats

Abstract

: We showed previously that 8-wk consumption of a diet containing palatinose (P, a slowly-absorbed sucrose analogue) and oleic acid (O) ameliorates but a diet containing sucrose (S) and linoleic acid (L) aggravates metabolic abnormalities in Zucker fatty (fa/fa) rats. In this study, we aimed to identify early changes in metabolism in rats induced by certain combinations of carbohydrates and fatty acids. Specifically, male Zucker fatty rats were fed an isocaloric diet containing various combinations of carbohydrates (P ; S) and fatty acids (O ; L). After 4 wk, no significant differences in body weight, visceral fat mass, plasma parameters (glucose, insulin, lipids, and adipokines), hepatic adiposity and gene expression, and adipose inflammation were observed between dietary groups. In contrast, pancreatic islets of palatinose-fed (PO and PL) rats were smaller and less fibrotic than sucrose-fed (SO and SL) rats. The abnormal ! -cell distribution and sporadic staining of active caspase-3 common to islets of linoleic-acid-fed rats were not observed in oleic-acid-fed (PO and SO) rats. Accordingly, progressive " -cell loss was seen in SL rats, but not in PO rats. These findings suggest that pancreatic islets may be initial sites that translate the effects of different combinations of dietary carbohydrates and fats into metabolic changes.

Effects of Endogenous PPAR Agonist Nitro-Oleic Acid on Metabolic Syndrome in Obese Zucker Rats

“…An issue arises as to whether the beneficial effects of OA-NO 2 observed in obese Zucker rats are attributable to the native OA. This possibility is not supported by a previous study showing that chronic administration of dietary oleic acid in obese Zucker at a dose roughly 500 times higher than that in the present study fails to affect body weight, plasma glucose and lipids despite the amelioration of pancreatic islet disruption [15]. Along this line, the benefits of omega-3 polyunsaturated fatty acid (LC omega-3 PUFA) are also seen with a substantially high dose [16].…”

Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

“…The most abundant saturated fatty acid present in the diet and serum is palmitic acid (PA, 16:0) [8], that is able to trigger lipotoxicity in β cells [9], hepatocytes [10], muscular cells [11], and so on. Contrarily, unsaturated fatty acids, including monounsaturated fatty acids (MUFA), are much nontoxic, and are proven able to combat PA induced lipotoxicity [12][13][14]. Human studies indicate that MUFA-rich diet has protective effects in cardiovascular risk, NAFLD and diabetes [15][16][17].…”

Dietary combination of sucrose and linoleic acid causes skeletal muscle metabolic abnormalities in Zucker fatty rats through specific modification of fatty acid composition

“…(38–41) Our results demonstrate that skeletal muscle and pancreatic islets (37) were an initial target tissue response to the adverse dietary interactions of the SL diet in Zucker fatty rats. Further research using other animal models is needed to determine the effect of deficient peripheral leptin signaling on the molecular mechanisms reported.…”

“…Nevertheless, 8-weeks feeding of the SL diet eventually lead to severe metabolic disorders in Zucker fatty rats, probably due to coincidental impaired insulin secretion. (1,37) Indeed, exogenous insulin administration was required for the high activity of glucose uptake and insulin signaling shown in the SL group. It is noteworthy that elevated arachidonic acid in the skeletal muscle and liver from the SL group was diminished after 8 weeks (data not shown).…”