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https://www.selleckchem.com/products/gc7-sulfate.html There were significant positive correlations between TG content and perirenal fat percentage, as well as FAS activity and perirenal fat percentage, but significant negative correlations between TG and NO levels, and FAS activity and IGF-1 level in rabbits after NCG treatment. NCG supplementation did not affect hepatic health indicators, except for serum ammonia concentrations, which were decreased in NCG-treated rabbits. Our results suggest that NCG can serve as a dietary supplement to reduce unfavorable fat deposition through inhibiting hepatic lipogenesis in animals since it appeared to have no negative effects on growth performance or hepatic health.Preliminary evidence suggested that high-fat diets (HFD) enriched with saturated fatty acids (SFA) but not monounsaturated fatty acids (MUFA), promoted hyperinsulinemia and pancreatic hypertrophy with insulin resistance. The objective of this study was to determine whether substitution of dietary MUFA within a HFD could attenuate the progression of pancreatic islet dysfunction seen with prolonged SFA-HFD. For 32 weeks, C57BL/6J mice were fed either 1) low fat diet, 2) SFA-HFD, or 3) SFA-HFD for 16 weeks then switched to MUFA-HFD for 16 weeks (SFA-to-MUFA-HFD). Fasting insulin was assessed throughout the study; islets were isolated following the intervention. Substituting SFA-to-MUFA-HFD prevented the progression of hyperinsulinemia observed in SFA-HFD mice (p less then 0.001). Glucose-stimulated insulin secretion from isolated islets was reduced by SFA-HFD, yet not fully affected by SFA-to-MUFA-HFD. Markers of β-cell identity (Ins2, Nkx6.1, Ngn3, Rfx6, Pdx1 and Pax6) were reduced, and islet inflammation was increased (IL-1β, 3.0-fold, p=0.007; CD68, 2.9-fold, p=0.001, Il-6, 1.1-fold, p=0.437), in SFA-HFD; effects not seen with SFA-to-MUFA-HFD. Switching to MUFA-HFD can partly attenuate progression of SFA-HFD-induced hyperinsulinemia, pancreatic inflammation, and im

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