Abstract Title:

Dietary substitution of saturated with monounsaturated fatty acids within high-fat diets attenuates hyperinsulinemia and pancreatic islet dysfunction.

Abstract Source:

Br J Nutr. 2020 Mar 3:1-22. Epub 2020 Mar 3. PMID: 32122411

Abstract Author(s):

Jessica C Ralston, Marie-Sophie Nguyen-Tu, Claire L Lyons, Aoife A Cooke, Aoife M Murphy, Aidan Falvey, Orla M Finucane, Fiona C McGillicuddy, Guy A Rutter, Helen M Roche

Article Affiliation:

Jessica C Ralston


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<0.001). Glucose-stimulated insulin secretion from isolated islets was reduced by SFA-HFD, yet not fully affected by SFA-to-MUFA-HFD. Markers ofβ-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 impairments in β-cell function. Whilst further work is required from a mechanistic perspective, dietary fat may mediate its effect in an IL-1β - AMPK dependent fashion. Future work should assess potential translation of the modulation ofmetabolic-inflammation in man.

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