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Monounsaturated Fatty Acid High‐Fat Diets Impede Adipose IL‐1β Secretion and Insulin Resistance
Author(s) -
Roche H,
Finucane O,
Lyons C,
Murphy A,
Reynolds C,
Healy N,
Tierney A,
Morine M,
AlcalaDiaz J,
LopezMiranda J,
O'Neill L,
McGillicuddy F
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.602.7
Subject(s) - endocrinology , medicine , insulin resistance , stromal vascular fraction , adipose tissue , ampk , hyperinsulinemia , oleic acid , chemistry , insulin , fatty acid , biology , phosphorylation , biochemistry , protein kinase a
Mice were placed on chow, MUFA or SFA‐HFD or switched to a MUFA‐HFD following SFA‐induced insulin resistance (IR). Glucose homeostasis was assessed. Stromal vascular fraction (SVF) was cultured ±ATP. Macrophages were LPS (10ng/ml:3h) primed, cultured ±oleic acid (OA;250µm)/palmitic acid (PA;250µm:24h), ±ATP(5mM:1h). Media was harvested to measure IL‐1β secretion. Protein AKT, AMPKα1, pro‐IL‐β were determined by immunoblot analysis. Implications of dietary fat on insulin sensitivity were examined in a sub‐cohort from the CORDIOPREV and LIPGENE studies. MUFA‐HFD fed mice displayed improved IR coincident with reduced pro and active IL‐1β, with sustained adipose pAMPK activation. We further demonstrate that monounsaturated fatty acid; oleic acid, can impede ATP‐induced IL‐1β secretion from LPS primed cells in an AMPK dependent manner, in vitro . MUFA‐HFD mice display hyperplastic adipose, with enhanced adipogenic potential of SVF and improved insulin sensitivity. Switching from SFA to MUFA‐HFD failed to reverse IR but improved hyperinsulinemia. This effect is recapitulated in man wherein high‐SFA consumers, but not high‐MUFA, display reduced insulin sensitivity according to habitual SFA:MUFA intake. These novel findings suggest that dietary MUFA can attenuate IL‐1β mediated IR and adipose dysfunction despite obesity via preservation of AMPK activity.

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