(27-02-15) Monounsaturated fatty acid enriched high fat-diets impede adipose NLRP3 inflammasome mediated IL-1â secretion and insulin resistance

Monounsaturated fatty acid enriched high fat-diets impede adipose NLRP3 inflammasome mediated IL-1â secretion and insulin resistance despite obesity.
Finucane OM1, Lyons CL1, Murphy AM1, Reynolds CM1, Klinger R2, Healy NP1, Cooke A1, Coll R3, McAllan L4, Nilaweera K4, O'Reilly M1, Tierney AC5, Morine MJ6, Alcala-Diaz JF7, Lopez-Miranda J7, O'Connor DP2, Neill LO3, McGillicuddy FC1, Roche HM8.
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Abstract
Saturated fatty acid (SFA) high-fat diets (HFD) enhance IL-1â mediated adipose inflammation and insulin resistance. However the mechanisms by which different fatty acids regulate IL-1â and subsequent effects on adipose tissue biology and insulin sensitivity in vivo remain elusive. We hypothesized that replacement of SFA for monounsaturated fatty acid (MUFA) in HFD would reduce pro-IL-1â priming in adipose tissue and attenuate insulin resistance via MUFA-driven AMPK activation. MUFA-HFD fed mice displayed improved insulin sensitivity coincident with reduced pro-IL-1â priming, attenuated adipose IL-1â secretion and sustained adipose AMPK activation compared to SFA-HFD fed mice. Furthermore, MUFA-HFD fed mice displayed hyperplastic adipose, with enhanced adipogenic potential of stromal vascular fraction and improved insulin sensitivity. In vitro, we demonstrated that the MUFA oleic acid can impede ATP-induced IL-1â secretion from LPS and SFA primed cells in an AMPK-dependent manner. Conversely, in a regression study, switching from SFA to MUFA-HFD failed to reverse insulin resistance but improved fasting plasma insulin levels. In man high-SFA, but not high-MUFA, consumers displayed reduced insulin sensitivity with elevated Pycard-1 and Caspase-1 expression in adipose tissue. These novel findings suggest that dietary MUFA can attenuate IL-1â mediated insulin resistance and adipose dysfunction despite obesity via preservation of AMPK activity.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

SOURCE: Diabetes. 2015 Jan 27. pii: db141098. [Epub ahead of print]

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