Monounsaturated Fatty Acid–Enriched High-Fat Diets Impede Adipose NLRP3 Inflammasome–Mediated IL-1β Secretion and Insulin Resistance Despite Obesity

Jan 29, 2015Diabetes

High-fat diets rich in healthy fats reduce fat tissue inflammation and insulin resistance despite causing obesity

AI simplified

Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Mice fed a monounsaturated fatty acid (MUFA) high-fat diet showed improved insulin sensitivity and reduced pro-IL-1β levels compared to those on a saturated fatty acid (SFA) high-fat diet.

Replacement of SFA with MUFA in high-fat diets is associated with reduced priming of pro-IL-1β in adipose tissue.
MUFA-fed mice exhibited less adipose IL-1β secretion and sustained activation of AMPK, which is linked to insulin sensitivity.
The MUFA oleic acid can inhibit IL-1β secretion from SFA-primed cells in a manner dependent on AMPK.
Shifting from SFA to MUFA high-fat diets improved fasting plasma insulin levels but did not reverse existing insulin resistance.
In humans, high-SFA consumers showed reduced insulin sensitivity and increased expression of pycard-1 and caspase-1 in adipose tissue, unlike high-MUFA consumers.

AI simplified

Saturated fatty acid (SFA) high-fat diets (HFDs) enhance interleukin (IL)-1β-mediated adipose inflammation and insulin resistance. However, the mechanisms by which different fatty acids regulate IL-1β and the subsequent effects on adipose tissue biology and insulin sensitivity in vivo remain elusive. We hypothesized that the replacement of SFA for monounsaturated fatty acid (MUFA) in HFDs would reduce pro-IL-1β 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-1β priming, attenuated adipose IL-1β secretion, and sustained adipose AMPK activation compared with SFA-HFD-fed mice. Furthermore, MUFA-HFD-fed mice displayed hyperplastic adipose tissue, with enhanced adipogenic potential of the stromal vascular fraction and improved insulin sensitivity. In vitro, we demonstrated that the MUFA oleic acid can impede ATP-induced IL-1β secretion from lipopolysaccharide- 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 humans, high-SFA consumers, 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-1β-mediated insulin resistance and adipose dysfunction despite obesity via the preservation of AMPK activity.

Full Text

Full text is available at the source.

View full text (PDF) ↗View full text ↗

Monounsaturated Fatty Acid–Enriched High-Fat Diets Impede Adipose NLRP3 Inflammasome–Mediated IL-1β Secretion and Insulin Resistance Despite Obesity

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief

Abstract

Full Text

Related papers

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief