Central s-resistin deficiency ameliorates hypothalamic inflammation and increases whole body insulin sensitivity.

Abstract:

:S-resistin, a non-secretable resistin isoform, acts as an intracrine factor that regulates adipocyte maduration, inflammatory and insulin response in 3T3-L1 cells. However, its intracellular function in vivo is still unknown. In this study, we analyze the central role of s-resistin, decreasing its hypothalamic expression using an intracerebroventricular injection of lentiviral RNAi. The data present herein support an improvement in the hypothalamic leptin and insulin signaling pathway upon s-resistin downregulation. Furthermore, hypothalamic levels of pro-inflammatory markers decrease, meanwhile those of the anti-inflammatory cytokine IL-10 increases. Interestingly, peripheral NEFA decreases alike circulating leptin and resistin levels. These data demonstrate that hypothalamic s-resistin controls fuel mobilization and adipokines secretion. Importantly, central s-resistin downregulation improves systemic insulin sensitivity, as demonstrated after an IPGTT. Interestingly, our data also indicate that s-resistin downregulation could improve hypothalamic inflammation in aged Wistar rats. Altogether, our findings suggest that hypothalamic s-resistin seems to be a key regulator of the brain-fat axis which links inflammation with metabolic homeostasis.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Rodríguez M,Pintado C,Moltó E,Gallardo N,Fernández-Martos CM,López V,Andrés A,Arribas C

doi

10.1038/s41598-018-22255-3

subject

Has Abstract

pub_date

2018-03-02 00:00:00

pages

3921

issue

1

issn

2045-2322

pii

10.1038/s41598-018-22255-3

journal_volume

8

pub_type

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