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

Citation

Rodriguez, M and Pintado, C and Molto, E and Gallardo, N and Fernandez-Martos, CM and Lopez, V and Andres, A and Arribas, C, Central s-resistin deficiency ameliorates hypothalamic inflammation and increases whole body insulin sensitivity, Scientific Reports, 8 Article 3921. ISSN 2045-2322 (2018) [Refereed Article]


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Copyright 2018 the authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

DOI: doi:10.1038/s41598-018-22255-3

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.

Item Details

Item Type:Refereed Article
Keywords:s-resistin deficiency, s-resistin downregulation, hypothalamic inflammation, insulin sensitivity, metabolic homeostasis
Research Division:Biological Sciences
Research Group:Biochemistry and cell biology
Research Field:Cell metabolism
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Fernandez-Martos, CM (Dr Carmen Fernandez-Martos)
ID Code:152589
Year Published:2018
Web of Science® Times Cited:3
Deposited By:Research Performance and Analysis
Deposited On:2022-08-22
Last Modified:2022-09-20
Downloads:1 View Download Statistics

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