IL-25 directly modulates adipocyte function and inflammation through the regulation of adiponectin View Full Text


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Article Info

DATE

2022-07-12

AUTHORS

Siranart Jeerawattanawart, Pilaiwan Siripurkpong, Sittiruk Roytrakul, Pornpimon Angkasekwinai

ABSTRACT

ObjectiveThis study aimed to investigate the direct role of IL-25 in modulating adipocyte function during homeostasis and low-grade inflammation induced by lipopolysaccharide (LPS).MethodsThe 3T3-L1 preadipocyte cell lines and primary cultures of adipose-derived stromal vascular precursor cells of wild-type and IL-17RB-deficient mice were used to determine the direct function of IL-25. The expression of IL-17RB in differentiating adipocyte was determined using real-time PCR and flow cytometry analysis. The effect of IL-25 on lipid accumulation, triglyceride content, lipolysis, glucose uptake, and adipokine expression in the mature adipocytes was evaluated. IL-25 modulating the expression of inflammatory cytokines in adipocytes induced by low dose LPS was determined using real-time PCR and ELISA.ResultsThe receptor for IL-25 was up-regulated during adipocyte differentiation and IL-25 directly modulated adipocyte function by reducing lipid accumulation and triglyceride concentration and enhancing lipolysis without affecting an insulin-stimulated glucose uptake. Interestingly, IL-25 induced adiponectin secretion through the PI3K/AKT signaling pathway. In 3T3-L1 adipocytes under low-grade inflammation, IL-25 attenuated the expression of IL-6 and CCL5 through the induction of adiponectin.ConclusionOur studies suggest that IL-25 directly regulates adipocyte function by maintaining the adiponectin level during homeostasis and by alleviating inflammatory response through the regulation of adiponectin during low-grade inflammation in adipocytes. More... »

PAGES

1229-1244

References to SciGraph publications

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  • 2014-12-22. Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity in NATURE
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    https://www.ncbi.nlm.nih.gov/pubmed/35819460


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