Adipocyte-specific deletion of IL-6 does not attenuate obesity-induced weight gain or glucose intolerance in mice

Martin Whitham, Martin Pal, Tim Petzold, Marit Hjorth, Casey L Egan, Julia S Brunner, Emma Estevez, Peter Iliades, Borivoj Zivanovic, Saskia Reibe, William E Hughes, Maria Findeisen, Juan Hidalgo, Mark A Febbraio

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

It has been suggested that interleukin-6 (IL-6) produced by adipocytes in obesity leads to liver insulin resistance, although this hypothesis has never been definitively tested. Accordingly, we did so by generating adipocyte-specific IL-6-deficient (AdipoIL-6-/-) mice and studying them in the context of diet-induced and genetic obesity. Mice carrying two floxed alleles of IL-6 (C57Bl/6J) were crossed with Cre recombinase-overexpressing mice driven by the adiponectin promoter to generate AdipoIL-6-/- mice. AdipoIL-6-/- and floxed littermate controls were fed a standard chow or high-fat diet (HFD) for 16 wk and comprehensively metabolically phenotyped. In addition to a diet-induced obesity model, we also examined the role of adipocyte-derived IL-6 in a genetic model of obesity and insulin resistance by crossing the AdipoIL-6-/- mice with leptin-deficient (ob/ob) mice. As expected, mice on HFD and ob/ob mice displayed marked weight gain and increased fat mass compared with chow-fed and ob/+ (littermate control) animals, respectively. However, deletion of IL-6 from adipocytes in either model had no effect on glucose tolerance or fasting hyperinsulinemia. We concluded that adipocyte-specific IL-6 does not contribute to whole body glucose intolerance in obese mice.

Original languageEnglish
Pages (from-to)E597-E604
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume317
Issue number4
DOIs
Publication statusPublished - 01 Oct 2019

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