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

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20 Citations (Scopus)


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 (C57B1/6J) were crossed with Cre recombinase-overexpressing mice driven by the adiponectin promoter to generate AdipoIL-6(-/-) mice. AdipoIL6(-/-) 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 IIFD 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
Number of pages8
JournalAmerican journal of physiology. Endocrinology and metabolism
Issue number4
Publication statusPublished - 1 Oct 2019


  • adiposity
  • floxed
  • glucose tolerance
  • IL-6
  • obesity


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