Adipocyte-specific deletion of IL-6 does not attenuate obesity-induced weight gain or glucose intolerance in mice
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.
|ISBN||1522-1555 (Electronic) 0193-1849 (Linking)|
|Authors||Whitham, M.; Pal, M.; Petzold, T.; Hjorth, M.; Egan, C. L.; Brunner, J. S.; Estevez, E.; Iliades, P.; Zivanovic, B.; Reibe, S.; Hughes, W. E.; Findeisen, M.; Hidalgo, J.; Febbraio, M. A.|
|Responsible Garvan Author||(missing name)|
|Publisher Name||AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM|
|URL link to publisher's version||https://www.ncbi.nlm.nih.gov/pubmed/31386565|