Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 317, Issue 4, Pages E597-E604Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00206.2019
Keywords
adiposity; floxed; glucose tolerance; IL-6; obesity
Categories
Funding
- National Health and Medical Research Council of Australia (NHMRC) [APP1062436]
- NHMRC [APP1116936]
- [SAF2014-56546-R]
- [RTI2018-101105-B-I00]
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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.
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