Adipocyte-specific deletion of IL-6 does not attenuate obesity-induced weight gain or glucose intolerance in mice
Research output: Contribution to journal › Article › peer-review
Colleges, School and Institutes
- Garvan Institute of Medical Research
- Medical University of Vienna
- Baker Heart and Diabetes Institute
- University of New South Wales
- Universitat Autonoma de Barcelona
- Monash University
OBJECTIVES: 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.
METHODS: Mice carrying 2 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 (FL) were fed a standard chow (CHOW) or high fat diet (HFD) for 16 weeks and comprehensively metabolically phenotyped. In addition to a diet-induced obesity (DIO) 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.
RESULTS: As expected, mice on a 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.
CONCLUSION: Adipocyte specific IL-6 does not contribute to whole body glucose intolerance in obese mice.
|Number of pages||8|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|Early online date||6 Aug 2019|
|Publication status||Published - 1 Oct 2019|