Journal
DIABETES
Volume 66, Issue 12, Pages 2952-2963Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db17-0296
Keywords
-
Categories
Funding
- National Institutes of Health [P30-DK-063720, P30-DK-098722, R01 DK-105175, CA-139158, DK-094641, DK-101064]
- Larry L. Hillblom Foundation
- JDRF
- Agency for Science, Technology and Research fellowship
Ask authors/readers for more resources
Uncoupling protein 1(+) beige adipocytes are dynamically regulated by environment in rodents and humans; cold induces formation of beige adipocytes, whereas warm temperature and nutrient excess lead to their disappearance. Beige adipocytes can form through de novo adipogenesis; however, how beiging characteristics are maintained afterward is largely unknown. In this study, we show that beige adipocytes formed postnatally in subcutaneous inguinal white adipose tissue lost thermogenic gene expression and multilocular morphology at the adult stage, but cold restored their beiging characteristics, a phenomenon termed beige adipocyte renaissance. Ablation of these postnatal beige adipocytes inhibited cold-induced beige adipocyte formation in adult mice. Furthermore, we demonstrated that beige adipocyte renaissance was governed by liver kinase b1 and histone deacetylase 4 in white adipocytes. Although neither presence nor thermogenic function of uncoupling protein 1(+) beige adipocytes contributed to metabolic fitness in adipocyte liver kinase b1-deficient mice, our results reveal an unexpected role of white adipocytes in maintaining properties of preexisting beige adipocytes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available