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Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming.

Citation
Holman, C. D., et al. “Aging Impairs Cold-Induced Beige Adipogenesis And Adipocyte Metabolic Reprogramming.”. Elife.
Center University of Pennsylvania
Author Corey D Holman, Alexander P Sakers, Ryan P Calhoun, Lan Cheng, Ethan C Fein, Christopher Jacobs, Linus Tsai, Evan D Rosen, Patrick Seale
Keywords UCP1, aging, beige adipocyte, beige adipogenesis, Cell Biology, cold exposure, Developmental Biology, mouse
Abstract

The energy-burning capability of beige adipose tissue is a potential therapeutic tool for reducing obesity and metabolic disease, but this capacity is decreased by aging. Here, we evaluate the impact of aging on the profile and activity of adipocyte stem and progenitor cells (ASPCs) and adipocytes during the beiging process in mice. We found that aging increases the expression of and other fibro-inflammatory genes in fibroblastic ASPCs and blocks their differentiation into beige adipocytes. Fibroblastic ASPC populations from young and aged mice were equally competent for beige differentiation in vitro, suggesting that environmental factors suppress adipogenesis in vivo. Examination of adipocytes by single nucleus RNA-sequencing identified compositional and transcriptional differences in adipocyte populations with aging and cold exposure. Notably, cold exposure induced an adipocyte population expressing high levels of de novo lipogenesis (DNL) genes, and this response was severely blunted in aged animals. We further identified , which encodes the natriuretic peptide clearance receptor, as a marker gene for a subset of white adipocytes and an aging-upregulated gene in adipocytes. In summary, this study indicates that aging blocks beige adipogenesis and dysregulates adipocyte responses to cold exposure and provides a resource for identifying cold and aging-regulated pathways in adipose tissue.

Year of Publication
2024
Journal
eLife
Volume
12
Date Published
05/2024
ISSN Number
2050-084X
DOI
10.7554/eLife.87756
Alternate Journal
Elife
PMID
38775132
PMCID
PMC11111218
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