Article Synopsis
- Starting in middle age, adults often experience increased visceral fat and related metabolic issues due to changes in their adipose progenitor cells (APCs).
- Research in mice shows that these APCs become much more active in generating fat cells during middle age, despite having lower activity in younger adults.
- A specific population of committed preadipocytes, which proliferate and form fat more readily as age increases, relies on leukemia inhibitory factor receptor signaling for their activity and contributes to the growth of visceral fat.
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Article Abstract
Starting at middle age, adults often suffer from visceral adiposity and associated adverse metabolic disorders. Lineage tracing in mice revealed that adipose progenitor cells (APCs) in visceral fat undergo extensive adipogenesis during middle age. Thus, despite the low turnover rate of adipocytes in young adults, adipogenesis is unlocked during middle age. Transplantations quantitatively showed that APCs in middle-aged mice exhibited high adipogenic capacity cell-autonomously. Single-cell RNA sequencing identified a distinct APC population, the committed preadipocyte, age-enriched (CP-A), emerging at this age. CP-As demonstrated elevated proliferation and adipogenesis activity. Pharmacological and genetic manipulations indicated that leukemia inhibitory factor receptor signaling was indispensable for CP-A adipogenesis and visceral fat expansion. These findings uncover a fundamental mechanism of age-dependent adipose remodeling, offering critical insights into age-related metabolic diseases.
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| http://dx.doi.org/10.1126/science.adj0430 | DOI Listing |
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