Estrogen Mediates Capacity for Hyperplastic Adipose Expansion and Preserves Adipose Progenitor Cell Availability in Subcutaneous Depots of Female Mice.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Female protection against cardiometabolic disease wanes after menopause, concomitant with a transition toward the male-like pattern of visceral adiposity. Since recruitment of adipose progenitor cells (APCs) to support adipose expansion is depot-specific and thought to maintain metabolic homeostasis, sex differences in the capacity for APC differentiation were explored as a mechanism underlying female cardiometabolic protection. Female APCs from subcutaneous depots were more proliferative and responsive to adipogenic stimuli and were enriched in pathways regulating cell cycle compared with male APCs. The female bias toward a higher number of committed preadipocytes in subcutaneous depots was reversed by ovariectomy (ovx) and restored in ovx females with 17β-estradiol (E2) replacement. In response to pharmacological stimulation of adipogenesis by rosiglitazone, intact females gained more fat mass and were protected against the diminished abundance of subcutaneous APCs that was observed in males. Ovx eliminated fat accumulation in response to rosiglitazone, but amplified diet-induced obesity and abolished female protection against metabolic dysfunction. E2 replacement restored female protection against obesity-associated adipose inflammation and metabolic dysfunction. Thus, we conclude that E2 mediates hyperplastic expansion in subcutaneous depots and preserves adipose function i

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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