J Clin Invest. 2019 Oct 1;129(10):4022-4031. doi: 10.1172/JCI129191.
The manner in which white adipose tissue (WAT) expands and remodels directly impacts the risk of developing metabolic syndrome in obesity. Preferential accumulation of visceral WAT is associated with increased risk for insulin resistance, whereas subcutaneous WAT expansion is protective. Moreover, pathologic WAT remodeling, typically characterized by adipocyte hypertrophy, chronic inflammation, and fibrosis, is associated with insulin resistance. Healthy WAT expansion, observed in the "metabolically healthy" obese, is generally associated with the presence of smaller and more numerous adipocytes, along with lower degrees of inflammation and fibrosis. Here, we highlight recent human and rodent studies that support the notion that the ability to recruit new fat cells through adipogenesis is a critical determinant of healthy adipose tissue distribution and remodeling in obesity. Furthermore, we discuss recent advances in our understanding of the identity of tissue-resident progenitor populations in WAT made possible through single-cell RNA sequencing analysis. A better understanding of adipose stem cell biology and adipogenesis may lead to novel strategies to uncouple obesity from metabolic disease.
白色脂肪组织（WAT）的扩张和重塑方式直接影响肥胖患者发生代谢综合征的风险。内脏 WAT 的优先积累与胰岛素抵抗的风险增加有关，而皮下 WAT 的扩张则具有保护作用。此外，病理性 WAT 重塑，通常表现为脂肪细胞肥大、慢性炎症和纤维化，与胰岛素抵抗有关。在“代谢健康”的肥胖者中观察到的健康 WAT 扩张通常与存在更小和更多数量的脂肪细胞、较低程度的炎症和纤维化有关。在这里，我们强调了最近的人类和啮齿动物研究，这些研究支持了这样一种观点，即通过脂肪生成招募新脂肪细胞的能力是肥胖症中健康脂肪组织分布和重塑的关键决定因素。此外，我们还讨论了通过单细胞 RNA 测序分析对 WAT 中组织驻留祖细胞群体的身份的最新理解。对脂肪干细胞生物学和脂肪生成的更好理解可能会导致将肥胖与代谢疾病分离的新策略。
