The Lemole Center for Integrated Lymphatic Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Cells. 2022 Mar 3;11(5):882. doi: 10.3390/cells11050882.
The prevalence of obesity and associated cardiometabolic diseases continues to rise, despite efforts to improve global health. The adipose tissue is now regarded as an endocrine organ since its multitude of secretions, lipids chief among them, regulate systemic functions. The loss of normal adipose tissue phenotypic flexibility, especially related to lipid homeostasis, appears to trigger cardiometabolic pathogenesis. The goal of this manuscript is to review lipid balance maintenance by the lean adipose tissue's propensity for phenotype switching, obese adipose tissue's narrower range of phenotype flexibility, and what initial factors account for the waning lipid regulatory capacity. Metabolic, hypoxic, and inflammatory factors contribute to the adipose tissue phenotype being made rigid. A better grasp of normal adipose tissue function provides the necessary context for recognizing the extent of obese adipose tissue dysfunction and gaining insight into how pathogenesis evolves.
尽管全球健康努力不断增加，但肥胖症和相关代谢性心血管疾病的患病率仍在持续上升。脂肪组织现在被认为是一种内分泌器官，因为它的多种分泌物（主要是脂质）调节全身功能。正常脂肪组织表型灵活性的丧失，尤其是与脂质动态平衡有关的丧失，似乎引发了代谢性心血管疾病的发病机制。本文的目的是回顾瘦脂肪组织通过表型转换维持脂质平衡的倾向、肥胖脂肪组织更窄的表型灵活性范围，以及最初是什么因素导致脂质调节能力下降。代谢、缺氧和炎症因素导致脂肪组织表型僵化。更好地掌握正常脂肪组织功能为认识肥胖脂肪组织功能障碍的程度以及深入了解发病机制的演变提供了必要的背景。
