Meister Benjamin M, Hong Soon-Gook, Shin Junchul, Rath Meghan, Sayoc Jacqueline, Park Joon-Young
Department of Kinesiology, College of Public Health and Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
J Obes Metab Syndr. 2022 Mar 30;31(1):37-50. doi: 10.7570/jomes21096.
Although the hallmark of obesity is the expansion of adipose tissue, not all adipose tissue expansion is the same. Expansion of healthy adipose tissue is accompanied by adequate capillary angiogenesis and mitochondria-centered metabolic integrity, whereas expansion of unhealthy adipose tissue is associated with capillary and mitochondrial derangement, resulting in deposition of immune cells (M1-stage macrophages) and excess production of pro-inflammatory cytokines. Accumulation of these dysfunctional adipose tissues has been linked to the development of obesity comorbidities, such as type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease, which are leading causes of human mortality and morbidity in modern society. Mechanistically, vascular rarefaction and mitochondrial incompetency (for example, low mitochondrial content, fragmented mitochondria, defective mitochondrial respiratory function, and excess production of mitochondrial reactive oxygen species) are frequently observed in adipose tissue of obese patients. Recent studies have demonstrated that exercise is a potent behavioral intervention for preventing and reducing obesity and other metabolic diseases. However, our understanding of potential cellular mechanisms of exercise, which promote healthy adipose tissue expansion, is at the beginning stage. In this review, we hypothesize that exercise can induce unique physiological stimuli that can alter angiogenesis and mitochondrial remodeling in adipose tissues and ultimately promote the development and progression of healthy adipogenesis. We summarize recent reports on how regular exercise can impose differential processes that lead to the formation of either healthy or unhealthy adipose tissue and discuss key knowledge gaps that warrant future research.
尽管肥胖的标志是脂肪组织的扩张，但并非所有的脂肪组织扩张都是相同的。健康脂肪组织的扩张伴随着充足的毛细血管生成和以线粒体为中心的代谢完整性，而不健康脂肪组织的扩张则与毛细血管和线粒体紊乱有关，导致免疫细胞（M1期巨噬细胞）沉积和促炎细胞因子的过量产生。这些功能失调的脂肪组织的积累与肥胖合并症的发生有关，如2型糖尿病、高血压、血脂异常和心血管疾病，这些是现代社会人类死亡和发病的主要原因。从机制上讲，肥胖患者的脂肪组织中经常观察到血管稀疏和线粒体功能不全（例如，线粒体含量低、线粒体碎片化、线粒体呼吸功能缺陷以及线粒体活性氧的过量产生）。最近的研究表明，运动是预防和减轻肥胖及其他代谢疾病的有效行为干预措施。然而，我们对运动促进健康脂肪组织扩张的潜在细胞机制的理解尚处于起步阶段。在这篇综述中，我们假设运动可以诱导独特的生理刺激，从而改变脂肪组织中的血管生成和线粒体重塑，并最终促进健康脂肪生成的发展和进程。我们总结了最近关于定期运动如何引发不同过程从而导致形成健康或不健康脂肪组织的报道，并讨论了需要未来研究的关键知识空白。
