Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Endocr Rev. 2024 Mar 4;45(2):190-209. doi: 10.1210/endrev/bnad028.
Over the past 4 decades, the clinical care of people living with HIV (PLWH) evolved from treatment of acute opportunistic infections to the management of chronic, noncommunicable comorbidities. Concurrently, our understanding of adipose tissue function matured to acknowledge its important endocrine contributions to energy balance. PLWH experience changes in the mass and composition of adipose tissue depots before and after initiating antiretroviral therapy, including regional loss (lipoatrophy), gain (lipohypertrophy), or mixed lipodystrophy. These conditions may coexist with generalized obesity in PLWH and reflect disturbances of energy balance regulation caused by HIV persistence and antiretroviral therapy drugs. Adipocyte hypertrophy characterizes visceral and subcutaneous adipose tissue depot expansion, as well as ectopic lipid deposition that occurs diffusely in the liver, skeletal muscle, and heart. PLWH with excess visceral adipose tissue exhibit adipokine dysregulation coupled with increased insulin resistance, heightening their risk for cardiovascular disease above that of the HIV-negative population. However, conventional therapies are ineffective for the management of cardiometabolic risk in this patient population. Although the knowledge of complex cardiometabolic comorbidities in PLWH continues to expand, significant knowledge gaps remain. Ongoing studies aimed at understanding interorgan communication and energy balance provide insights into metabolic observations in PLWH and reveal potential therapeutic targets. Our review focuses on current knowledge and recent advances in HIV-associated adipose tissue dysfunction, highlights emerging adipokine paradigms, and describes critical mechanistic and clinical insights.
在过去的 40 年中，人类免疫缺陷病毒（HIV）感染者的临床护理已经从急性机会性感染的治疗演变为慢性非传染性合并症的管理。与此同时，我们对脂肪组织功能的认识也逐渐成熟，认识到它对能量平衡的重要内分泌贡献。HIV 感染者在开始接受抗逆转录病毒治疗之前和之后，脂肪组织库的质量和组成会发生变化，包括区域性损失（脂肪萎缩）、增加（脂肪肥大）或混合性脂肪营养不良。这些情况可能与 HIV 感染者的全身性肥胖并存，并反映了 HIV 持续存在和抗逆转录病毒治疗药物引起的能量平衡调节紊乱。脂肪细胞肥大是内脏和皮下脂肪组织库扩张以及肝、骨骼肌和心脏中广泛发生的异位脂质沉积的特征。内脏脂肪组织过多的 HIV 感染者表现出脂肪因子失调，同时伴有胰岛素抵抗增加，使他们患心血管疾病的风险高于 HIV 阴性人群。然而，传统疗法对该患者群体的心血管代谢风险管理无效。尽管 HIV 感染者复杂心血管代谢合并症的知识不断增加，但仍存在重大知识空白。目前正在进行的旨在了解器官间通讯和能量平衡的研究为 HIV 感染者的代谢观察提供了深入了解，并揭示了潜在的治疗靶点。我们的综述重点介绍了与 HIV 相关的脂肪组织功能障碍的最新知识和进展，强调了新兴的脂肪因子范式，并描述了关键的机制和临床见解。
