Zhu JingJing, Wilding John P H, Hu Ji
Department of Endocrinology and Metabolism, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Department of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
Med Hypotheses. 2023 Feb;171:111020. doi: 10.1016/j.mehy.2023.111020. Epub 2023 Jan 27.
Research evidence suggests that adipocytes in obesity might facilitate SARS-CoV-2 replication, for it was only found in adipose tissue of individuals with overweight or obesity but not lean individuals who died from COVID-19. As lipid metabolism is key to adipocyte function, and viruses are capable of exploiting and manipulating lipid metabolism of host cells for their own benefit of infection, we hypothesize that adipocytes could not only impair host immune defense against viral infection, but also facilitate SARS-CoV-2 entry, replication and assembly as a reservoir to boost the viral infection in obesity. The latter of which could mainly be mediated by SARS-CoV-2 hijacking the abnormal lipid metabolism in the adipocytes. If these were to be confirmed, an approach to combat COVID-19 in people with obesity by taking advantage of the abnormal lipid metabolism in adipocytes might be considered, as well as modifying lipid metabolism of other host cells as a potential adjunctive treatment for COVID-19.
研究证据表明，肥胖中的脂肪细胞可能促进SARS-CoV-2复制，因为仅在超重或肥胖个体而非死于COVID-19的瘦个体的脂肪组织中发现了该病毒。由于脂质代谢是脂肪细胞功能的关键，且病毒能够利用和操纵宿主细胞的脂质代谢以利于自身感染，我们推测脂肪细胞不仅会损害宿主对病毒感染的免疫防御，还会促进SARS-CoV-2作为一个储存库进入、复制和组装，从而加剧肥胖中的病毒感染。后者可能主要由SARS-CoV-2劫持脂肪细胞中异常的脂质代谢介导。如果这些得到证实，那么可以考虑利用脂肪细胞中异常的脂质代谢来对抗肥胖人群中的COVID-19，以及调节其他宿主细胞的脂质代谢作为COVID-19的潜在辅助治疗方法。
