Gammone Maria Alessandra, D'Orazio Nicolantonio
Human and Clinical Nutrition Unit, Department of Medical, Oral and Biotechnological Sciences, University G. D'Annunzio, Chieti, Italy.
Front Endocrinol (Lausanne). 2021 Apr 30;12:652639. doi: 10.3389/fendo.2021.652639. eCollection 2021.
Obesity has been recognized as an independent risk factor for critical illness and major severity in subjects with coronavirus disease 2019 (COVID-19). The role of fat distribution, particularly visceral fat (often linked to metabolic abnormalities), is still unclear. The adipose tissue represents a direct source of cytokines responsible for the pathological modifications occurring within adipose tissue in obese subjects. Adipokines are a crucial connection between metabolism and immune system: their dysregulation in obesity contributes to chronic low-grade systemic inflammation and metabolic comorbidities. Therefore the increased amount of visceral fat can lead to a proinflammatory phenotypic shift. This review analyzes the interrelation between obesity and COVID-19 severity, as well as the cellular key players and molecular mechanisms implicated in adipose inflammation, investigating if adipose tissue can constitute a reservoir for viral spread, and contribute to immune activation and cytokines storm. Targeting the underlying molecular mechanisms might have therapeutic potential in the management of obesity-related complications in COVID-19 patients.
肥胖已被公认为是2019冠状病毒病(COVID-19)患者发生危重症和严重病情的独立危险因素。脂肪分布的作用,尤其是内脏脂肪(通常与代谢异常有关),仍不明确。脂肪组织是细胞因子的直接来源,这些细胞因子导致肥胖个体脂肪组织内发生病理改变。脂肪因子是代谢与免疫系统之间的关键联系:它们在肥胖状态下的失调会导致慢性低度全身炎症和代谢合并症。因此,内脏脂肪量增加会导致促炎表型转变。本综述分析了肥胖与COVID-19严重程度之间的相互关系,以及参与脂肪炎症的细胞关键因子和分子机制,探讨脂肪组织是否可能成为病毒传播的储存库,并促进免疫激活和细胞因子风暴。针对潜在的分子机制可能对COVID-19患者肥胖相关并发症的管理具有治疗潜力。