Vitamin C protects against hypoxia, inflammation, and ER stress in primary human preadipocytes and adipocytes.

Dysregulation of adipose tissue involves increased cellular hypoxia, ER stress, and inflammation and altered adipokine production, contributing to the aetiology of obesity-related diseases including type 2 diabetes and cardiovascular disease. This study aimed to investigate the effects of Vitamin C supplementation on these processes in primary human preadipocytes and adipocytes. Treatment of preadipocytes and adipocytes with the proinflammatory cytokine TNFα and palmitic acid (PA), to mimic the obesogenic milieu, significantly increased markers of hypoxia, ER stress and inflammation and reduced secretion of high molecular weight (HMW) adiponectin. Importantly, Vitamin C abolished TNFα+PA induced hypoxia and significantly reduced the increases in ER stress and inflammation in both cell types. Vitamin C also significantly increased the secretion of HMW adiponectin from adipocytes. These findings indicate that Vitamin C can reduce obesity-associated cellular stress and thus provide a rationale for future investigations.

脂肪组织的失调涉及细胞缺氧增加、内质网应激和炎症以及脂肪因子产生的改变，这促成了包括2型糖尿病和心血管疾病在内的肥胖相关疾病的病因。本研究旨在探讨补充维生素C对原代人前脂肪细胞和脂肪细胞中这些过程的影响。用促炎细胞因子肿瘤坏死因子α（TNFα）和棕榈酸（PA）处理前脂肪细胞和脂肪细胞以模拟致肥胖环境，显著增加了缺氧、内质网应激和炎症的标志物，并减少了高分子量（HMW）脂联素的分泌。重要的是，维生素C消除了TNFα + PA诱导的缺氧，并显著降低了两种细胞类型中内质网应激和炎症的增加。维生素C还显著增加了脂肪细胞中高分子量脂联素的分泌。这些发现表明维生素C可以减轻与肥胖相关的细胞应激，从而为未来的研究提供了理论基础。