In their recent study, Nicholas et al. challenge the current dogma that T cell inflammation must be fueled by glycolysis and demonstrate a novel metabolic mechanism for Th17 inflammation in human type 2 diabetes mellitus (T2DM): a combination of increased environmental long-chain fatty acid metabolites coupled with decreased fatty acid oxidation.

中文翻译：

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人类 2 型糖尿病中 Th17 炎症的新机制

在他们最近的研究中，Nicholas 等人。挑战目前 T 细胞炎症必须由糖酵解助长的教条，并证明了人类 2 型糖尿病 (T2DM) 中 Th17 炎症的新代谢机制：环境长链脂肪酸代谢物增加与脂肪酸氧化减少相结合。