Nature子刊:短期和长期生酮饮食对代谢的不同影响,γδ T细胞是关键
创作:szx 审核:szx 01月23日
  • 喂食1周生酮饮食,可显著降低小鼠的血糖水平,并增加脂肪质量;
  • 对脂肪组织驻留性免疫细胞进行单细胞RNA测序分析,发现生酮饮食可促进代谢保护性γδ T细胞的扩增,以抑制脂肪组织中的炎症反应;
  • 长期喂食生酮饮食可增加脂肪组织中的巨噬细胞,而减少γδ T细胞,并造成小鼠肥胖,促进脂肪组织的炎症反应,增加血糖及空腹血糖水平;
  • 相比于野生型小鼠,缺失γδ T细胞的小鼠在长期喂食生酮饮食后,血糖水平进一步升高。
主编推荐语
szx
生酮饮食对脂肪组织的影响尚未明确。Nature Metabolism上发表的一项最新研究,发现短期喂食生酮饮食,可激活脂肪组织中的γδ T细胞以促进组织修复及代谢稳态,降低小鼠血糖水平并增加脂肪质量;而长期喂食生酮饮食则减少脂肪组织中的γδ T细胞,并导致肥胖及葡萄糖耐受不良。
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Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue

生酮作用激活内脏脂肪组织中的代谢保护性γδ T细胞

10.1038/s42255-019-0160-6

01-20, Article

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Ketone bodies are essential alternative fuels that allow humans to survive periods of glucose scarcity induced by starvation and prolonged exercise. A widely used ketogenic diet (KD), which is extremely high in fat with very low carbohydrates, drives the host into using β-hydroxybutyrate for the production of ATP and lowers NLRP3-mediated inflammation. However, the extremely high fat composition of KD raises the question of how ketogenesis affects adipose tissue to control inflammation and energy homeostasis. Here, by using single-cell RNA sequencing of adipose-tissue-resident immune cells, we show that KD expands metabolically protective γδ T cells that restrain inflammation. Notably, long-term ad libitum KD feeding in mice causes obesity, impairs metabolic health and depletes the adipose-resident γδ T cells. In addition, mice lacking γδ T cells have impaired glucose homeostasis. Our results suggest that γδ T cells are mediators of protective immunometabolic responses that link fatty acid–driven fuel use to reduced adipose tissue inflammation.

First Authors:
Emily L Goldberg

Correspondence Authors:
Vishwa Deep Dixit

All Authors:
Emily L Goldberg,Irina Shchukina,Jennifer L Asher,Sviatoslav Sidorov,Maxim N Artyomov,Vishwa Deep Dixit

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Nature Reviews Endocrinology期刊

Ketogenic diet affects immune cells in mice

2020-01-30

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