Journal
CELL DEATH & DISEASE
Volume 12, Issue 4, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-021-03608-9
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Funding
- Ministry of Science and Technology [MOST 108-2320-B-016-017-MY3, MOST 109-2811-B-016-500, MOST 108-2314-B-016-045-, MOST 109-2314-B-016-030-]
- Ministry of National Defense-Medical Affairs Bureau [MAB-108-065, MAB-109-085, MAB109-010, MND-MAB-110-082]
- Tri-Service General Hospital [TSGH-C03109025]
- Taoyuan Armed Force General Hospital of the Republic of China [10818, 10735]
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This study found that the upregulated expression of GRAIL gene in the liver of NAFLD patients, and Grail knockout significantly alleviated hepatic fat accumulation induced by a high-fat diet. Conversely, overexpression of GRAIL exacerbated lipid accumulation. The results demonstrated that Grail regulates hepatic steatosis through interaction with sirtuin 1, showing its significance as a molecular regulator in the development of NAFLD.
In obese adults, nonalcoholic fatty liver disease (NAFLD) is accompanied by multiple metabolic dysfunctions. Although upregulated hepatic fatty acid synthesis has been identified as a crucial mediator of NAFLD development, the underlying mechanisms are yet to be elucidated. In this study, we reported upregulated expression of gene related to anergy in lymphocytes (GRAIL) in the livers of humans and mice with hepatic steatosis. Grail ablation markedly alleviated the high-fat diet-induced hepatic fat accumulation and expression of genes related to the lipid metabolism, in vitro and in vivo. Conversely, overexpression of GRAIL exacerbated lipid accumulation and enhanced the expression of lipid metabolic genes in mice and liver cells. Our results demonstrated that Grail regulated the lipid accumulation in hepatic steatosis via interaction with sirtuin 1. Thus, Grail poses as a significant molecular regulator in the development of NAFLD.
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