Authors
Chong Cao, Yanyang Liu, Xiaozhuo Tan, Yian Zhao, Huang Jaime, Yuxiao Chu, Mengcheng He, Rong Hua, Qiyuan Yao, Yikai Shao
Published in
International journal of obesity (2005). Sep 08, 2026. Epub Sep 08, 2026.
Abstract
Intestinal hypoxia-inducible factor 1α (HIF1α) orchestrates epithelial adaptation to luminal hypoxia and has been linked to metabolic homeostasis, yet its contribution to obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), and bariatric surgery-mediated benefits remain unclear.
In this study, we combined diet-induced models and genetic approaches to interrogate intestinal epithelial HIF1α function in obesity/MASLD progression and in the metabolic improvements elicited by sleeve gastrectomy (SG).
Intestinal epithelial HIF1α deletion did not alter diet-induced weight gain, glucose homeostasis, or the metabolic and hepatoprotective effects of SG under either High-fat diet (HFD) or high-fat/high-fructose diets (HFFD) feeding. Notably, despite largely unchanged systemic metabolic phenotypes, intestinal HIF1α deficiency increased hepatic triglyceride and cholesterol accumulation and reshaped hepatic metabolic gene expression, indicating a selective impact on liver lipid handling. In contrast, activation of intestinal HIF1α protected against diet-induced obesity and hepatic steatosis. 16S rRNA profiling showed that intestinal HIF1α activation was associated with a distinct microbial shift, including enrichment of Ruminococcus and reduction of Desulfovibrio.
Although activated after SG, intestinal epithelial HIF1α is not required for SG-induced metabolic improvements but exerts context-dependent protection against diet-induced obesity and hepatic steatosis, accompanied by gut microbial remodeling.
PMID:
42711457
Bibliographic data and abstract were imported from PubMed on 09 Sep 2026.
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