2. Academic Validation
  3. Total parenteral nutrition impairs glucose metabolism by modifying the gut microbiome

Total parenteral nutrition impairs glucose metabolism by modifying the gut microbiome

  • Nat Metab. 2023 Feb 13. doi: 10.1038/s42255-023-00744-8.
Peng Wang # 1,  Haifeng Sun # 1,  Gulisudumu Maitiabula # 1,  Li Zhang 1,  Jianbo Yang 1,  Yupeng Zhang 1,  Xuejin Gao 1,  Jieshou Li 1,  Bin Xue 2 3,  Chao-Jun Li 4,  Xinying Wang 5
Affiliations

Affiliations

  • 1 Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
  • 2 MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center of the Medical School of Nanjing University, Nanjing, China. xuebin@njmu.edu.cn.
  • 3 Core Laboratory, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China. xuebin@njmu.edu.cn.
  • 4 State Key Laboratory of Reproductive Medicine and China International Joint Research Center on Environment and Human Health, Center for Global Health, School of Public Health, Gusu School, Nanjing Medical University, Nanjing, China. lichaojun@njmu.edu.cn.
  • 5 Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China. wangxinying@nju.edu.cn.
  • # Contributed equally.
PMID: 36782071 DOI: 10.1038/s42255-023-00744-8
Abstract

Total parenteral nutrition (TPN) can lead to complications, such as glucose metabolism disorders. While TPN is associated with impairments in intestinal function, the gut barrier and mucosal immunity, the relationship between the gut microbiome and TPN-related glucose metabolism disorders remains to be explored. In a cohort of 256 participants with type 2 intestinal failure, we show that parenteral nutrition providing >80% of total energy induces Insulin resistance and a higher risk of complications. Using various male mouse models, we demonstrate that changes in Lactobacillaceae and indole-3-acetic acid (IAA) levels underlie these complications. Lactobacillaceae and IAA levels decrease in TPN-treated mice and participants, while their abundances in the latter are negatively correlated with Insulin resistance and serum lipopolysaccharide levels. Furthermore, IAA activates the Aryl Hydrocarbon Receptor and increases glucagon-like peptide-1 secretion through upregulation of Gcg expression and increased stem cell differentiation towards L cells. Finally, liraglutide, a glucagon-like peptide-1 receptor agonist, completely prevents TPN-induced glucose metabolism disorders in mice. Thus, TPN induces glucose metabolism disorders by altering the gut microbiota and its metabolites.

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