Identification of gut microbiota and microbial metabolites regulated by an antimicrobial peptide lipocalin 2 in high fat diet-induced obesity.

Autor: Qiu X; Department of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, 55455, USA., Macchietto MG; Clinical Translational Science Institute, University of Minnesota, Twin Cities, MN, 55455, USA., Liu X; Department of Computer Science and Engineering, Graduate Program in Bioinformatics and Computational Biology, University of Minnesota, Twin Cities, MN, 55455, USA., Lu Y; Department of Plant and Microbial Biology, Microbial and Plant Genomics Institute, University of Minnesota, Twin Cities, MN, 55455, USA., Ma Y; Department of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, 55455, USA., Guo H; Department of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, 55455, USA., Saqui-Salces M; Department of Animal Science, University of Minnesota, Twin Cities, MN, 55455, USA., Bernlohr DA; Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Twin Cities, MN, 55455, USA., Chen C; Department of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, 55455, USA., Shen S; Clinical Translational Science Institute, University of Minnesota, Twin Cities, MN, 55455, USA., Chen X; Department of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, 55455, USA. xlchen@umn.edu.
Jazyk: angličtina
Zdroj: International journal of obesity (2005) [Int J Obes (Lond)] 2021 Jan; Vol. 45 (1), pp. 143-154. Date of Electronic Publication: 2020 Nov 19.
DOI: 10.1038/s41366-020-00712-2
Abstrakt: Lipocalin 2 (Lcn2), as an antimicrobial peptide is expressed in intestine, and the upregulation of intestinal Lcn2 has been linked to inflammatory bowel disease. However, the role of Lcn2 in shaping gut microbiota during diet-induced obesity (DIO) remains unknown. We found that short-term high fat diet (HFD) feeding strongly stimulates intestinal Lcn2 expression and secretion into the gut lumen. As the HFD feeding prolongs, fecal Lcn2 levels turn to decrease. Lcn2 deficiency accelerates the development of HFD-induced intestinal inflammation and microbiota dysbiosis. Moreover, Lcn2 deficiency leads to the remodeling of microbiota-derived metabolome, including decreased production of short-chain fatty acids (SCFAs) and SCFA-producing microbes. Most importantly, we have identified Lcn2-targeted bacteria and microbiota-derived metabolites that potentially play roles in DIO and metabolic dysregulation. Correlation analyses suggest that Lcn2-targeted Dubosiella and Angelakisella have a novel role in regulating SCFAs production and obesity. Our results provide a novel mechanism involving Lcn2 as an antimicrobial host factor in the control of gut microbiota symbiosis during DIO.
Databáze: MEDLINE
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