Exploring the interplay of gut microbiota, inflammation, and LDL-cholesterol: a multiomics Mendelian randomization analysis of their causal relationship in acute pancreatitis and non-alcoholic fatty liver disease

J Transl Med. 2024 Feb 19;22(1):179. doi: 10.1186/s12967-024-04996-0.

Abstract

Background: Acute pancreatitis and non-alcoholic fatty liver disease are both serious diseases in the digestive system. The pathogenesis of both diseases is extremely complex closely and it related to gut microbiota, inflammation, and blood fat. There is a close relationship between gut microbiota and blood lipids.

Methods: In this study, we used three types of exposure: 412 gut microbiota, 731 inflammatory cells, and 91 inflammatory proteins (pqtls), with LDL-C as an intermediary and acute pancreatitis and non-alcoholic fatty liver disease as outcomes. We mainly used MR-IVW, co-localization analysis, and reverse MR analysis methods for analysis.

Results: 7 gut microbiota, 21 inflammatory cells, and 3 inflammatory proteins can affect LDL-C levels. LDL-C is associated with acute pancreatitis and non-alcoholic fatty liver disease.

Conclusions: Three omics were used: 412 gut microbiota, 731 inflammatory cells, and 91 inflammatory proteins (pqtls). It explains the causal relationship between multiomics, LDL- cholesterol, acute pancreatitis, and non-alcoholic fatty liver disease.

Keywords: Gut microbiota; Inflammatory cells; Inflammatory proteins; Multiomics.

MeSH terms

  • Acute Disease
  • Cholesterol, LDL
  • Gastrointestinal Microbiome*
  • Genome-Wide Association Study
  • Humans
  • Inflammation
  • Mendelian Randomization Analysis
  • Multiomics
  • Non-alcoholic Fatty Liver Disease* / genetics
  • Pancreatitis* / genetics

Substances

  • Cholesterol, LDL