Abstract

Intestinal dysbiosis and its functional implications in chronic pancreatitis (CP) have not been elaborately studied. We evaluated the taxonomic and functional alterations in intestinal microbiota in 30 well-characterised patients with CP (16 without, 14 with diabetes) and 10 healthy controls. The patients with CP and diabetes had significantly longer disease duration and greater degree of malnutrition. There was increase in plasma endotoxin concentrations from controls to CP non-diabetics to CP diabetics. We observed significant differences in richness and alpha diversity between the groups. We also observed increase in the Firmicutes:Bacteroidetes ratio in CP patients without and with diabetes. There was reduction in abundance of Faecalibacterium prausnitzii and Ruminococcus bromii from controls to CP non-diabetics to CP diabetics. On the other hand, there was increase in LPS (endotoxin) synthetic pathways (KEGG orthology) in the groups. Faecalibacterium prausnitzii abundance correlated negatively with plasma endotoxin and glycemic status; while plasma endotoxin correlated positively with blood glucose and negatively with plasma insulin. Our results have important implications for future studies exploring mechanistic insights on secondary diabetes in CP.

Highlights

  • Intestinal dysbiosis and its functional implications in chronic pancreatitis (CP) have not been elaborately studied

  • In this study we have shown significant association of intestinal dysbiosis with host metabolic functions, including diabetes, in patients with Chronic pancreatitis (CP)

  • The CP patients with DM had a significantly longer disease duration and higher degree of malnutrition compared to the CP patients without diabetes

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Summary

Introduction

Intestinal dysbiosis and its functional implications in chronic pancreatitis (CP) have not been elaborately studied. We evaluated the taxonomic and functional alterations in intestinal microbiota in 30 wellcharacterised patients with CP (16 without, 14 with diabetes) and 10 healthy controls. There was reduction in abundance of Faecalibacterium prausnitzii and Ruminococcus bromii from controls to CP non-diabetics to CP diabetics. Pancreatic exocrine insufficiency (PEI) results in maldigestion of fat and other nutrients thereby culminating in malnutrition and metabolic abnormalities. We hypothesized that nutrient maldigestion in CP could result in alteration of the gut microbiota which could eventually contribute to the related metabolic abnormalities. With this premise, we conducted the current study, wherein we evaluated for alterations in the intestinal microbiota and their associations with metabolic abnormalities, including DM, in patients with CP

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