Abstract
Intestinal gluconeogenesis (IGN), gastric bypass (GBP) and gut microbiota positively regulate glucose homeostasis and diet-induced dysmetabolism. GBP modulates gut microbiota, whether IGN could shape it has not been investigated. We studied gut microbiota and microbiome in wild type and IGN-deficient mice, undergoing GBP or not, and fed on either a normal chow (NC) or a high-fat/high-sucrose (HFHS) diet. We also studied fecal and urine metabolome in NC-fed mice. IGN and GBP had a different effect on the gut microbiota of mice fed with NC and HFHS diet. IGN inactivation increased abundance of Deltaproteobacteria on NC and of Proteobacteria such as Helicobacter on HFHS diet. GBP increased abundance of Firmicutes and Proteobacteria on NC-fed WT mice and of Firmicutes, Bacteroidetes and Proteobacteria on HFHS-fed WT mice. The combined effect of IGN inactivation and GBP increased abundance of Actinobacteria on NC and the abundance of Enterococcaceae and Enterobacteriaceae on HFHS diet. A reduction was observed in the amounf of short-chain fatty acids in fecal (by GBP) and in both fecal and urine (by IGN inactivation) metabolome. IGN and GBP, separately or combined, shape gut microbiota and microbiome on NC- and HFHS-fed mice, and modify fecal and urine metabolome.
Highlights
Intestinal gluconeogenesis (IGN), gastric bypass (GBP) and gut microbiota positively regulate glucose homeostasis and diet-induced dysmetabolism
We assessed the effect of IGN inactivation on both gut microbiota and microbiome in normal chow (NC)-fed mice (these mice underwent a laparotomy to serve as control for mice that underwent GBP)
We evaluated separately and combinedly the effects of both IGN inactivation and GBP on gut microbiota and microbiome in NC- and HFHS-fed mice
Summary
Intestinal gluconeogenesis (IGN), gastric bypass (GBP) and gut microbiota positively regulate glucose homeostasis and diet-induced dysmetabolism. Abbreviations ANOVA Analysis of variance GBP Gastric bypass HFHS High-fat high-sucrose IGN Intestinal glucose production iG6PC-KO Intestinal glucose-6-phosphatase catalytic subunit knock-out Lap Laparotomized LDA Linear discriminant analysis NC Normal chow PF Pair-fed SCFAs Short chain fatty acids T2DM Type 2 diabetes mellitus TMA Trimethylamine WT Wild-type. It is noteworthy that the changes in cecal SCFAs content and composition induced by fiber-enriched diet are modulated acccording to the presence or absence of IGN11 It was a first question of this study to know whether IGN inactivation per se might shape gut microbiota influencing SCFAs production. We addressed this question using IGN-deficient mice (knocked-out for the catalytic subunit of glucose-6-phosphatase in the intestine (iG6PC-KO)) compared to wild-type (WT) mice
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