GLP-1 {90000646}

Shared Reference Notes

• [1.1] [#Diabetes Type 2] [#Dipeptidyl peptidase 4] [#High Fat Diet] 
  - microbial DPP4 was mainly produced by #Bacteroides spp. - Gut microbial DPP4 (mDPP4) could degrade active GLP-1(7-37) in vitro. - mDPP4 could not affect active GLP-1 levels in chow-fed mice but could decrease active GLP-1 activity and impair #Glucose homeostasis in high-fat diet (HFD)–fed mice or dextran #Sulfate sodium/indomethacin–treated mice, suggesting that a damaged gut barrier is required for mDPP4 to affect the activity of host GLP-1. - Gut microbial DPP4 isozyme can impair host #Glucose homeostasis, and variations in microbial DPP4 activities could possibly contribute to the heterogeneous responses to sitagliptin observed among patients with T2D.
• [1.2] [#Para-cresol] 
  - The absence of gut microbiota also reduces the production of amino acid-derived microbial metabolites (e.g., #Indole and p-cresol), which are reported to modulate GLP-1 expression and secretion, and gut motility. - supplementing mice with the tyrosine-derived microbial metabolite p-cresol reversed the enteropeptidase inhibition mediated effects on Gcg expression and small intestinal transit.
• [#Short Chain Fatty Acid] - gut microbiota regulated metabolites, such as SCFAs, modulate GLP-1 levels, either as energy substrates4 or as FFAR2/3 agonists.
• [1.3] [#High temperature and humidity] 
  - HTH caused a distinct alteration of gut microbiota charactered as increased #Firmicutes/ #Bacteroidetes ratio, decreased #Prevotellaceae UCG-001 accompanied with increased #Lachnoclostridium and #Candidatus saccharimonas at day 7. #Prevotellaceae UCG-001, involved in saccharolytic fermentation, probably contributed to the decreased plasma #Butyric acid level. - the decreased #Butyric acid recovered rapidly and could not explain the GLP-1 suppression as butyrate supplement could not alleviate GLP-1 decline
• - #Bile Acids and gut microbiota are reciprocally regulated and collaboratively control GLP-1 production mainly through the binding of BAs to their receptors, FXR. - The activation of FXR decreases GLP-1 secretion.
• [#Bile Acids] [#High temperature and humidity] - ambient HTH affected the crosstalk between gut microbiota and BAs and thereby caused an aberrant FXR activation and GLP-1 suppression.
• - #Lithocholic acid increases glucagon-like peptide-1 secretion in NCI-H716 cells.
• - combination of #Lithocholic acid with farnesoid X receptor inhibitors resulted in a significant increase in GLP-1 levels compared to #Lithocholic acid alone. - alteration of BAs composition, especially the reduced LCA, contributed to HTH induced GLP-1 suppression through FXR activation.
• [1.4] [#Short Chain Fatty Acid] 
  - The activation of G-protein-coupled receptors by SCFAs triggers the release of peptide YY and GLP-1, contributing to feelings of satiety and reduced food intake. - SCFAs activate #Adenosine monophosphate-activated protein kinase, promoting hepatic autophagy and lipid oxidation.
• [#Diabetes Type 2] [#Secondary bile acids] - stimulating the G-protein-coupled receptor 5 by gut-bacteria-derived secondary BAs influences #Glucose homeostasis through glucagon-like peptide-1 (GLP-1) action.
• [1.5] [#Diabetes Type 2] 
  - duodenal single dose infusion of #Anaerobutyricum soehngenii stimulated glucagon-like peptide-1 (GLP-1) production, ameliorated glycemic control

References Notes