ArticleDiabetologia2020
The glucose-lowering effects of α-glucosidase inhibitor require a bile acid signal in mice.
Article in Diabetologia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Habitual Dietary Intake Affects the Altered Pattern of Gut Microbiome by Acarbose in Patients with Type 2 Diabetes.Nutrients · 2021Trial
- Declining FXR expression coordinates neonatal beta cell mass development with microbial bile acid metabolism maturation in mice.Diabetologia · 2026Article
- Acarbose impairs gutmBio · 2024Article
- LPS-related muscle loss is associated with the alteration of Bacteroidetes abundance, systemic inflammation, and mitochondrial morphology in a weaned piglet model.Science China. Life sciences · 2024Article
- Identification and characterization of a calcium-binding peptide from salmon bone for the targeted inhibition of α-amylase in digestion.Food chemistry: X · 2024Article
- Acarbose Impairs GutbioRxiv : the preprint server for biology · 2024Article
- Regulation of bile acids and their receptor FXR in metabolic diseases.Frontiers in nutrition · 2024Review
- Hepatic retinaldehyde deficiency is involved in diabetes deterioration by enhancing PCK1- and G6PC-mediated gluconeogenesis.Acta pharmaceutica Sinica. B · 2023Article
- Bile acids-gut microbiota crosstalk contributes to the improvement of type 2 diabetes mellitus.Frontiers in pharmacology · 2022Review
- Depletion of gut microbiota induces skeletal muscle atrophy by FXR-FGF15/19 signalling.Annals of medicine · 2021Article
- Review
- Effect of different bile acids on the intestine through enterohepatic circulation based on FXR.Gut microbesReview
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisBile-acid (BA) signalling is crucial in metabolism homeostasis and has recently been found to mediate the therapeutic effects of glucose-lowering treatments, including α-glucosidase inhibitor (AGI). However, the underlying mechanisms are yet to be clarified. We hypothesised that BA signalling may be required for the glucose-lowering effects and metabolic benefits of AGI.
methodsLeptin receptor (Lepr)-knockout (KO) db/db mice and high-fat high-sucrose (HFHS)-fed Fxr (also known as Nr1h4)-KO mice were treated with AGI. Metabolic phenotypes and BA signalling in different compartments, including the liver, gut and endocrine pancreas, were evaluated. BA pool profiles were analysed by mass spectrometry. The islet transcription profile was assayed by RNA sequencing. The gut microbiome were assayed by 16S ribosomal RNA gene sequencing.
resultsAGI lowered microbial BA levels in BA pools of different compartments in the body, and increased gut BA reabsorption in both db/db and HFHS-fed mouse models via altering the gut microbiome. The AGI-induced changes in BA signalling (including increased activation of farnesoid X receptor [FXR] in the liver and inhibition of FXR in the ileum) echoed the alterations in BA pool size and composition in different organs. In Fxr-KO mice, the glucose- and lipid-lowering effects of AGI were partially abrogated, possibly due to the Fxr-dependent effects of AGI on decelerating beta cell replication, alleviating insulin hypersecretion and improving hepatic lipid and glucose metabolism. CONCLUSIONS/
interpretationBy regulating microbial BA metabolism, AGI elicited diverse changes in BA pool composition in different host compartments to orchestrate BA signalling in the whole body. The AGI-induced changes in BA signalling may be partly required for its glucose-lowering effects. Our study, hence, sheds light on the promising potential of regulating microbial BA and host FXR signalling for the treatment of type 2 diabetes. DATA AVAILABILITY: Sequencing data are available from the BioProject Database (accession no. PRJNA600345; www.ncbi.nlm.nih.gov/bioproject/600345).
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