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甘氨熊脱氧胆酸可调节胆汁酸水平，并改变肠道微生物群和糖脂代谢，从而减轻糖尿病。

Glycoursodeoxycholic acid regulates bile acids level and alters gut microbiota and glycolipid metabolism to attenuate diabetes.

机构信息

College of Pharmacy, Xinjiang Medical University, Urumqi, China.

Nanshan Hospital, The First Affiliated Hospital of Guangzhou University of Chinese Medicine (Shenzhen Nanshan Hospital of Chinese Medicine), Shenzhen, China.

出版信息

Gut Microbes. 2023 Jan-Dec;15(1):2192155. doi: 10.1080/19490976.2023.2192155.

DOI:10.1080/19490976.2023.2192155
PMID:36967529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10054359/
Abstract

Accumulating evidence suggests that the bile acid regulates type 2 diabetes mellitus (T2DM) through gut microbiota-host interactions. However, the mechanisms underlying such interactions have been unclear. Here, we found that glycoursodeoxycholic acid (GUDCA) positively regulates gut microbiota by altering bile acid metabolism. GUDCA in mice resulted in higher taurolithocholic acid (TLCA) level and abundance. Together, these changes resulted in the activation of the adipose G-protein-coupled bile acid receptor, GPBAR1 (TGR5) and upregulated expression of uncoupling protein UCP-1, resulting in elevation of white adipose tissue thermogenesis. The anti-T2DM effects of GUDCA are linked with the regulation of the bile acid and gut microbiota composition. This study suggests that altering bile acid metabolism, modifying the gut microbiota may be of value for the treatment of T2DM.

摘要

越来越多的证据表明，胆汁酸通过肠道微生物群-宿主相互作用来调节 2 型糖尿病（T2DM）。然而，这种相互作用的机制尚不清楚。在这里，我们发现甘氨熊脱氧胆酸（GUDCA）通过改变胆汁酸代谢来正向调节肠道微生物群。GUDCA 在小鼠中导致较高的牛磺胆酸（TLCA）水平和丰度。这些变化共同导致脂肪 G 蛋白偶联胆汁酸受体，GPBAR1（TGR5）的激活和解偶联蛋白 UCP-1 的表达上调，导致白色脂肪组织产热增加。GUDCA 的抗 T2DM 作用与胆汁酸和肠道微生物群组成的调节有关。这项研究表明，改变胆汁酸代谢、修饰肠道微生物群可能对 T2DM 的治疗具有价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/f80b486a74e9/KGMI_A_2192155_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/3f70b4374b3f/KGMI_A_2192155_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/0693b93dd798/KGMI_A_2192155_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/988cfb617a2a/KGMI_A_2192155_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/88d4d51878c1/KGMI_A_2192155_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/51426eeb9046/KGMI_A_2192155_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/f80b486a74e9/KGMI_A_2192155_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/3f70b4374b3f/KGMI_A_2192155_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/0693b93dd798/KGMI_A_2192155_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/988cfb617a2a/KGMI_A_2192155_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/88d4d51878c1/KGMI_A_2192155_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/51426eeb9046/KGMI_A_2192155_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/10054359/f80b486a74e9/KGMI_A_2192155_F0006_OC.jpg

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[1]
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Gut Microbiota-Derived Metabolites Orchestrate Metabolic Reprogramming in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Frontiers.

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[2]
Cholecystectomy-related gut microbiota dysbiosis exacerbates colorectal tumorigenesis.

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[3]
Unraveling Genetic Causality Between Type 2 Diabetes Mellitus and Hemiplegia Based on Mendelian Randomization.

J Multidiscip Healthc. 2025-8-7

[4]
DHLCA Alleviates Diabetic Kidney Disease via TGR5/FXR Activation and Gut Microbiota Remodeling.

Drug Des Devel Ther. 2025-7-29

[5]
Novel Approaches in Glucose and Lipid Metabolism Disorder Therapy: Targeting the Gut Microbiota-Bile Acid Axis.

Biology (Basel). 2025-7-2

[6]
Bile Acids and Type 2 Diabetes: Roles in Glucose Homeostasis and Therapeutic Opportunities.

Metabolites. 2025-6-13

[7]
The gut microbiota-bile acid axis: a crucial regulator of immune function and metabolic health.

World J Microbiol Biotechnol. 2025-6-25

[8]
Pig bile powder maintains blood glucose homeostasis by promoting glucagon-like peptide-1 secretion inhibiting farnesoid X receptor.

World J Diabetes. 2025-6-15

[9]
Multi-strain probiotics attenuate carbohydrate-lipid metabolic dysregulation in type 2 diabetic rats via gut-liver axis modulation.

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[10]
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本文引用的文献

[1]
Combined berberine and probiotic treatment as an effective regimen for improving postprandial hyperlipidemia in type 2 diabetes patients: a double blinded placebo controlled randomized study.

Gut Microbes. 2022

[2]
Myricetin supplementation decreases hepatic lipid synthesis and inflammation by modulating gut microbiota.

Cell Rep. 2021-8-31

[3]
Intestinal hypoxia-inducible factor 2α regulates lactate levels to shape the gut microbiome and alter thermogenesis.

Cell Metab. 2021-10-5

[4]
A Preliminary Study Showing the Impact of Genetic and Dietary Factors on GC-MS-Based Plasma Metabolome of Patients with and without -Genetic Predisposition to T2DM up to 5 Years Prior to Prediabetes Appearance.

Curr Issues Mol Biol. 2021-6-29

[5]
Glycoursodeoxycholic Acid Ameliorates Atherosclerosis and Alters Gut Microbiota in Apolipoprotein E-Deficient Mice.

J Am Heart Assoc. 2021-4-6

[6]
Linderae Radix Ethanol Extract Alleviates Diet-Induced Hyperlipidemia by Regulating Bile Acid Metabolism Through gut Microbiota.

Front Pharmacol. 2021-2-17

[7]
The bile acid TUDCA improves glucose metabolism in streptozotocin-induced Alzheimer's disease mice model.

Mol Cell Endocrinol. 2021-2-5

[8]
Gut microbiota-derived metabolites as central regulators in metabolic disorders.

Gut. 2021-6

[9]
Host variables confound gut microbiota studies of human disease.

Nature. 2020-11

[10]
Gut microbiome-related effects of berberine and probiotics on type 2 diabetes (the PREMOTE study).

Nat Commun. 2020-10-6

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