Intestinal Trefoil Factor 3: a new biological factor mediating gut-kidney crosstalk in diabetic kidney disease.

Biological markers DKD Gut-kidney axis Trefoil factor 3 Type 2 diabetes mellitus

Journal

Endocrine
ISSN: 1559-0100
Titre abrégé: Endocrine
Pays: United States
ID NLM: 9434444

Informations de publication

Date de publication:
26 Dec 2023
Historique:
received: 20 07 2023
accepted: 29 09 2023
medline: 27 12 2023
pubmed: 27 12 2023
entrez: 26 12 2023
Statut: aheadofprint

Résumé

To investigate the effect of TFF3 in the pathogenesis of Diabetic Kidney Disease (DKD), and explore the dynamic changes of TFF3 expression pattern in renal injury process. DKD animal model was established by streptozotocin (STZ) (40 mg/kg/d, ip, for 5 days, consecutively) combined with the high fat diet (HFD) for 12 weeks. While animals were sacrificed at different time stages in DKD process (4 weeks, 8 weeks and 12 weeks, respectively). STZ combined with high-fat diet induced weight gain, increased blood glucose and decreased glucose tolerance in DKD mice. Compared to the control group, the DKD group exhibits extracellular matrix (ECM) accumulation and the renal injury was aggravated in a time-dependent manner. The TFF3 expression level was decreased in kidney, and increased in colon tissue. TFF3 is not only expressed in colon, but also expressed in renal medulla and cortex. TFF3 might be play a pivotal role in renal mucosal repair by gut-kidney crosstalk, and protect renal from high glucose microenvironment damage.

Identifiants

DOI: 10.1007/s12020-023-03559-5 PMID: 38148440
pubmed: 38148440
doi: 10.1007/s12020-023-03559-5
pii: 10.1007/s12020-023-03559-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : National Natural Science Foundation of China
ID : 82204704
Organisme : Basic and Applied Basic Research Special Project, Guangzhou Science and Technology Bureau
ID : SL2024A04J00581

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Tao Zhang (T)

Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education; Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou Higher Education Mega Center, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

Yinghui Zhang (Y)

Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education; Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou Higher Education Mega Center, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

Jie Tao (J)

Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education; Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou Higher Education Mega Center, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

Xianglu Rong (X)

Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education; Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou Higher Education Mega Center, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

Yiqi Yang (Y)

Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education; Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou Higher Education Mega Center, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China. yangyiqi2011@163.com.

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