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Trimethylamine N-oxide impairs β-cell function and glucose tolerance.
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- Author(s): Kong L;Kong L;Kong L;Kong L; Zhao Q; Zhao Q; Zhao Q; Zhao Q; Jiang X; Jiang X; Jiang X; Jiang X; Hu J; Hu J; Jiang Q; Jiang Q; Jiang Q; Jiang Q; Sheng L; Sheng L; Peng X; Peng X; Peng X; Wang S; Wang S; Chen Y; Chen Y; Chen Y; Chen Y; Wan Y; Wan Y; Wan Y; Wan Y; Hou S; Hou S; Hou S; Hou S; Liu X; Liu X; Liu X; Liu X; Ma C; Ma C; Ma C; Ma C; Li Y; Li Y; Quan L; Quan L; Chen L; Chen L; Chen L; Cui B; Cui B; Cui B; Li P; Li P; Li P; Li P
- Source:
Nature communications [Nat Commun] 2024 Mar 21; Vol. 15 (1), pp. 2526. Date of Electronic Publication: 2024 Mar 21.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
- Publication Information: Original Publication: [London] : Nature Pub. Group
- Subject Terms:
- Abstract: β-Cell dysfunction and β-cell loss are hallmarks of type 2 diabetes (T2D). Here, we found that trimethylamine N-oxide (TMAO) at a similar concentration to that found in diabetes could directly decrease glucose-stimulated insulin secretion (GSIS) in MIN6 cells and primary islets from mice or humans. Elevation of TMAO levels impairs GSIS, β-cell proportion, and glucose tolerance in male C57BL/6 J mice. TMAO inhibits calcium transients through NLRP3 inflammasome-related cytokines and induced Serca2 loss, and a Serca2 agonist reversed the effect of TMAO on β-cell function in vitro and in vivo. Additionally, long-term TMAO exposure promotes β-cell ER stress, dedifferentiation, and apoptosis and inhibits β-cell transcriptional identity. Inhibition of TMAO production improves β-cell GSIS, β-cell proportion, and glucose tolerance in both male db/db and choline diet-fed mice. These observations identify a role for TMAO in β-cell dysfunction and maintenance, and inhibition of TMAO could be an approach for the treatment of T2D.
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J Biol Chem. 1999 Jul 16;274(29):20197-205. (PMID: 10400636) - Accession Number: FLD0K1SJ1A (trimethyloxamine)
IY9XDZ35W2 (Glucose)
0 (Methylamines)
0 (Insulin) - Publication Date: Date Created: 20240322 Date Completed: 20240325 Latest Revision: 20240325
- Publication Date: 20240325
- Accession Number: PMC10957989
- Accession Number: 10.1038/s41467-024-46829-0
- Accession Number: 38514666
- Source:
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