Regulation of Transporters for Organic Cations by High Glucose.
diabetes
glucose
organic cation transporters
regulation
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
13 Sep 2023
13 Sep 2023
Historique:
received:
01
08
2023
revised:
08
09
2023
accepted:
11
09
2023
medline:
4
10
2023
pubmed:
28
9
2023
entrez:
28
9
2023
Statut:
epublish
Résumé
Endogenous positively charged organic substances, including neurotransmitters and cationic uremic toxins, as well as exogenous organic cations such as the anti-diabetic medication metformin, serve as substrates for organic cation transporters (OCTs) and multidrug and toxin extrusion proteins (MATEs). These proteins facilitate their transport across cell membranes. Vectorial transport through the OCT/MATE axis mediates the hepatic and renal excretion of organic cations, regulating their systemic and local concentrations. Organic cation transporters are part of the remote sensing and signaling system, whose activity can be regulated to cope with changes in the composition of extra- and intracellular fluids. Glucose, as a source of energy, can also function as a crucial signaling molecule, regulating gene expression in various organs and tissues. Its concentration in the blood may fluctuate in specific physiological and pathophysiological conditions. In this work, the regulation of the activity of organic cation transporters was measured by incubating human embryonic kidney cells stably expressing human OCT1 (hOCT1), hOCT2, or hMATE1 with high glucose concentrations (16.7 mM). Incubation with this high glucose concentration for 48 h significantly stimulated the activity of hOCT1, hOCT2, and hMATE1 by increasing their maximal velocity (V
Identifiants
pubmed: 37762353
pii: ijms241814051
doi: 10.3390/ijms241814051
pmc: PMC10531077
pii:
doi:
Substances chimiques
Organic Cation Transport Proteins
0
Organic Cation Transporter 2
0
Metformin
9100L32L2N
Cations
0
RNA, Messenger
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : CI107/11-1-2 and CI107/14-1
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