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Moxonidine and S43126 Enhance Glucose Uptake into Cells and Cause Insulin Release
Author(s) -
Edwards Lincoln Paul,
Tesfai Jerusalem,
Crane Louis,
BaziardMouysset Genevieve
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1095.9
Subject(s) - moxonidine , imidazoline receptor , insulin , endocrinology , medicine , chemistry , insulin resistance , glucose uptake , blood pressure , agonist , pharmacology , receptor
Certain imidazoline compounds have the potential to act as monotherapy for hypertension and hyperglycemia. We hypothesize that I 1 ‐imidazoline agonists act centrally to lower blood pressure and enhance glucose uptake by causing insulin release and phosphorylation of protein kinase B (PKB). Novel I 1 ‐imidazoline agonist S43126 (5 nmol) and moxonidine (5nmol) were injected cumulatively into the brain of spontaneously hypertensive rats, followed by measurement of blood pressure. Rat‐tail arterial strips were tested for contractile response to imidazoline compounds. Time‐course and dose‐response studies were carried out in A7R5 rat smooth muscle cells, followed by Western blotting. ELISA was used to measure insulin release from Min 6 pancreatic beta cells. Our results showed that both S43126 and moxonidine lowered arterial pressure by 20 mmHg and 45 mmHg respectively. Moxonidine, but not S43126 caused contraction of tail artery. Moxonidine caused phosphorylation of PKB in a time and dose‐dependent manner, and enhanced glucose uptake in A7R5 cells, in a dose‐dependent manner following 30 min treatment. Both compounds enhanced insulin secretion in Min 6 cells in a dose‐dependent manner following 60 min of treatment. These data indicate that I 1 ‐imidazoline agonists should be further studied as agents to reduce blood pressure and improve insulin resistance associated with metabolic diseases.