The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats.
Hyperinsulinemia in obesity has been attributed to insulin oversecretion by pancreatic beta-cells. Beta-cells are equipped with cholinergic and adrenergic receptors; whereas overall acetylcholine action is to potentiate, catecholamines' effect is to inhibit glucose-induced insulin release (GIIR) via alpha2-adrenoceptor. However, it has been shown that beta-adrenergic agonists potentiate glucose response. GIIR was studied in pancreatic islets from hyperinsulinemic adult obese rats, obtained by L-glutamate monosodium (MSG) neonatal treatment. Islets from MSG-rats were more glucose responsive than control ones. Isoproterenol, a beta-adrenergic agonist, inhibited the GIIR in islets from MSG-obese rats. Results indicate that MSG treatment causes alteration on function of beta-cell adrenoceptors.
Marçal
Anderson Carlos
AC
Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Maringá, PR, Brazil.
Grassiolli
Sabrina
S
da Rocha
Diego Neves
DN
Puzzi
Marcelo Aguilar
MA
Gravena
Clarice
C
Scomparin
Dionízia Xavier
DX
de Freitas Mathias
Paulo Cezar
PC
D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000032:analysis; D006946:Hyperinsulinism / Q000139:chemically induced; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D009765:Obesity / Q000139:chemically induced / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate / Q000494:pharmacology
D001786:Blood Glucose; D007328:Insulin; D007545:Isoproterenol; D012970:Sodium Glutamate