Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

Original Data

Rev Diabet Stud, 2007, 4(3):185-194

DOI 10.1900/RDS.2007.4.185

Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

Sylvie Durant¹, Josiane Coulaud², Francoise Homo-Delarche²

¹INSERM U530, Centre Universitaire-UFR biomedicale, 45, rue des Saints-Peres, 75006 Paris, France
²CNRS UMR 7059, Universite Paris 7 / D. Diderot, 2, place Jussieu, 75271 Paris Cedex 05, France
Address correspondence to: Francoise Homo-Delarche, e-mail: fhomodel@wanadoo.fr

Keywords: type 1 diabetes, NOD mouse, bromocriptine, insulin, glucagon, corticosterone, dopamine, L-Dopa

Abstract

The effects of bromocriptine (10 mg/kg), known to inhibit prolactin secretion and lower autoimmune processes, were studied on glucose homeostasis in non-fasted non-obese diabetic mice, a spontaneous model of type 1 diabetes. Hyperglycemia was observed 120 and 240 min after i.p. but not s.c. injection. Bromocriptine administration i.p. led to rapid and marked hyperglycemia characterized by sexual dimorphism with males having higher glycemia than females. Bromocriptine induced a rapid but transient decrease in insulinemia in males only and biphasic increases in glucagon levels and a sustained stimulatory effect on circulating corticosterone in both sexes. Bromocriptine-induced hyperglycemia involved D2-dopaminergic receptors, as demonstrated by the inhibitory effect of the D2-dopamine antagonist, metoclopramide (10 mg/kg). Simultaneous injection of bromocriptine and metoclopramide also blocked the rise in blood corticosterone. In conclusion, by inducing hyperglycemia, i.p. bromocriptine administration to prediabetic autoimmune mice may counteract its beneficial anti-immunostimulatory effects.

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