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ORIGINAL RESEARCH ARTICLE

Effects of Every-Other-Day Feeding on Prolactin Regulatory Mechanism in Transgenic Human Growth Hormone Mice

Vanesa Jiménez-Ortega^*, Michal M. Masternak, Jacob A. Panici, Zhihui Wang, Andrzej Bartke and Ana I. Esquifino^*,1

^* Departamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense, 28040 Madrid, Spain; and Departments of Physiology and Internal Medicine, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9628

To whom requests for reprints should be addressed at ¹ Departamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense, 28040 Madrid, Spain. E-mail: pelayos{at}med.ucm.es

Transgenic mice overexpressing human growth hormone (hGH) exhibit accelerated aging with functional hyperprolactinemia and greatly depressed endogenous prolactin. Calorie restriction (CR) is widely recognized as the most effective experimental intervention to delay aging. The aim of the present work was to analyze the effects of lifelong overexpression of hGH on prolactin-gene expression as well as the dopamine production at the pituitary level and discern whether this mechanism changes as a function of feeding patterns. Ten-month-old mice fed every other day (EOD) were killed after one day of fasting. The results confirmed typical phenotypic features of these transgenic mice: an increase in body weight, very high hGH plasma concentrations, and hyperinsulinemia. There was a marked inhibition of the expression of the prolactin gene, together with an increased tyrosine hydroxylase (TH) and the long isoform of dopamine receptor type 2 (D2LR) gene expression at the pituitary level. These parameters were not affected by the EOD feeding pattern. These data may suggest an autocrine or paracrine effect of dopamine at the hypophyseal level on prolactin secretion that is independent of the feeding pattern.

Key Words: growth hormone • prolactin • every-other-day feeding • tyrosine hydroxylase • dopamine receptor type 2