In earlier studies it has been shown that prolactin (PRL) is a stimulating factor for the immune system, and it has been suggested that PRL might antagonize immunosuppressive effects of glucocorticoids. PRL has been reported to affect the cytokine secretion pattern, by elevating cytokine gene expression in macrophages, after the onset of sepsis. It also promotes the antibody response in mice where it increases the production of interferon-gamma (IFN-gamma) and inhibits interleukin-1 (IL-1) production. Due to these properties, PRL might influence the development of autoimmune type 1 diabetes. The aim of the present study was to examine the effects of two drugs; PRL and bromocriptine (BC) in vivo on the development of hyperglycemia and pancreatic insulitis in mice treated with multiple doses of streptozotocin (STZ) (40 mg/kg body weight, i.p.). The dopaminergic agonist BC is known to inhibit PRL secretion. In another set of experiments, the direct effects of PRL on the function of pancreatic islets exposed to STZ in vitro were studied. Mice treated with STZ became gradually hyperglycemic, and concomitant treatment with PRL (4 mg/kg body weight) for 21 days significantly reduced the elevation in blood glucose levels from day 10 onwards (P<0.05). Morphologic examinations of the pancreas on day 21 of mice receiving STZ injections revealed a marked insulitis, but only moderate insulitis in the STZ treated animals given PRL. BC administration (10 mg/kg body weight) in combination with STZ did not significantly affect the elevation in blood glucose levels or the insulitis. PRL or BC administration alone did not change the serum glucose concentration. This study indicates that PRL may affect hyperglycemia in the early phase of autoimmune diabetes. We suggest that it might be due to counteraction of autoimmune immunologic mechanisms and/or enhancement of beta-cell regeneration.

This article has been cited by other articles:

				R. Arumugam, E. Horowitz, D. Lu, J. J. Collier, S. Ronnebaum, D. Fleenor, and M. Freemark The Interplay of Prolactin and the Glucocorticoids in the Regulation of {beta}-Cell Gene Expression, Fatty Acid Oxidation, and Glucose-Stimulated Insulin Secretion: Implications for Carbohydrate Metabolism in Pregnancy Endocrinology, November 1, 2008; 149(11): 5401 - 5414. [Abstract] [Full Text] [PDF]

				R. Shao, M. Nutu, B. Weijdegard, E. Egecioglu, J. Fernandez-Rodriguez, E. Tallet, V. Goffin, C. Ling, and H. Billig Differences in Prolactin Receptor (PRLR) in Mouse and Human Fallopian Tubes: Evidence for Multiple Regulatory Mechanisms Controlling PRLR Isoform Expression in Mice Biol Reprod, October 1, 2008; 79(4): 748 - 757. [Abstract] [Full Text] [PDF]

				M. Jackerott, A. Moldrup, P. Thams, E. D. Galsgaard, J. Knudsen, Y. C. Lee, and J. H. Nielsen STAT5 Activity in Pancreatic {beta}-Cells Influences the Severity of Diabetes in Animal Models of Type 1 and 2 Diabetes. Diabetes, October 1, 2006; 55(10): 2705 - 2712. [Abstract] [Full Text] [PDF]