Study of the relationship between type-1 diabetes mellitus, prolactin hormone and immune system in rats

ABSTRACT

The effects of prolactin [PRL] on lactation and reproductive organs are well known. However, its effects on other target organs and its physiological consequences remain poorly understood. Prolactin was shown earlier to act as a stimulating factor for the immune system and thus it might influence the development of autoimmune diseases, as in type-I diabetes mellitus [DM]. The aim of the present work was to clarify the role of PRL in the development of autoimmune type-1 DM aiming to answer the question of whether PRL may have a beneficial effect in type-1 DM or not. The study was conducted on sixty male albino rats matched for age and weight. Rats were divided into six groups each of ten rats; group 1 a control group [C], group 2 a vehicle-treated group [V], group 3 Streptozotocin [STZ] treated group [STZ was given intraperitoneally [i.p.] in a dose of 40 mg/kg body weight [b.w] daily for 5 consequetive days], group 4 a group of STZ + PRL [PRL was given i.p. in a dose of 4 mg/Kg b.w starting with STZ and continuing for 21 days, group 5 a group of STZ + Bromocriptine [BC], a PRL antagonist. BC was given i.p. in a dose of 10 mg/kg b.w for 21 days and group 6 a group of STZ + PRL + BC. The study showed significant elevations of serum glucose, glycosylated Hb, [HAlc], serum Interleukin-1 beta [IL-1 beta], and interferon-gamma [IFN-gamma] levels in STZ treated rats, compared to the control and vehicle treated groups. Administration of PRL with STZ induced a significant decrease in the mean values of the previous parameters compared to STZ-only treated rats, still these parameters were not close to the mean control values. BC administration with STZ and PRL prevented the induced changes found with STZ and PRL. The results of the present study indicated that PRL might affect the associated immunological changes occurring in the early phases of developing type-1 DM. The partial protective effect of PRL was suggested to be due to suppression of autoimmune mechanisms as indicated by the significant reduction of IL-1 beta and IFN-gamma in PRL + STZ treated group as compared to control mean values