SUMMARY Pseudopregnancy was induced in 61% of C57BL/St mice that were stimulated cervically with a glass rod for 30 s on the day of oestrus. Within 60 min of stimulation, the concentration of prolactin in the serum increased threefold and appeared to be released in a phasic manner. Subsequently, prolactin was secreted at an enhanced rate for approximately two-thirds of pseudopregnancy, as the level in the serum rose and the level in the pituitary gland dropped. The concentrations of growth hormone (GH) in the serum showed only a minor increase 8 h after cervical stimulation, with no significant rise during the course of pseudopregnancy. Pituitary GH concentrations increased between early and late pseudopregnancy. The DNA and RNA contents of the mammary glands, indices of mammary gland growth and metabolic activity, were both enhanced during pseudopregnancy and paralleled the increases in the secretion of prolactin, whereas mammary gland weight generally followed changes in the level of GH in the pituitary gland. Administration of the prolactin inhibitor 2-bromo-α-ergocryptine reduced the incidence of pseudopregnancy, but neither an inhibitor of GH release, somatostatin, nor an antiserum to mouse GH had any appreciable effects. Injections of ovine prolactin and mouse GH induced the dioestrous state in mice, but only ovine prolactin stimulated the growth of corpora lutea. These results suggest that prolactin is the main hormone involved in the induction and maintenance of pseudopregnancy in the mouse. Injections of ovine prolactin or mouse GH suppressed endogenous levels of the respective hormone; however, prolactin also reduced the level of GH and GH reduced the level of prolactin, suggesting that pituitary hormones can influence not only their own secretion but that of other pituitary hormones as well.
Monomeric mouse prolactin containing small amounts of 125I-labelled prolactin was administered to adult female mice of a high (C3H/St) and low (C57BL/St) mammary tumour strain. Their endogenous prolactin had been suppressed with 2-bromo-alpha-ergocryptine. The chromatographic profile, on Sephadex G-100, of prolactin in the serum of mice injected with mouse prolactin was compared by direct measurement (radioactivity count) and by radioimmunoassay (RIA) at several intervals after injection. With both methods, the injected hormone was found in the serum in predominantly two molecular sizes, the so-called 'big' and 'little' forms. Although 'little' prolactin in both strains constituted a constant 80% of the total hormone at most intervals by direct measurement, it comprised a comparatively smaller proportion by RIA. In addition, the RIA-determined 'little' prolactin, after reaching maximum levels at 15 min, progressively decreased with time, the decrease being greater in the C3H/St than in the C57BL/St strain. Similar experiments with mouse growth hormone revealed no such discrepancies between the radioactivity counts and the RIA measurements. A fraction of both 'big' and 'little' forms in the C3H/St strain failed to precipitate completely after the material had been incubated with an antiserum to mouse prolactin. These results demonstrate that the prolactin injected into mice is metabolized in serum into two non-immunoreactive forms, one that elutes with the same elution volume on Sephadex G-100 column as the monomer and the other that elutes as the 'big' form. Furthermore, the loss of immunoreactivity of monomeric mouse prolactin is greater in the high-tumour C3H/St strain than in the low-tumour C57BL/St strain. Endogenous immunoreactive prolactin, on the other hand, was found mainly in the 'big' form in the serum of female mice of the C3H/St strain under basal conditions, whereas it was present only in the 'little' form in comparable mice of the C57BL/St strain, even though pituitary extracts of both strains contained mainly the 'little' form. These results support the concept that monomeric prolactin in the systemic circulation of the tumour-prone C3H/St strain is largely in a non-immunoreactive form.
The mutant diabetic (db/db) mouse was first described by Hummel et al. in 1966 (1). These mice suffer from metabolic disturbances resembling not insulin-dependent diabetes mellitus in man. The symptoms include hyperglycemia, polyuria, glycosuria and marked obesity. Like the obese mutant ob/ ob, the db/db mice exhibit a paradoxical hyperglycemia concomitant with hyperinsulinemia in early stages of development (2). In later life, the insulin levels of db/db mice return towards normal, but the hyperglycemia persists. Glucose homeostasis under normal conditions is maintained by the interaction of several hormonal factors, which include insulin, growth hormone (GH), somatostatin and glucagon. Desjardins (3) found by bioassay that pituitary G H concentrations and GH-releasing factor (GH-RF) in the hypothalamus were both below normal in mildly hyperglycemic, 4-to 5 week-old db/ db mice. In contrast, the two hormones were present at higher than normal levels in severely hyperglycemic, 12-to I3-week-old diabetics. However, the concentrations of G H in the sera of db/db mice have not been measured. In this study, we have determined the serum levels of immunoreactive GH, insulin, and prolactin (PRL), another pituitary hormone shown to influence glucose homeostasis (4), in normal and db/db mice of both sexes. The observations covered a period from 5 to 32 weeks of age.Materials and methods. Mice used were of the C57BL/KsJ-db m strain, purchased from the Jackson Laboratory, Bar Harbor, Me. Twenty diabetic (db+/db+) and 20 related
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