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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolactin deficiency, induced by bromocryptine treatment, brought about reciprocal changes in the ability of adipocytes and acini isolated from lactating rats to synthesize lipids. The capacity to synthesize fatty acids and phospholipids decreased in the mammary gland and increased in adipocytes by bromocryptine treatment. In the mammary gland, the maximum potential activity of the pentose shunt as well as the specific activities of the pathway dehydrogenases were significantly reduced by bromocryptine treatment. Simultaneously, adipose tissue increased its lipogenic capacity but neither the maximum potential of the shunt nor the specific activities of the pentose phosphate shunt dehydrogenases were significantly changed with respect to the control lactating rats. Thus, a differential regulatory mechanism(s) of the pentose phosphate shunt activity appears to operate in these two tissues. Adipocytes from lactating rats showed a poor responsiveness to insulin in terms of lipid synthesis from glucose. In contrast, in adipocytes from bromocryptine treated rats insulin was able to increase lipid synthesis (105%). Sheep prolactin administration 'in vivo' partially reversed the effects of bromocryptine. These data suggest that prolactin mediates adipocytes resistance to insulin during lactation. Phospholipid synthesis, as occurred in fatty acid synthesis, is increased in adipose tissue and decreased in mammary gland by bromocryptine treatment. However, alpha 1-adrenergic stimulation increases phosphatidylinositol turnover to about the same percentages in both mammary gland acini and adipocytes from lactating rats independently of bromocryptine treatment.
Mol Cell Biochem 1990 Mar 27
PMID:Integration of lipid metabolism in the mammary gland and adipose tissue by prolactin during lactation. 234 43

The effects of a GnRH antagonist analogue (N-acetyl-Ala1,D-p-Cl-Phe2,D-Trp3,6-GnRH, Ant.) and a GnRH antiserum (A/S) on the development of pituitary-testicular function were studied in immature (23/24-31/32-day-old) rats. In another experiment the Ant. treatment was combined with bromocriptine (BR)-induced hypoprolactinaemia. Ant. and A/S decreased serum and pituitary levels of LH and FSH, and BR those of Prl (P less than 0.01-0.05). Testicular testosterone (T) and progesterone (P) contents were significantly decreased only by Ant. (P less than 0.01). Ant. decreased the weights of the testes, ventral prostates and seminal vesicles, as well as testicular LH, FSH and Prl receptors (R) (P less than 0.01-0.05). BR decreased LH-R but had no effect on Prl-R. Both Ant. and A/S decreased available pituitary GnRH-R (P less than 0.01), but free testicular GnRH-R were reduced only by Ant. BR increased GnRH receptors in the pituitaries. It is concluded that Ant.-induced low gonadotropin levels in immature animals inhibit the developmental increase of testicular weight, gonadotropin and Prl-R, steroidogenesis and androgen action on accessory sex glands. Hypoprolactinaemia had an additive inhibitory effect to the antigonadal effects of Ant. The testis tissue of immature (23/24-day-old) animals already contains GnRH-R. In general, developing animals are clearly very sensitive to the antigonadal actions of Ant. and BR, whereas the effect of GnRH-A/S is less pronounced than in adults.
Mol Cell Endocrinol 1984 Feb
PMID:Pituitary-testicular function in immature rats after treatment with GnRH antagonist, GnRH antiserum and bromocriptine. 632 70

An ontogenetic and endocrinological study has been designed on developing rats in uterus of mothers tryptophan deprived at day 1 (exp. 1) and day 14.5 (exp. 2) of conception to verify the supposed determining role of the serotoninergic system (SS) in sexual differentiation in mammals. Tryptophan-free feeding has been pursued uninterruptedly in the litter after birth, during lactation and postnatal development. Tryptophan-free pregnant rats were obtained by exclusion of tryptophan sources from chow. In both exp. 1 and exp. 2 the litter showed at birth a significant physical under evolution, that worsened, during post-natal development, to a much more marked dwarfism in exp. 1 pups. At 30 days postnatal age, whereas the female exp. 1 rats showed a right-timed onset of puberty, neither descensus of the testes nor spermatogenesis could be observed in the male rats of the same experiment. Endocrinologically the males showed a significant reduction of plasma FSH levels, but also a slight increase of those of LH. Moreover, a marked hypoandrogenism and a severe hypoprolactinemia characterized the males of this group. Hypoprolactinemia was the major endocrinological finding also in the female litter, which, however, at 30 days p.n. age showed the typical histological patterns of a cycling ovary, i.e. growing secondary follicles with scattered antral spaces, and thus a right-timed pubertal maturation, in spite of the significant lower plasma levels of pituitary gonadotropins and sex steroids. When mothers were tryptophan deprived at 14.5 of pregnancy (exp. 2), the litters showed a less marked dwarfism, persistent, severe hypoprolactinemia as in exp. 1 rats, but a normal right-timed onset of puberty in both male and female rats. Taken together these findings confirm on the one hand the close relationship between SS and PRL. On the other hand, they suggest a major, crucial role of PRL played in the male rat before day 14.5 of intrauterine development, presumably intervening in the synthesis of LH receptors sites by the maturing Leydig cells in the male gonads. Growth hormone concentrations in both sexes dwarf rats were lower than in control rats.
J Mol Histol 2008 Oct
PMID:Embryonic and postnatal development in experimental tryptophan deprived rats. A preliminary study. 1871 58