Intermediary Metabolism in the Liver and Adipose Tissue of Rats with Hormone-Secreting Pituitary Tumors

MacLeod, Robert M.; Bass, Mary B.; Huang, Shih‐Tsung; Smith, M. Carolyn

doi:10.1210/endo-82-2-253

Cited by 20 publications

(6 citation statements)

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“…Studies in animals suggest that prolactin may have potent and complex effects on lipid metabolism. In particular prolactin is reported to increase glucose uptake and fatty acid synthesis in adipose tissue (Hamid, et al, 1965) and lipogenesis in liver (MacLeod et al, 1968). Prolactin is also reported to cause accelerated lipid hydrolysis in adipose tissue (Hamid et al, 1965) and raises fatty acid levels in children (Elsair & Denine, 1970).…”

Section: Discussionmentioning

confidence: 99%

Plasma lipids and prolactin in patients with breast cancer

Bani¹,

Williams²,

Boulter³

et al. 1986

Br J Cancer

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Summary In a comparative study of pre-and postmenopausal women with benign and malignant breast disease, a number of differences were observed in circulating plasma prolactin and lipid concentrations. Plasma lipids, phospholipids, triglycerides, cholesterol and free fatty acids were all higher in blood obtained from breast cancer patients prior to surgery. HDL-Cholesterol levels were significantly lower in these patients. These differences remained when the patient groups were sub-divided according to menopausal status. Plasma prolactin concentrations were also found to be higher in cancer compared with non-cancer patients, this effect being more marked in premenopausal than in postmenopausal patients. Premenopausal patients with invasive or poorly differentiated disease had significantly higher prolactin levels than those with non-invasive disease. No correlations were found between plasma prolactin and any of the lipid fractions.

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Section: Discussionmentioning

confidence: 99%

Plasma lipids and prolactin in patients with breast cancer

Bani¹,

Williams²,

Boulter³

et al. 1986

Br J Cancer

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“…The adenoma was chosen since it is an abundant source of mammotrophs which constitute more than 95% of the cell population (I@, and since it is sensitive to the inhibitory effects of D A exerted on PRL release and tumor size (19,20) through high affinity D, receptors which are normal from a pharmacological point of view (21). The 7315a and MtTWIS tumors secrete PRL and small amounts of POMC-derived peptides and growth hormone, respectively (22,23). Although containing high affinity D, receptors, they are resistant to the inhibitory effects of D A exerted on baseline PRL release and on tumor growth (24,25).…”

mentioning

confidence: 99%

Regulation of Basal and Stimulated Prolactin Release in Prolactin‐Secreting Rat Pituitary Tumors*

Lafond

Bouvier

Forget

et al. 1989

J Neuroendocrinology

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To better understand the mechanisms of the inhibitory effects of dopamine on pituitary prolactin release, we have utilized an estrone-induced, benign and dopamine-sensitive rat pituitary adenoma and two malignant, transplantable and dopamine-resistant rat pituitary tumors, 7315a and MtTW15. Enzymatically dispersed and Percoll purified cells obtained from the three tissues were incubated for 30 min in media with or without Na+ and in the presence or the absence of dopamine and/or various prolactin releasers for evaluating the secretion of prolactin under baseline and experimental conditions. In some experiments, the cells were pretreated for 16 h with pertussis toxin to evaluate the eventual presence and role of pertussis toxin-sensitive G proteins. Dopamine inhibited baseline prolactin release by adenomatous lactotrophs in a Na+-dependent manner, but was totally inactive with 7315a and MtTWl5 cells. The Caz+ channel agonist BAY K 8644 stimulated prolactin release with all three preparations and its effects were enhanced by a Na+-free medium. Dopamine antagonized the stimulatory effects of BAY K 8644 with adenomatous and 7315a cells only, even in the absence of Na+. Pertussis toxin pretreatment significantly increased baseline prolactin release by adenomatous and MtTW15 cells and abolished dopamine inhibition of adenomatous lactotrophs baseline hormone release. BAY K 8644, TRH and vasoactive intestinal peptide, stimulated prolactin release by adenomatous cells and this effect was antagonized by dopamine in a pertussis toxin-sensitive manner. All prolactin releasers, except TRH, were effective also with 7315a cells, and its actions were not blocked by pertussin toxin. The stimulatory effects of BAY K 8644 and vasoactive intestinal peptide on 7315a cells were enhanced by pertussis toxin pretreatment. The results obtained with an almost pure preparation of adenomatous lactotrophs confirm the existence of a dual mechanism of dopamine inhibitory action on prolactin release: 1) a Na+-dependent action exerted on baseline, and 2) a Na+-independent action exerted on stimulated prolactin release. They also indicate that both actions are exerted through pertussis toxin-sensitive G proteins. Furthermore, our results show the presence in transplantable pituitary tumors 7315a and MtTW15 of multiple and diverse anomalies in the regulation of prolactin release probably due, at least partly, to anomalies of one or more G proteins andlor neurotransmitter receptors.

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“…1969). A different approach to the study of the role of GH in the regulation of pathways leading to R5P formation and thus to PRPP synthesis was provided by the use of rats bearing a transplantable GH hormone‐secreting pituitary tumour, thus providing an animal exposed to a continuously high concentration of the hormone (MacLeod et al. 1968; Gumaa et al.…”

Section: Discussionmentioning

confidence: 99%

“…Measurements of hepatic changes in hypophysectomized rats showed that transketolase, the rate-limiting enzyme of the non-oxidative route of R5P formation, was decreased significantly and restored to normal by treatment with GH (Novello et al 1969). A different approach to the study of the role of GH in the regulation of pathways leading to R5P formation and thus to PRPP synthesis was provided by the use of rats bearing a transplantable GH hormone-secreting pituitary tumour, thus providing an animal exposed to a continuously high concentration of the hormone (MacLeod et al 1968;Gumaa et al 1969). The examination of both the oxidative and non-oxidative segments of the PPP showed only marginal changes in the activities of G6P dehydrogenase and 6PG dehydrogenase, contrasting with the nonoxidative route where striking increases were observed, in the case of transketolase up to +70%.…”

Section: Discussionmentioning

confidence: 99%

Effects of long‐term experimental diabetes on adrenal gland growth and phosphoribosyl pyrophosphate formation in growth hormone‐deficient dwarf rats

Kunjara

Greenbaum

McLean

et al. 2012

Int J Experimental Path

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The availability of growth hormone (GH)-deficient dwarf rats with otherwise normal pituitary function provides a powerful tool to examine the relative role of hyperglycaemia and the reordering of hormonal factors in the hypertrophy-hyperfunction of the adrenal gland that is seen in experimental diabetes. Here, we examine the effects of long-term (6 months) experimental diabetes on the growth of the adrenal glands; their content of phosphoribosyl pyrophosphate (PRPP); and the activity of the PRPP synthetase, G6P dehydrogenase and 6PG dehydrogenase enzymes in GH-deficient dwarf rats compared to heterozygous controls. These parameters were selected in view of the known role of PRPP in both de novo and salvage pathways of purine and pyrimidine synthesis and in the formation of NAD, and in view of the role of the oxidative enzymes of the pentose phosphate pathway in both R5P formation and the generation of the NADPH that is required in reductive synthetic reactions. This study shows that GH deficiency prevents the increase in adrenal gland weight, PRPP synthetase, PRPP content and G6P dehydrogenase and 6PG dehydrogenase. This contrasts sharply with the heterozygous group that showed the expected increase in these parameters. The blood glucose levels of the groups of long-term diabetic rats, both GH-deficient and heterozygous, remained at an elevated level throughout the experiment. These results are fully in accord with earlier evidence from studies with somatostatin analogues which showed that the GH-insulin-like growth factor I (IGF-I)-axis plays a key role in the adrenal diabetic hypertrophy-hyperfunction syndrome.

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Intermediary Metabolism in the Liver and Adipose Tissue of Rats with Hormone-Secreting Pituitary Tumors

Cited by 20 publications

References 0 publications

Plasma lipids and prolactin in patients with breast cancer

Plasma lipids and prolactin in patients with breast cancer

Regulation of Basal and Stimulated Prolactin Release in Prolactin‐Secreting Rat Pituitary Tumors*

Effects of long‐term experimental diabetes on adrenal gland growth and phosphoribosyl pyrophosphate formation in growth hormone‐deficient dwarf rats

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