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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large subcutaneous doses (2 mg/21 days) of estradiol valerate (EV) given over several months will induce a prolactin and growth hormone-secreting pituitary tumor in female rats. The medial basal hypothalami (MBHs) of such EV-treated animals were examined at different time intervals with light and electron microscopes to determine whether EV affects the MBH and to relate any observed effects to the process of tumorigenesis. The MBHs of extensively treated rats exhibited profound glial and neuronal changes. The filament content of astrocytes was greatly increased and large dense pleomorphic inclusions filled both astrocytic perikarya and processes. Degenerating neuronal elements have been observed in the neuropil of extensively treated animals. Dark cells identified as M cells were seen to engage in phagocytosis and were loaded with dense inclusions. Some neurons in MBH contained large quantities of lipofuscin that was different in appearance from that of normal females of the same age. The glial reaction developed gradually. At earlier stages of EV treatment there were fewer reactive glia and these contained fewer inclusions. Myelin figures often occurred in these early inclusions. Reactive glia in EV-treated rats did not appear in the preoptic area, dorsomedial nucleus or lateral hypothalamus but were found in ventromedial nucleus. Retired breeders and starvation-stressed rats resembled normal controls. These pathological changes in MBH may result from a direct effect of EV on the hypothalamus. It is possible that, in addition to its effects on the hypophysis, EV suppresses or injures hypophysiotropic cells in MBH, thus releasing pituitary chromophobes from inhibitory hypothalamic influences. This could result in hypersecretion and neoplasia.
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PMID:Cytopathological effects of estradiol on the arcuate nucleus of the female rat. A possible mechanism for pituitary tumorigenesis. 17 Aug 18

To investigate further the alterations in pituitary-thyroid function seen during starvation, we have measured basal and TRH-stimulated serum levels of thyrotropin (TSH), prolactin (PRL), growth hormone, thyroxine (T4), triiodothyronine (T3), free T4, free T3, and reverse T3 during prolonged fasting in seven obese men. Fasting was associated with a significant decrease in serum (4, (3, and free T3, while there was an increase in serum reverse T3; these values tended to return toward pre-fast levels as the fast continued beyond 3 weeks. No significant changes were seen in basal serum TSH, PRL, growth hormone, or free T4. Although the TSH response to TRH was diminished during fasting, PRL, T4, and T3 responses were unchanged. In addition to transient alterations in the peripheral metabolism of T4, these findings suggest that alterations in the thyroid hormone binding capacity of serum carrier proteins may occur during fasting. The blunted TSH response to TRH despite reduction of serum T3 concentration suggests that subtle alterations in hypothalamic-pituitary function may also occur.
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PMID:Alterations in basal and TRH-stimulated serum levels of thyrotropin, prolactin, and thyroid hormones in starved obese men. 41 Aug 22

GH12C1, a clonal strain of rat pituitary tumor cells in culture (GH cells), does not produce detectable amounts of prolactin. 5-Bromodeoxyuridine (BrdUrd), the thymidine analogue, at sublethal concentrations (3-5 microgram/ml) induces prolactin synthesis in these cells. BrdUrd also induces prolactin synthesis in F1BGH12C1 cells, a BrdUrd resistant (BrdUrdr) substrain isolated from GH12C1 cells. The F1BGH12C1 strain is not drug dependent, but its resistance to BrdUrd is a stable phenotype. The significant features of the induction of prolactin synthesis in the BrdUrdr strain are the increased net synthesis of prolactin and the shortening of the lag period of prolactin induction. As BrdUrd concentration in the growth medium is increased, the rise in prolactin synthesis parallels the increased incorporation of BrdUrd into DNA. Prolactin synthesis is first detected when BrdUrd replaces 20-25% of the thymidine in DNA. BrdUrd can replace up to 75-80% of the thymidine within 2 d of treatment. Partial starvation of these cells under specified growth conditions does not affect the general growth pattern of the cells, general protein synthesis, and thymidine uptake, but does affect DNA synthesis. When cells are cultured under conditions in which DNA synthesis is preferentially inhibited, BrdUrd does not induce prolactin synthesis, suggestive of a DNA-mediated mechanism of action for the drug.
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PMID:On the mechanism of 5-bromodeoxyuridine induction of prolactin synthesis in rat pituitary tumor cells. 47 83

Fatty acid synthesis in the mammary gland of lactating rats in vivo was 5-fold higher than in the liver. Starvation decreased fatty acid synthesis in the gland 50-fold, whereas refeeding for 2h completely reversed this change. The plasma insulin concentration decreased 2-fold in starvation and was restored to the fed-rat value on refeeding. Glucagon and prolactin concentrations did not always change in parallel with lipogenesis, suggesting that insulin may be a regulator of this process in the gland.
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PMID:Evidence for a role of insulin in the regulation of lipogenesis in lactating rat mammary gland. Measurements of lipogenesis in vivo and plasma hormone concentrations in response to starvation and refeeding. 72 15

Growth hormone (GH) cells of rats were studied on days, 2, 4 and 7 of starvation. Immunoperoxidase staining for light microscopy confirmed the presence of GH in the pituitaries of all groups of animals. Electron microscopy revealed crinophagy in the cytoplasm of GH cells on days 4 and 7. By ultrastructural morphometry, volume density and the diameter of secretory granules in the cytoplasm of GH cells remained unchanged. Blood GH determinations showed a significant decrease on day 4 of the starvation period. On day 7 most of the values were in the range of the controls. Blood prolactin levels fell significantly on day 7. It appears that the pituitary is capable of secreting GH even in rats completely deprived of exogenous nutrients.
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PMID:Effect of starvation on pituitary growth hormone cells and blood growth hormone and prolactin levels in the rat. 95 50

Male and female wild Norway rats (Rattus norvegicus Erxleben) and males and female albino outbred rats (Ipf:RIZ) were crossbred. The resulting animals (F1 hybrids) were the control, noninbred group (0% inbred). By systematic full-sib mating, two experimental groups (50 and 91% of inbred) were produced. Half of each group (both males and females) was exposed to physical stress (3 days of starvation and 3 hr of swimming). The other half of each group was anesthetized using ether to collect blood. The anterior pituitary hormone concentrations of prolactin (PRL), corticotropin (ACTH), and growth hormone (rGH) in blood serum were determined by the radioimmunoassay method. Significant relationships between the PRL, ACTH, and rGH concentrations in blood serum and the inbreeding coefficient were observed: A significant PRL content decrease in blood serum occurred (linear function) and the rGH and ACTH content diminished significantly rapidly (quadratic function). These changes were affected by an increase in homozygosity. Stress significantly influenced PRL, ACTH, and rGH concentrations as well. The sex of rats significantly determined PRL and ACTH content only. Hormone levels were also influenced by interactions between the factors studied (inbred level, sex, stress).
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PMID:The effect of genetic variability (degree of homozygosity) on serum levels of the anterior pituitary hormones prolactin, corticotropin, and growth hormone in rats. 133 58

Recent pharmacological studies have more precisely characterised the nature of the inhibitory effect of brain serotonin (5-hydroxytryptamine) on feeding behaviour. Thus, the brain sites and receptors involved have been identified, and a possible physiological role of endogenous serotonin in controlling natural patterns of eating and nutrient selection has been defined. The medial hypothalamus is believed to be a critical location in the mediation of serotonin's action. Specifically, the paraventricular and ventromedial nuclei are known to be involved in controlling energy balance, while the suprachiasmatic nucleus determines circadian patterns of eating. Serotonergic stimulation of these 3 nuclei with exogenous serotonin or drugs that release endogenous serotonin, preferentially reduces carbohydrate intake in naturally feeding animals through satiety mechanisms involved in the termination of feeding. This phenomenon is mediated by serotonin and possibly serotonin receptors, in contrast to serotonin autoreceptors which potentiate feeding possibly by inhibiting serotonin release. The activity of serotonergic function in the medial hypothalamus exhibits a circadian rhythm which is characterised by a peak at the beginning of the active cycle when the motivation to eat is strongest and is triggered by deficits in energy stores. At this time, carbohydrate is found to be the naturally preferred macronutrient, and it appears that serotonin becomes most activated under these conditions to terminate the carbohydrate-rich meal, possibly by activating satiety neurons localised in the medial hypothalamus. In this process, serotonin may interact antagonistically with noradrenaline (norepinephrine) and its alpha 2-noradrenergic receptors that normally function to enhance carbohydrate intake at the onset of the natural feeding cycle. Moreover, while inducing satiety for carbohydrate, serotonin may also play a role in switching the animal's preference towards protein. The regulation of this macronutrient is closely linked to that of carbohydrate, and it is normally preferred in the second meal of the natural feeding cycle. Most of the pharmacological evidence to date generally supports the hypothesis that disturbances in serotonin function occur in eating disorders. Decreases in plasma tryptophan, urinary 5-hydroxyindoleacetic acid (5-HIAA), platelet serotonin binding and basal cerebrospinal fluid 5-HIAA in anorexia nervosa normalise upon weight restoration and appear to be starvation effects. These alterations in serotonergic function may however perpetuate the symptomatology of anorexia nervosa once the illness is set in motion. Some drugs which in part affect serotonergic function facilitate weight gain in conjunction with an integrated psychotherapeutic and behavioural programme. Patients with bulimia nervosa, regardless of the presence of anorexia nervosa or major depression, who have been relatively weight stable and free of binge/vomit episodes for at least 3 weeks, have significantly blunted prolactin responses to the serotonin agonists. These findings indicate that post-synaptic responsiveness in hypothalamic-pituitary serotonergic pathways is reduced in bulimia. Similar alterations in other serotonin pathways at or above the level of the hypothalamus may contribute to binge eating and other behavioural symptoms in bulimic patients. The clinical response to several psychotropic agents known to potentiate serotonergic transmission further substantiates a serotonin dysregulation hypothesis of bulimia nervosa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of serotonin in eating disorders. 219 74

This paper discusses hormonal and metabolic reactions of healthy volunteers exposed to 14-day starvation. This exposure led to many-fold increase of plasma and urinary epinephrine (E); drastic increase of ACTH and beta-endorphin (BE), morning and integrated concentrations of cortisol and STH, aldosterone, T3, glucagon, cAMP, cGMP, cAMP-cGMP, acetyl choline (AC), free fatty acids (FFA), lactate, metanephrine (MN) excretion; decrease of plasma norepinephrine (NE) and unchanged NE excretion; decrease of plasma concentrations of TTH, T4, T3, prolactin (PL), insulin (morning and integrated concentrations), C-peptide, FSH, LH, testosterone, histamine, prostaglandins (PG) A + E, PG F2, glucose and pH, as well as decrease of excretion of homovanillic acid (HVA), vanillyl mandelic acid (VMA), normetanephrine (NMN) and MN-E, NMN:NE. On recovery day 14 concentrations of E, NE, BE, STH, AC, cAMP, cGMP, FFA as well as E and dopamine excretion remained elevated while concentrations of T3, PL, FT, LT, testosterone PG A + E, PG 2 and excretion of MN, HVA, VMA, MN:E remained decreased, while other parameters returned to the normal.
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PMID:[Hormonal and metabolic reactions in the human body during prolonged starvation]. 237 73

Metoclopramide has previously been shown to inhibit the ketosis of starvation in rats and humans. The effect of D2-dopaminergic blockade on post-exercise ketosis was, therefore, studied in 6 carbohydrate-starved non-athletic persons who had just completed a 9-km walk in mountainous terrain. There were nine control subjects who went on the walk, but who did not ingest metoclopramide. Metoclopramide (0.15 mg.kg-1 body mass) caused a highly significant rise in the plasma prolactin concentration, but did not influence blood concentrations of 3-hydroxybutyrate, free fatty acid, glucose, insulin or glucagon. Unlike ketosis in starvation, therefore, neither prolactin, nor the D2-dopaminergic system play a part in the genesis of post-exercise ketosis.
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PMID:D2-dopaminergic blockade does not influence post-exercise ketosis in non-athletes. 268 63

1. Rats submitted to starvation or water deprivation showed a decrease in LH and prolactin serum levels. 2. 5-HT was increased without changes in DA and NA in cerebral cortex of starved rats. 3. Neurotransmitters did not change in hypothalamus of starved rats but water deprivation decreased NA and increased 5-HT.
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PMID:Starvation and dehydration: effect on hypothalamic monoamines and serum LH and prolactin. 270 68


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