UMLS:C0038187 - FACTA Search

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

The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160-169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSH beta mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160-169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160-169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that alpha-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0.2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSH beta mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone.
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PMID:Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland. 779 20

It is well recognized that starvation and malnutrition are associated with a low-T3 syndrome in man. A similar condition has been observed after intake of a low carbohydrate hypocaloric diet. However, little is known about the influence of iodine on these conditions. Therefore, we evaluated the effect of iodine supplementation on thyroid function before and after a short-term intake of a low carbohydrate diet in normal subjects residing in an iodine-deficient area. The study was performed in 16 young euthyroid, nonobese volunteers (11 males, 5 females). The subjects were placed on a low carbohydrate (800 kcal) diet for 4 days. Eight subjects received 500 micrograms iodine (oral) daily beginning 4 weeks before diet. The control group (n = 8) received no iodine. After iodine supplementation, iodine excretion increased from 52 to 405 micrograms iodine/g of creatinine. Total T4 showed a slight but significant increase (104.2 nmol/l vs. 115.8 micrograms/dl; p < 0.001); fT4 was unchanged. The intake of the hypocaloric low carbohydrate diet resulted in a striking decrease in both total and free T3 and an increase of rT3 irrespective of iodine supplementation. T4 and fT4 were not affected in either group. During diet, iodine administration resulted in a decrease of basal TSH from 2.3 to 1.2 mU/l (p < 0.05), delta TSH from 10.3 to 4.5 mU/l (p < 0.01) and delta T3 (T3 180 min after TRH) from 0.7 to 0.3 nmol/l (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of small doses of iodine on thyroid function during caloric restriction in normal subjects. 826 74

In the rat, 48 h of food deprivation significantly reduces hypothalamic paraventricular nucleus (PVN) thyrotropin-releasing hormone (TRH) gene expression, anterior pituitary thyrotropin (TSH) gene expression and circulating triiodothyronine (T3). Using in situ hybridization histochemistry, we have now assessed the effect of selective nutritional deprivation, by comparing protein-free and protein and fat-free diets with a normal diet matched for total energy content. As previously demonstrated, fasting markedly reduced PVN TRH transcripts, pituitary TSB beta transcripts, circulating T3 and body weight. Compared to rats fed a control diet, rats fed a protein-free or a protein and fat-free diet of similar energy content showed a highly significant decrease in PVN TRH transcripts, pituitary TSB beta transcripts and circulating T3 levels. The exclusion of fat from the protein-free diet did not produce any further decline in the parameters measured. This indicates that variations in the protein composition alone of the diet are sufficient to reduce hypothalamic TRH mRNA, pituitary TSB beta mRNA and plasma T3, and are the predominant factors in the TRH response to starvation.
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PMID:The effect of dietary protein on thyrotropin-releasing hormone and thyrotropin gene expression. 846 89

We have investigated the effects of food deprivation on nitric oxide synthase (NOS) transcript levels in the rat paraventricular (PVN) and supraoptic nuclei (SON), using in situ hybridization histochemistry. Food deprivation for 48 h significantly and consistently reduced NOS transcript prevalence by approximately 50% in both sites. Since there is considerable evidence for an important role of 5-HT in feeding behaviour, we then examined the effect of food deprivation on NOS gene expression in the PVN following para-chlorophenylalanine (PCPA)-induced hypothalamic 5-HT depletion. As starvation causes central down-regulation of the thyroid axis, changes in thyrotropin-releasing hormone (TRH) and pituitary thyrotrophin (TSH) transcript prevalence were used as internal controls. PCPA pretreatment (200 mg/kg body weight as a single daily dose ip for 2 days) had no significant effect on basal levels of NOS, TRH or TSH transcripts, or on the effect of a subsequent 48 h fast, which significantly reduced all three. These results show for the first time, that food deprivation for 48 h significantly reduces NOS gene expression in the rat PVN and SON. Secondly, that basal levels and the fasting-induced reductions in the prevalence of NOS, TRH and TSH transcripts were not affected by PCPA-induced hypothalamic 5-HT depletion. Therefore, at least under the experimental conditions used here, 5-HT does not appear to be involved in setting baseline levels- or in the starvation-induced inhibition of NOS or thyroid axis gene expression in the PVN.
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PMID:Inhibition of hypothalamic nitric oxide synthase gene expression in the rat paraventricular nucleus by food deprivation is independent of serotonin depletion. 874 23

The reduced thyroid activity during short-term starvation is associated with a lowered hypothalamic synthesis and secretion of TRH. However, little is known about the cause of the reduced thyroid function during prolonged malnutrition. We have therefore studied the effects of food reduction to one-third of normal (FR33) on the hypothalamus-pituitary-thyroid axis of male and female Wistar rats. After 3 weeks body weights of FR33 rats were almost 50% lower than those of controls. In both sexes, FR33 caused marked increases in serum corticosterone, and decreases in serum TSH, thyroxine (T4), free T4, tri-iodothyronine (T3) and free T3. While the free T3 fraction (FFT3) in serum decreased, the free T4 fraction (FFT4) tended to increase. Electrophoretic analysis indicated that decreased FFT3 was correlated with an increased thyroxine-binding globulin, while the increase in FFT4 seemed due to a decreased thyroxine-binding prealbumin binding capacity. Total RNA and proTRH mRNA in the hypothalamus were not affected by FR33. Median eminence and posterior pituitary TRH content tended to increase in FR33 rats, suggesting that hypothalamic TRH release is reduced in FR33 rats. Anterior pituitary TSH content was decreased by FR33 in both sexes, but pituitary TSH beta mRNA and TRH receptor status were not affected except for increased pituitary TSH beta mRNA in female FR33 rats. Although FR33 had no effect on pituitary weight, pituitary RNA and membrane protein content in FR33 rats were 50-70% lower than values in controls. In conclusion, prolonged food reduction suppresses the pituitary-thyroid axis in rats. In contrast to short-term food deprivation, the mechanism whereby serum TSH is suppressed does not appear to involve decreases in proTRH gene expression, but may include effects on pituitary mRNA translation. Our results further support the hypothesis that TSH release may be lowered by increased corticosterone secretion, although the mechanism of this effect may differ between acute starvation and prolonged food reduction.
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PMID:Effects of long-term food reduction on the hypothalamus-pituitary-thyroid axis in male and female rats. 886 83

Prolonged fasting is associated with a number of changes in the thyroid axis manifested by low serum T3 and T4 levels and, paradoxically, low or normal TSH. This response is, at least partly, caused by suppression of proTRH gene expression in neurons of the hypothalamic paraventricular nucleus (PVN) and reduced hypothalamic TRH release. Because the fall in thyroid hormone levels can be blunted in mice by the systemic administration of leptin, we raised the possibility that leptin may have an important role in the neuroendocrine regulation of the thyroid axis, through effects on hypophysiotropic neurons producing proTRH. Adult male, Sprague-Dawley rats were either fed normally, fasted for 3 days, or fasted and administered leptin at a dose of 0.5 microg/gm BW i.p. every 6 h. Fasted animals showed significant reduction in plasma total and free T4 and T3 levels compared with controls, that were restored toward normal by the administration of leptin. Percent free T4, but not percent free T3, increased during fasting, further suggesting a reduction in plasma transthyretin levels that did not return to fed levels after leptin administration. By semiquantitative analysis of in situ hybridization autoradiograms, proTRH messenger RNA in medial parvocellular PVN neurons was markedly suppressed in the fasting animals but was restored to normal by leptin administration [fed vs. fast vs. fast/leptin (density units x 10(8)): 8.5 +/- 0.4, 3.2 +/- 0.2, 8.1 +/- 0.8]. In contrast, proTRH messenger RNA in adjacent neurons in the lateral hypothalamus that do not have a hypophysiotropic function remained unchanged by any of the experimental manipulations. These findings indicate that leptin has a selective, central action to modulate the hypothalamic-pituitary-thyroid axis by regulating proTRH gene expression in the PVN but does not have peripheral effects on thyroid-binding proteins. We propose that the fall in circulating leptin levels during fasting resets the set point for feedback inhibition by thyroid hormones on the biosynthesis of hypophysiotropic proTRH, thereby allowing adaptation to starvation.
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PMID:Leptin prevents fasting-induced suppression of prothyrotropin-releasing hormone messenger ribonucleic acid in neurons of the hypothalamic paraventricular nucleus. 916 50

The effects of the stable expression of E1A and/or middle T oncogenes on the proliferative activity of PC Cl3 normal thyroid cells are reported. The proliferation of PC Cl3 cells is mainly regulated by insulin and TSH in a stimulatory way and by somatostatin in an inhibitory fashion. The transformed cell lines, named PC Py and PC E1A Py, show an autonomous pattern of proliferation. The blockade of phosphotyrosine phosphatase activity with vanadate increased the proliferation rate of PC Cl3 under basal and stimulated conditions and completely prevented the inhibitory activity of somatostatin, suggesting that in PC Cl3 cells, a tonic tyrosine phosphatase activity regulates basal and stimulated proliferation, and that a somatostatin-dependent increase in this activity may represent a cytostatic signal. Conversely, in both PC Py and PC E1A Py, vanadate did not modify basal and stimulated proliferation. We analyzed tyrosine phosphatase activity in the different cell lines basally and under conditions leading to the arrest of cell proliferation: confluence (contact inhibition), growth factor deprivation (starvation), and somatostatin treatment. Under basal conditions, tyrosine phosphatase activity was significantly lower in PC Py and PC E1APy cell lines than that in the normal cells. The inhibition of the proliferation induced by contact inhibition or somatostatin treatment was accompanied by an increase in tyrosine phosphatase activity only in PC Cl3 cells. The reduction in tyrosine phosphatase activity in PC E1APy cells correlated with a significant reduction in the expression of R-PTP eta, a tyrosine phosphatase cloned from PC Cl3 cells. Conversely, the expression of another receptor-like PTP, PTP mu, was unchanged. Thus, PTP eta may be a candidate to mediate inhibitory signals (i.e. activation of somatostatin receptors or cell to cell contact) on the proliferative activity of PC Cl3 cells, and the reduction of its expression in the transformed cell lines may lead to an alteration in the control of cell proliferation.
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PMID:Oncogene transformation of PC Cl3 clonal thyroid cell line induces an autonomous pattern of proliferation that correlates with a loss of basal and stimulated phosphotyrosine phosphatase activity. 927 62

We describe a "physiological" cell cycle synchronization model system. FRTL5 cells, TSH-dependent for proliferation, were starved from TSH. The cell cycle phases and the expression of markers associated to different cycle phases were evaluated. TSH starvation blocks proliferation without provoking death and induces virtually all the cells to accumulate in G0/G1 phase. TSH readdition allows 30% of these cells to enter the S phase. DNA topoisomerase II 170-kDa isoform is not expressed in G0/G1 synchronized cells while it is expressed in logarithmic growing cells. The 180-kDa isoform is not expressed in G0/G1 synchronized cells while it is expressed in 20% of logarithmic growing cells regardless of the cycle phase. c-myc mRNA is not expressed in G0/G1 synchronized cells while it is detectable upon TSH readdition. This system provides a tool for the analysis of events associated with the G0/G1 phase and the transition from G0/G1 to S phase.
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PMID:Cell cycle synchronization of FRTL5 cells. A physiological model system. 1008 79

Fasting and refeeding have considerable effects on thyroid hormone metabolism. In the present study, 8-day-old meat-type cockerels were subjected to a 2-day starvation period followed by 3 days' refeeding. Blood and tissue samples were collected at the start of the experiment, at 4, 24, and 48 h of starvation, and at 4, 8, 24, 48, and 72 h of refeeding. This study demonstrates that in chicken, fasting decreased plasma T(3) and TSH levels and increased plasma T(4) concentrations. This was accompanied by increased hepatic type III deiodinase (D3) and decreased renal D3 activity. There were no changes in hepatic or renal type I deiodinase (D1). Refeeding restored normal plasma T(3), T(4), and TSH levels, while hepatic D3 and renal D3 activities returned to prefasting levels. Again hepatic D1 was not affected, but renal D1 was lower than the ad libitum values during the entire refeeding period. These results confirm that liver D3 is involved in the regulation of plasma T(3) during fasting and refeeding in the chicken. Northern blot analysis demonstrated increased hepatic D3 mRNA levels during the first day of starvation that disappeared by the end of the second day; refeeding had no additional effects. These results suggest that in fasted chickens the rapid upregulation of hepatic D3 occurs predominantly at a pretranslational level, whereas the drop in hepatic D3 activity after refeeding is probably regulated at a posttranslational level. In addition, renal D3 may play a role in the regulation of local T(3) availability.
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PMID:Regulation of thyroid hormone metabolism during fasting and refeeding in chicken. 1056 57

Bullfrog (Rana catesbeiana) tadpoles are of value to amphibian researchers because of their large size, and year-round availability due to overwintering in many latitudes. Concern over a possible difference in hormonal parameters in tadpoles obtained at different times of the year prompted us to investigate thyroid gland secretion in vitro, plasma and ocular melatonin, and plasma corticosteroids in late pre- to early prometamorphic larvae on 12L:12D. Winter tadpoles exposed to 22 degrees C for 3 weeks of acclimation (winter group) were compared to summer tadpoles kept at 22 degrees C (summer group), as well as to summer tadpoles exposed to cold (12 degrees C) for the 3 weeks (cold group), or kept at 22 degrees C and starved for the last week of acclimation (starved group). Thyroids from the summer group had a significantly higher response to 0.2 microg/ml ovine thyrotropin (TSH) than the other groups, indicating that cold and starvation inhibited subsequent in vitro thyroid sensitivity to TSH. The thyroids of the starved tadpoles had significantly higher baseline (unstimulated) thyroxine (T4) secretion into the culture media, a finding that might be related to starvation-induced acceleration of metamorphosis. Plasma melatonin was lower, and ocular melatonin significantly higher in both summer and starved groups, while the reverse occurred in the winter and cold groups. Thus, seasonal or induced cold brought on a shift in the relationship of plasma to ocular melatonin but starvation had no effect. There were no significant differences among the treatment groups in plasma hydrocortisone (HC) and aldosterone (ALDO) levels, except that HC was lower than ALDO only in the plasma of winter tadpoles. We conclude that seasonal variation needs to be taken into account in endocrine experiments utilizing tadpoles obtained at different times of the year.
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PMID:Hormonal profiles correlated with season, cold, and starvation in Rana catesbeiana (bullfrog) tadpoles. 1057 55

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