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

This study investigated the influence of starvation over seven days on avian thyroidal superoxide radical levels and superoxide dismutase activity profiles in the Indian rock pigeon Columba livia intermeida, in relation with iodine metabolism. The serum thyroid hormone profile was assayed to correlate the thyroidal redox status with the circulating thyroid hormone levels. The spin-trapping results suggest a role for thyroidal superoxide anion (O2.-) in causing a hypothyroid state in pigeons during long term energy withdrawal. Pigeons starved for 1 day generated superoxide and iodide free radicals in their thyroids, with a significant decrease in SOD activity. Regain of SOD activity in 2nd- and 3rd-day starved birds is marked by complete scavenging of radicals in the thyroid, suggesting the significance of SOD in thyroid glands as a potential antioxidant sink against reactive oxygen species, O2.- Resurgence of O2.- radicals with a parallel decrease in SOD activity in the thyroid gland on 5th- and 7th-day of starvation provides evidence of disruption of homeostasis between pro-oxidant and antioxidant states, leading to oxidative stress in avian thyroid during long-term calorie crisis. Following starvation both thyroid hormones thyroxine (T4) and triiodothyronine (T3) decreased, putting pigeons in a hypothyroid state. We argue that oxidative inactivation of thyroid peroxidase and other thyroid proteins by radical attack during starvation invoked oxidative stress, which could be one of the factors responsible for the hypothyroid state in pigeons.
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PMID:Starvation induced hypothyroidism involves perturbations in thyroid superoxide-SOD system in pigeons. 963 31

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

Anorexia nervosa is one of the most common forms of malnutrition observed in Western society in individuals without physical diseases, with an average risk of mortality of 20% in a younger population aged between 15 and 25 years. It is characterised by an initial dramatic decrease in food intake that leads to profound depletion in muscle and fat mass. During the course of the disease, the resting energy expenditure decreases proportionally to the loss of lean body mass with a decrease in thyroid hormone secretion. The metabolic adaptation during anorexia nervosa is similar to that observed during starvation with a relative sparing of protein stores. After an initial weight loss, the total energy expenditure is similar to that in normal individuals, with a decrease in resting energy expenditure and an increased energy-related physical activity. At the end stage of wasting, however, physical activity dramatically decreases as well as energy intake. This metabolic adaptation of semi-starvation is impaired during refeeding with an increase in the thermic effect of food and a high risk of refeeding syndrome with severe hypophosphatemia.
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PMID:From malnutrition to refeeding during anorexia nervosa. 1056 98

Hormonal regulation of a major 20 kDa protein of hamster exorbital lacrimal gland (LG) was studied by SDS-PAGE profile analysis and the purified protein's antisera was used to screen tissues of hamster and other species for crossreacting proteins. This protein was seen in female LG but not in males and late-pregnant or hCG-treated females. Low estrogen state in females after gonadectomy, prolonged light-deprivation, prolonged starvation or lactation increased its level several folds to approximately 20% of LG soluble proteins and similar levels were induced in males after gonadectomy (low androgen state). However, light-deprivation or melatonin treatment-induced low androgen state in males had no effect. In gonadectomized hamsters, this LG protein was obliterated on treatment with androgens, estrogens or thyroid hormones. Only estrogen inhibition of LG 20 kDa was prevented by simultaneous tamoxifen administration. Simultaneous treatment of gonadectomized hamsters with gonadotrophins and estrogen/androgen did not prevent the LG 20 kDa protein's inhibition. Relative potencies of estrogens (3.6 microg daily dose) were: estradiol-17beta approximately diethylstilbestrol > estrone > estradiol-17alpha, while estriol and chlorotrianisene had no effect. Dexamethasone, progesterone, prolactin, hypothyroid state or adrenalectomy had no effect on LG 20 kDa expression. Western blot studies confirmed the marked repression of LG 20 kDa by estrogen androgen and thyroid hormone and detected the protein in tears of females and gonadectomized hamsters but not in males. Interestingly, among other tissues tested, crossreaction was only seen with the estrogen-repressed 24 and 20.5 kDa major male-specific secretory proteins of hamster submandibular glands (SMG) which were previously reported by us. This strongly indicated that the LG and SMG proteins are products of the same or closely related genes. A possible role for these hamster sex-specific LG and SMG major secretory proteins in olfactory communication is suggested.
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PMID:Hormonal effects on hamster lacrimal gland female-specific major 20 kDa secretory protein and its immunological similarity with submandibular gland major male-specific proteins. 1062 3

Glucocorticoids are primarily recognized for their profound anti-inflammatory actions and their ability to induce lymphocyte apoptosis. We report here that, in contrast to their effect on cells of the immune system, glucocorticoids suppress serum deprivation induced apoptosis of rat hepatoma (HTC) cells. Suppression of apoptosis in these cells occurs at physiological concentrations of glucocorticoid and is abrogated by the glucocorticoid antagonist RU486. Although HTC cells also express receptors for progesterone, estrogen, and thyroid hormone, ligands for these receptors fail to rescue these cells from programmed cell death. Because the sensitivity of cells to apoptotic stimuli is often regulated by the ratio of antiapoptotic to proapoptotic Bcl-2 family members, we analyzed the influence of glucocorticoids and induction of apoptosis by serum starvation on the expression of these proteins. Bcl-2, Bcl-xL, Bad, Bak, and Bax levels were not altered by either treatment. Mitochondrial function has recently been implicated as a critical early regulator of apoptosis in many cells including hepatocytes. Dexamethasone treatment blocked a decrease in this potential (delta psi(m)) during serum deprivation induced apoptosis in HTC cells, indicating an action of this hormone upstream of mitochondria. We also show that the induction of apoptosis in HTC cells is associated with a decrease in nuclear factor (NF)-kappaB. Treatment with dexamethasone effectively blocked the loss of nuclear NF-kappaB, suggesting that this hormone acts to suppress apoptosis of HTC cells via regulation of this nuclear transcription factor. This hypothesis was confirmed by transfection experiments that show that expression of a superrepressor of NF-kappaB inhibits the ability of dexamethasone to rescue HTC cells from apoptosis induced by serum deprivation.
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PMID:Delineation of an antiapoptotic action of glucocorticoids in hepatoma cells: the role of nuclear factor-kappaB. 1080 96

Starvation causes a rapid reduction in thyroid hormone levels in rodents. This adaptive response is caused by a reduction in thyrotropin-releasing hormone (TRH) expression that can be reversed by the administration of leptin. Here we examined hypothalamic signaling pathways engaged by leptin to upregulate TRH gene expression. As assessed by leptin-induced expression of suppressor of cytokine signaling-3 (SOCS-3) in fasted rats, TRH neurons in the paraventricular nucleus are activated directly by leptin. To a greater degree, they also contain melanocortin-4 receptors (MC4Rs), implying that leptin can act directly or indirectly by increasing the production of the MC4R ligand, alpha-melanocyte stimulating hormone (alpha-MSH), to regulate TRH expression. We further demonstrate that both pathways converge on the TRH promoter. The melanocortin system activates the TRH promoter through the phosphorylation and DNA binding of the cAMP response element binding protein (CREB), and leptin signaling directly regulates the TRH promoter through the phosphorylation of signal transducer and activator of transcription 3 (Stat3). Indeed, a novel Stat-response element in the TRH promoter is necessary for leptin's effect. Thus, the TRH promoter is an ideal target for further characterizing the integration of transcriptional pathways through which leptin acts.
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PMID:Transcriptional regulation of the thyrotropin-releasing hormone gene by leptin and melanocortin signaling. 1113 86

Dietary carbohydrate content is a major factor determining endocrine and metabolic regulation. The aim of this study was to evaluate the relation between thyroid hormone levels and metabolic parameters during eucaloric carbohydrate deprivation. We measured thyroid hormone levels, resting energy expenditure (by indirect calorimetry) and urinary nitrogen excretion in six healthy males after 11 days of three isocaloric diets containing 15% of energy equivalents as protein and 85%, 44% and 2% as carbohydrates. In contrast to the high and intermediate carbohydrate diets, carbohydrate deprivation decreased plasma T3 values (1.78 +/- 0.09 and 1.71 +/- 0.07 vs. 1.33 +/- 0.05 nmol/l, respectively, P < 0.01), whereas reverse T3, T3 uptake and free T4 levels increased simultaneously compared to the other two diets. TSH values were not different among the three diets. Although dietary carbohydrate content did not influence resting energy expenditure, carbohydrate deprivation increased urinary nitrogen excretion (10.91 +/- 0.67 and 12.79 +/- 1.14 vs. 15.89 +/- 1.10 g/24 h, respectively, P = 0.03). Eucaloric carbohydrate deprivation increases protein catabolism despite decreased plasma T3 levels. Because it has previously been shown that starvation decreases plasma T3 levels, resting energy expenditure and nitrogen excretion, these discordant endocrine and metabolic changes following carbohydrate deprivation indicate that the effects of starvation on endocrine and metabolic regulation are not merely the result of carbohydrate deprivation.
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PMID:Isocaloric carbohydrate deprivation induces protein catabolism despite a low T3-syndrome in healthy men. 1116 29

Branched-chain amino acids are toxic in excess but have to be conserved for protein synthesis. This is accomplished in large part by control of the activity of the branched-chain alpha-keto acid dehydrogenase complex by phosphorylation/dephosphorylation. Regulation of the activity of the hepatic enzyme appears particularly important, at least in rats, since an exceptional high activity of the complex in this tissue makes the liver the primary clearing house for excess branched-chain alpha-keto acids released by other tissues. The degree to which the branched-chain alpha-keto acid dehydrogenase complex is inactivated by phosphorylation is determined by the activity of the branched-chain alpha-keto acid dehydrogenase kinase, which is itself regulated by allosteric effectors as well as factors that affect its level of expression. Well established among these are the alpha-keto acid produced by leucine transamination, which is a potent inhibitor of the kinase, and starvation for dietary protein, which causes increased expression of the branched-chain alpha-keto acid dehydrogenase kinase. The latter finding resulted in the working hypothesis that nutrients and hormones regulate expression of the branched-chain alpha-keto acid dehydrogenase kinase. Evidence has been obtained for the involvement of thyroid hormone, glucocorticoids and ligands for peroxisome proliferator-activated receptor alpha. Thyroid hormone induces, whereas glucocorticoids and peroxisome proliferator-activated receptor alpha ligands repress, expression of the kinase. Increased blood levels of thyroid hormone are proposed to be responsible for increased expression of branched-chain alpha-keto acid dehydrogenase kinase in animals starved for protein.
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PMID:Regulation of branched-chain alpha-keto acid dehydrogenase kinase expression in rat liver. 1123 71

Thyroid hormones and leptin have effects on similar aspects of body homeostasis, such as energy expenditure, thermogenesis, and metabolic efficiency. Thus, the cross-talk between the thyrostat and the lipostat might play a crucial role in the maintenance of body homeostasis. To investigate the relationship between the hypothalamic-pituitary-thyroid (HPT) axis and leptin under physiological conditions, we evaluated the pulsatility and circadian rhythmicity and time-cross-correlated the 24-h secretory patterns of leptin and TSH in 12 short normal prepubertal children (6 girls and 6 boys). In both male and female subjects, leptin was secreted in a pulsatile and circadian fashion, with a nocturnal leptin surge that was more pronounced in males than in females. Mean 24-h leptin levels and total area under the curve were significantly higher in girls than in boys. This was mainly due to the nighttime mean leptin levels and total area under the curve, which were higher than those in boys. The cross-correlated 24-h leptin and TSH levels revealed significant positive and negative correlations. The positive one, of leptin over TSH, suggests a positive feedback regulation by leptin on the HPT axis, which might play an important role in triggering the neuroendocrine response to starvation, including decreased thyroid hormone levels. The negative correlation, of TSH over leptin, could explain the compensatory changes in adipocyte metabolism, and indirectly in circulating leptin levels, in response to alterations in thyroid status. In conclusion, we suggest that under baseline physiological conditions, the HPT axis has a prevailing inhibitory effect on leptin secretion, whereas leptin has a prevailing positive effect on the HPT axis. The sexual dimorphism in leptin levels does not seem to influence in a major way the interactions between the HPT axis and leptin.
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PMID:Interactions of leptin and thyrotropin 24-hour secretory profiles in short normal children. 1134 8

Although it was originally believed that thyroid hormones enter target cells by passive diffusion, it is now clear that cellular uptake is effected by carrier-mediated processes. Two stereospecific binding sites for each T4 and T3 have been detected in cell membranes and on intact cells from humans and other species. The apparent Michaelis-Menten values of the high-affinity, low-capacity binding sites for T4 and T3 are in the nanomolar range, whereas the apparent Michaelis- Menten values of the low-affinity, high-capacity binding sites are usually in the lower micromolar range. Cellular uptake of T4 and T3 by the high-affinity sites is energy, temperature, and often Na+ dependent and represents the translocation of thyroid hormone over the plasma membrane. Uptake by the low-affinity sites is not dependent on energy, temperature, and Na+ and represents binding of thyroid hormone to proteins associated with the plasma membrane. In rat erythrocytes and hepatocytes, T3 plasma membrane carriers have been tentatively identified as proteins with apparent molecular masses of 52 and 55 kDa. In different cells, such as rat erythrocytes, pituitary cells, astrocytes, and mouse neuroblastoma cells, uptake of T4 and T3 appears to be mediated largely by system L or T amino acid transporters. Efflux of T3 from different cell types is saturable, but saturable efflux of T4 has not yet been demonstrated. Saturable uptake of T4 and T3 in the brain occurs both via the blood-brain barrier and the choroid plexus-cerebrospinal fluid barrier. Thyroid hormone uptake in the intact rat and human liver is ATP dependent and rate limiting for subsequent iodothyronine metabolism. In starvation and nonthyroidal illness in man, T4 uptake in the liver is decreased, resulting in lowered plasma T3 production. Inhibition of liver T4 uptake in these conditions is explained by liver ATP depletion and increased concentrations of circulating inhibitors, such as 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid, indoxyl sulfate, nonesterified fatty acids, and bilirubin. Recently, several organic anion transporters and L type amino acid transporters have been shown to facilitate plasma membrane transport of thyroid hormone. Future research should be directed to elucidate which of these and possible other transporters are of physiological significance, and how they are regulated at the molecular level.
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PMID:Plasma membrane transport of thyroid hormones and its role in thyroid hormone metabolism and bioavailability. 1149 79


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