neuropeptide-y and Hyperthyroidism

Despite well documented anabolic effects of GH in mammals, a clear demonstration of such responses in domestic poultry is lacking. Recently, comprehensive dose-response studies of GH have been conducted in broilers during late post-hatch development (8 to 9 weeks of age). GH reduced feed intake (FI) and body weight gain in a dose-dependent manner, whereas birds pair-fed to the level of voluntary FI of GH-infused birds did not differ from controls. The reduction in voluntary FI may involve centrally mediated mechanisms, as hypothalamic neuropeptide Y protein and mRNA were reduced with GH, coincident with the maximal depression in FI. Growth of breast muscle was also reduced in a dose-dependent manner. Circulating IGF-I was not enhanced by GH, despite evidence that early events in the GH signaling pathway were intact. A GH dose-dependent increase in circulating 3,3',5-triiodothyronine(T3) paralleled decreases in hepatic 5D-III monodeiodinase activity, whereas 5'D-I activity was not altered. This confirms that a marked hyperthyroid response to GH occurs in late posthatch chickens, resulting from a decrease in the degradative pathway of T3 metabolism. This secondary hyperthyroidism would account for the decreased skeletal muscle mass (52) and lack of enhanced IGF-I (53) in GH-treated birds. Based upon these studies, it is now evident that GH does in fact have significant effects in poultry, but metabolic responses may confound the anabolic potential of the hormone.

Topics: Animals; Chickens; Dose-Response Relationship, Drug; Eating; Female; Gene Expression Regulation; Growth Hormone; Hyperthyroidism; Insulin-Like Growth Factor I; Iodide Peroxidase; Neuropeptide Y; Signal Transduction; Thyroxine; Triiodothyronine

Background Melatonin, an important neurohormone released from the pineal gland, is generally accepted to exercise an inhibitor effect on the thyroid gland. Zinc mediates the effects of many hormones and is found in the structure of numerous hormone receptors. Aim The present study aims to examine the effect of melatonin supplementation and pinealectomy on leptin, neuropeptide Y (NPY), melatonin and zinc levels in rats with hypothyroidism and hyperthyroidism. Methods This study was performed on the 70 male rats. Experimental animals in the study were grouped as follows: control (C); hypothyroidism (PTU); hypothyroidism + melatonin (PTU + M); hypothyroidism + pinealectomy (PTU + Pnx); hyperthyroidism (H); hyperthyroidism + melatonin (H + M) and hyperthyroidism + pinealectomy (H + Pnx). Blood samples collected at the end of 4-week procedures were analyzed to determine melatonin, leptin, NPY and zinc levels. Results It was found that thyroid parameters thyroid stimulating hormone (TSH), free triiodthyronine (FT3), free thyroxine (FT4), total T3 (TT3) and total T4 (TT4) decreased in hypothyroidism groups and increased in the groups with hyperthyroidism. The changes in these hormones remained unaffected by melatonin supplementation and pinealectomy. Melatonin levels rose in hyperthyroidism and fell in hypothyroidism. Leptin and NPY levels increased in both hypothyroidism and hyperthyroidism. Zinc levels, on the other hand, decreased in hypothyroidism and pinealectomy, but increased in hyperthyroidism. Conclusion The results of the study demonstrate that hypothyroidism and hyperthyroidism affect leptin, NPY, melatonin and zinc values in different ways in rats. However, melatonin supplementation and pinealectomy do not have any significant influence on the changes occurring in leptin, NPY and zinc levels in thyroid dysfunction.

Topics: Animals; Biomarkers; Dietary Supplements; Disease Models, Animal; Hyperthyroidism; Hypothyroidism; Leptin; Male; Melatonin; Neuropeptide Y; Pineal Gland; Rats; Thyroid Function Tests; Zinc

Since zinc mediates the effects of many hormones or is found in the structure of numerous hormone receptors, zinc deficiency leads to various functional impairments in the hormone balance. And also thyroid hormones have important activity on metabolism and feeding. NPY and leptin are affective on food intake and regulation of appetite. The present study is conducted to determine how zinc supplementation and deficiency affect thyroid hormones (free and total T3 and T4), melatonin, leptin, and NPY levels in thyroid dysfunction in rats. The experiment groups in the study were formed as follows: Control (C); Hypothyroidism (PTU); Hypothyroidism+Zinc (PTU+Zn); Hypothyroidism+Zinc deficient; Hyperthyroidism (H); Hyperthyroidism+Zinc (H+Zn); and Hyperthyroidism+Zinc deficient. Thyroid hormone parameters (FT

Topics: Animals; Biomarkers; Enzyme-Linked Immunosorbent Assay; Hyperthyroidism; Hypothyroidism; Leptin; Male; Melatonin; Neuropeptide Y; Rats; Rats, Sprague-Dawley; Thyroid Hormones; Zinc

There is insufficient information about the appetite-related hormones orexin-A, nesfatin-1, agouti-related peptide (AgRP), and neuropeptide Y (NPY) in hyperthyroidism. The aim of the present study was to investigate the effects of hyperthyroidism on the basal metabolic rate (BMR) and energy intake, orexin-A, nesfatin-1, AgRP, NPY, and leptin levels in the circulation, and their relationship with each other and on appetite.. In this prospective study, patients were evaluated in hyperthyroid and euthyroid states in comparison with healthy subjects. Twenty-one patients with overt hyperthyroidism and 33 healthy controls were included in the study.. Daily energy intake in the hyperthyroid state was found to be higher than that in the euthyroid state patient group (p=0.039). BMR was higher in hyperthyroid patients than the control group (p=0.018). Orexin-A was lower and nesfatin-1 was higher in hyperthyroid patients compared to the controls (p<0.001), whereas orexin-A increased and nesfatin-1 decreased after euthyroidism (p=0.003, p<0.001). No differences were found in the AgRP, NPY, and leptin levels between the hyperthyroid and euthyroid states and controls (p>0.05). Orexin-A correlated negatively with nesfatin-1 (p=0.042), BMR (p=0.013), free triiodothyronine (fT3; p<0.001), and free thyroxine (fT4; p<0.001) and positively with thyrotropin (TSH; p<0.001). Nesfatin-1 correlated negatively with orexin-A (p=0.042) and TSH (p<0.001) and positively with fT3 (p=0.005) and fT4 (p=0.001). In the regression analysis, "diagnosis of hyperthyroidism" was the main factor affecting orexin-A (p<0.001).. Although it seems that no relationship exists among orexin-A, nesfatin-1, and increased appetite in hyperthyroidism, the orexin-A and nesfatin-1 levels are markedly affected by hyperthyroidism.

Topics: Adult; Agouti-Related Protein; Appetite; Basal Metabolism; Calcium-Binding Proteins; Case-Control Studies; DNA-Binding Proteins; Energy Intake; Female; Graves Disease; Humans; Hyperthyroidism; Leptin; Longitudinal Studies; Male; Middle Aged; Nerve Tissue Proteins; Neuropeptide Y; Nucleobindins; Orexins; Prospective Studies; Thyrotropin; Thyroxine; Triiodothyronine; Young Adult

Hyperthyroidism is characterized in rats by increased energy expenditure and marked hyperphagia. Alterations of thermogenesis linked to hyperthyroidism are associated with dysregulation of hypothalamic AMPK and fatty acid metabolism; however, the central mechanisms mediating hyperthyroidism-induced hyperphagia remain largely unclear. Here, we demonstrate that hyperthyroid rats exhibit marked up-regulation of the hypothalamic mammalian target of rapamycin (mTOR) signalling pathway associated with increased mRNA levels of agouti-related protein (AgRP) and neuropeptide Y (NPY), and decreased mRNA levels of pro-opiomelanocortin (POMC) in the arcuate nucleus of the hypothalamus (ARC), an area where mTOR co-localizes with thyroid hormone receptor-α (TRα). Central administration of thyroid hormone (T3) or genetic activation of thyroid hormone signalling in the ARC recapitulated hyperthyroidism effects on feeding and the mTOR pathway. In turn, central inhibition of mTOR signalling with rapamycin in hyperthyroid rats reversed hyperphagia and normalized the expression of ARC-derived neuropeptides, resulting in substantial body weight loss. The data indicate that in the hyperthyroid state, increased feeding is associated with thyroid hormone-induced up-regulation of mTOR signalling. Furthermore, our findings that different neuronal modulations influence food intake and energy expenditure in hyperthyroidism pave the way for a more rational design of specific and selective therapeutic compounds aimed at reversing the metabolic consequences of this disease.

Topics: Agouti-Related Protein; AMP-Activated Protein Kinases; Animals; Disease Models, Animal; Eating; Feeding Behavior; Hyperphagia; Hyperthyroidism; Hypothalamus; Male; Neural Pathways; Neuropeptide Y; Phosphorylation; Pro-Opiomelanocortin; Protein Kinase Inhibitors; Rats; Rats, Sprague-Dawley; RNA, Messenger; Signal Transduction; Sirolimus; Thyroid Hormone Receptors alpha; Time Factors; TOR Serine-Threonine Kinases; Triiodothyronine; Weight Loss

The possible role of neuropeptide Y (NPY) was studied in rats with hypermetabolism and hyperphagia induced by thyroxine (50-100-200 microg/day s.c. for 3-4 weeks). Both metabolic rate and body temperature increased quickly with thyroxine treatment, while hyperphagia started to develop only after 2 weeks of treatment. The weight gain rate progressively decreased or stopped. The NPY-induced hyperphagia was not altered significantly during thyroxine treatment (in severe thyrotoxicosis it was rather suppressed); the fasting-induced hyperphagia was smaller than in controls following 1 week of treatment, and it became enhanced only after 3 weeks, when the deficit in body weight indicated a certain level of starvation already prior to the food deprivation. The NPY-antagonist D-Tyr27,36,D-Thr32-NPY27,36 suppressed this fasting-induced hyperphagia, suggesting that endogenous NPY is involved in this late phase. In conclusion, hyperthyroidism per se does not increase the NPY activity, instead the quickly developing hyperthermia may inhibit the NPY actions; NPY may, however, be activated by a concurrent hypermetabolism-induced starvation.

Topics: Animals; Body Temperature; Body Weight; Eating; Energy Metabolism; Female; Food Deprivation; Hyperphagia; Hyperthyroidism; Male; Neuropeptide Y; Rats; Rats, Wistar; Thyroxine

Neuropeptide Y (NPY) is present in thyroid sympathetic nerve fibers. To assess the involvement of endogenous NPY in the regulation of thyroid function, a NPY antiserum was produced in a rabbit, characterized, and used for immunization of normal and hyperthyroid rats. Plasma thyroxine, thyroid-stimulating hormone (TSH), thyroidal, and other organ blood flows (BF) were measured in anesthetized (ketamine and pentobarbital sodium) male Sprague-Dawley rats at 1 h after intravenous administration of 1 ml of the antiserum, normal rabbit serum, or saline. Immunization against NPY had no effect on the plasma levels of thyroxine, TSH, or arterial blood pressure, but it significantly increased thyroidal BF in normal rats. In the hyperthyroid rats (treated with 5 micrograms.100 g body wt-.day-1 thyroxine for 6 days), the NPY antiserum reversed the hyperthyroidism-induced decrease in thyroid BF and significantly increased duodenal and testicular BF values, but it did not alter BF values in four other organs. These results indicate that endogenous NPY regulates thyroid BF in normal rats. They also provide an example of NPY involvement in the pathophysiological adjustment of some organs to hyperthyroidism.

Topics: Animals; Blood Pressure; Hyperthyroidism; Immune Sera; Male; Neuropeptide Y; Organ Specificity; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Thyroid Gland; Thyrotropin; Thyroxine

Plasma levels of the neuropeptides, vasoactive intestinal polypeptide (VIP, neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), substance P, and galanin were determined in 15 hyperthyroid patients before and at 3 occassions during 38 weeks of treatment. Treatment was performed with either 131I alone or with carbimazole, with combination of carbimazole and thyroxine, or with subtotal thyroidectomy. Before and after 11 (+/- 4), 24 (+/- 6) and 38 (+/- 5) weeks of treatment, plasma neuropeptide levels were analysed. A group of 9 premenopausal women served as controls. During hyperthyroidism, mean plasma level of CGRP was higher than in controls (P less than 0.001). In contrast, the mean plasma levels of the other measured neuropeptides did not differ from those in the controls. Mean serum level of tree T4 was lowered from 81.9 +/- 30.1 to 23.9 +/- 8.6 pmol/l and mean serum level of free T3 was lowered from 27.3 +/- 7.9 to 6.7 +/- 2.3 pmol/l during the course of the treatment. After 11 weeks of treatment, mean plasma NPY level was significantly increased (P = 0.004) compared to pretreatment levels. However, after 38 weeks of treatment, mean plasma NPY level had returned to control values. The mean plasma CGRP level was significantly reduced at 11 and 38 weeks of treatment compared to pre-treatment value (P = 0.002 and P = 0.004, respectively). Mean plasma level of neurotensin slowly declined during the treatment (P = 0.003). In contrast, mean plasma level of VIP, of substance P, and of galanin did not differ from control value before or after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Calcitonin Gene-Related Peptide; Carbimazole; Drug Therapy, Combination; Female; Galanin; Humans; Hyperthyroidism; Iodine Radioisotopes; Male; Middle Aged; Neuropeptide Y; Neuropeptides; Peptides; Substance P; Thyroidectomy; Thyroxine; Triiodothyronine; Vasoactive Intestinal Peptide