Serum Ghrelin Levels Are Increased in Hypothyroid Patients and Become Normalized by l-Thyroxine Treatment

Gjedde, Signe; Vestergaard, Esben Thyssen; Gormsen, Lars Christian; Riis, Anne Lene; Rungby, Jørgen; Møller, Niels; Weeke, Jørgen; Jørgensen, Jens Otto Lunde

doi:10.1210/jc.2007-2619

Cited by 40 publications

(26 citation statements)

References 22 publications

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“…A rat model of hypothyroidism showed increased circulating ghrelin and gastric ghrelin mRNA levels (Caminos et al, 2002). Following thyroxine replacement in hypothyroid patients, serum ghrelin levels showed a significant reduction (Braclik et al, 2008;Gjedde et al, 2008).…”

Section: Page 21 Of 44mentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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Section: Page 21 Of 44mentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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“…NKX2.2 in mice resulted in a dramatic expansion of ghrelinproducing cells at the expense of b-cells (18). Interestingly, patients with hypothyroidism were reported to have elevated serum ghrelin levels (acylated and unacylated), which was normalized by T4 treatment (19). Although the chronic hypothyroid mice in our study did not produce elevated circulating ghrelin levels, there was clearly an effect of thyroid hormone deficiency to induce ghrelin locally within hESC-derived grafts.…”

Section: Discussionmentioning

confidence: 49%

Hypothyroidism Impairs Human Stem Cell–Derived Pancreatic Progenitor Cell Maturation in Mice

et al. 2016

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Pancreatic progenitors derived from human embryonic stem cells (hESCs) are a potential source of transplantable cells for treating diabetes and are currently being tested in clinical trials. Yet, how the milieu of pancreatic progenitor cells, including exposure to different factors after transplant, may influence their maturation remains unclear. Here, we examined the effect of thyroid dysregulation on the development of hESC-derived progenitor cells in vivo. Hypothyroidism was generated in SCID-beige mice using an iodine-deficient diet containing 0.15% propyl-2-thiouracil, and hyperthyroidism was generated by addition of L-thyroxine (T4) to drinking water. All mice received macroencapsulated hESC-derived progenitor cells, and thyroid dysfunction was maintained for the duration of the study (“chronic”) or for 4 weeks posttransplant (“acute”). Acute hyperthyroidism did not affect graft function, but acute hypothyroidism transiently impaired human C-peptide secretion at 16 weeks posttransplant. Chronic hypothyroidism resulted in severely blunted basal human C-peptide secretion, impaired glucose-stimulated insulin secretion, and elevated plasma glucagon levels. Grafts from chronic hypothyroid mice contained fewer β-cells, heterogenous MAFA expression, and increased glucagon+ and ghrelin+ cells compared to grafts from euthyroid mice. Taken together, these data suggest that long-term thyroid hormone deficiency may drive the differentiation of human pancreatic progenitor cells toward α- and ε-cell lineages at the expense of β-cell formation.

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“…the presence of symptoms characteristic for thyroid function disease: -a newly diagnosed hypothyroidism with free T3 (fT3) < 3.95 pmol/L, free T4 (fT4) <11pmol/L and TSH > 4.5 µU/mL) or -hyperthyroidism with fT3 > 6.80 pmol/L, fT4 > 21. 5 pmol/L and TSH < 0.27 µU/mL. Additional requirements were: -completing all visits during the follow-up; -a restoration of euthyreosis no later than during the third follow-up visit.…”

Section: Methodsmentioning

confidence: 99%

“…An abnormal amount of T3 disturbs a number of metabolic processes [2]: shortage of T3 in hypothyroidism reduces basic metabolic rate and thermogenesis, inhibits catabolism and gains total body weight [5]; excess of T3 in hyperthyroidism reverses these processes [6]. Specific therapy of hypo- [7,8] and hyperthyroidism [9][10][11] restores proper body mass.…”

Section: Introductionmentioning

confidence: 99%

Zmiany w składzie tkankowym obserwowane w trakcie terapii ciężkich zaburzeń funkcji tarczycy

Stangierski

Ruchała

Krauze

et al. 2015

Endokrynologia Polska

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Introduction: Hyper-and hypothyroidism are accompanied by altered metabolic rate, thermogenesis, and body weight. The aim of this study was to estimate the relation between treatment-induced changes in thyroid function, and the accompanying body composition in patients with either severe hypo-or hyperthyroidism. Material and methods: Body composition analysis and hormonal assessment were measured at the initial diagnosis of thyroid disorder, after three-month treatment, and finally after complete recovery from hyperthyroidism (n = 18) or hypothyroidism (n = 27). Nonparametric Spearman correlation was used to analyse the relation between thyroid hormones and body composition as well as their respective changes. Results:In hypothyroid patients applied treatment significantly reduced (p < 0.05) total body weight, mainly due to a decrease in fat mass, whereas in hyperthyroid patients it caused a weight gain, with a simultaneous increase in muscle, water and fat mass. Total body weight and fat mass were significantly correlated with thyroid hormones' concentrations in all patients. Changes of fat, water, or muscle mass were strongly correlated with the changes in the patients' hormonal status.

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Serum Ghrelin Levels Are Increased in Hypothyroid Patients and Become Normalized by l-Thyroxine Treatment

Abstract: Serum ghrelin levels are reversibly increased in hypothyroid patients. It remains to be investigated whether this represents a direct effect of iodothyronines on ghrelin secretion or clearance or a compensatory response to the abnormal energy metabolism in hypothyroid patients.

Cited by 40 publications

References 22 publications

Ghrelin in obesity and endocrine diseases

Ghrelin in obesity and endocrine diseases

Hypothyroidism Impairs Human Stem Cell–Derived Pancreatic Progenitor Cell Maturation in Mice

Zmiany w składzie tkankowym obserwowane w trakcie terapii ciężkich zaburzeń funkcji tarczycy

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