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Signe Frøssing Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Malin Nylander Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark
Department of Obstetrics & Gynecology, Herlev Gentofte Hospital, Copenhagen, Denmark

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Caroline Kistorp Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Sven O Skouby Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark
Department of Obstetrics & Gynecology, Herlev Gentofte Hospital, Copenhagen, Denmark

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Jens Faber Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Context

Women with polycystic ovary syndrome (PCOS) have an increased risk of cardiovascular disease (CVD), and biomarkers can be used to detect early subclinical CVD. Midregional-pro-adrenomedullin (MR-proADM), midregional-pro-atrial natriuretic peptide (MR-proANP) and copeptin are all associated with CVD and part of the delicate system controlling fluid and hemodynamic homeostasis through vascular tonus and diuresis. The GLP-1 receptor agonist liraglutide, developed for treatment of type 2 diabetes (T2D), improves cardiovascular outcomes in patients with T2D including a decrease in particular MR-proANP.

Objective

To investigate if treatment with liraglutide in women with PCOS reduces levels of the cardiovascular biomarkers MR-proADM, MR-proANP and copeptin.

Methods

Seventy-two overweight women with PCOS were treated with 1.8 mg/day liraglutide or placebo for 26 weeks in a placebo-controlled RCT. Biomarkers, anthropometrics, insulin resistance, body composition (DXA) and visceral fat (MRI) were examined.

Results

Baseline median (IQR) levels were as follows: MR-proADM 0.52 (0.45–0.56) nmol/L, MR-proANP 44.8 (34.6–56.7) pmol/L and copeptin 4.95 (3.50–6.50) pmol/L. Mean percentage differences (95% CI) between liraglutide and placebo group after treatment were as follows: MR-proADM −6% (−11 to 2, P = 0.058), MR-proANP −25% (−37 to −11, P = 0.001) and copeptin +4% (−13 to 25, P = 0.64). Reduction in MR-proANP concentration correlated with both increased heart rate and diastolic blood pressure in the liraglutide group. Multiple regression analyses with adjustment for BMI, free testosterone, insulin resistance, visceral fat, heart rate and eGFR showed reductions in MR-proANP to be independently correlated with an increase in the heart rate.

Conclusion

In an RCT, liraglutide treatment in women with PCOS reduced levels of the cardiovascular risk biomarkers MR-proANP with 25% and MR-proADM with 6% (borderline significance) compared with placebo. The decrease in MR-proANP was independently associated with an increase in the heart rate.

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Alexander V Amram Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Stephen Cutie Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Guo N Huang Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA

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Research conducted across phylogeny on cardiac regenerative responses following heart injury implicates endocrine signaling as a pivotal regulator of both cardiomyocyte proliferation and heart regeneration. Three prominently studied endocrine factors are thyroid hormone, vitamin D, and glucocorticoids, which canonically regulate gene expression through their respective nuclear receptors thyroid hormone receptor, vitamin D receptor, and glucocorticoid receptor. The main animal model systems of interest include humans, mice, and zebrafish, which vary in cardiac regenerative responses possibly due to the differential onsets and intensities of endocrine signaling levels throughout their embryonic to postnatal organismal development. Zebrafish and lower vertebrates tend to retain robust cardiac regenerative capacity into adulthood while mice and other higher vertebrates experience greatly diminished cardiac regenerative potential in their initial postnatal period that is sustained throughout adulthood. Here, we review recent progress in understanding how these three endocrine signaling pathways regulate cardiomyocyte proliferation and heart regeneration with a particular focus on the controversial findings that may arise from different assays, cellular-context, age, and species. Further investigating the role of each endocrine nuclear receptor in cardiac regeneration from an evolutionary perspective enables comparative studies between species in hopes of extrapolating the findings to novel therapies for human cardiovascular disease.

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M L M Barreto-Chaves Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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N Senger Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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M R Fevereiro Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A C Parletta Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A P C Takano Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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The cardiac growth process (hypertrophy) is a crucial phenomenon conserved across a wide array of species and is critically involved in the maintenance of cardiac homeostasis. This process enables an organism to adapt to changes in systemic demand and occurs due to a plethora of responses, depending on the type of signal or stimuli received. The growth of cardiac muscle cells in response to environmental conditions depends on the type, strength and duration of stimuli, and results in adaptive physiological responses or non-adaptive pathological responses. Thyroid hormones (TH) have a direct effect on the heart and induce a cardiac hypertrophy phenotype, which may evolve to heart failure. In this review, we summarize the literature on TH function in the heart by presenting results from experimental studies. We discuss the mechanistic aspects of TH associated with cardiac myocyte hypertrophy, increased cardiac myocyte contractility and electrical remodeling, as well as the associated signaling pathways. In addition to classical crosstalk with the sympathetic nervous system (SNS), emerging work pointing to the new endocrine interaction between TH and the renin-angiotensin system (RAS) is also explored. Given the inflammatory potential of the angiotensin II peptide, this new interaction may open the door for new therapeutic approaches which target the key mechanisms responsible for TH-induced cardiac hypertrophy.

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Peiwen Zheng School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Fan Wang Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China

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Hui Li Psychosomatic Medicine Research Division, Inner Mongolia Medical University, Huhhot, China

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Hanlu Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Mengtong Li School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Haozheng Ma School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Jue He School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Li Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Yanlong Liu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Haiyun Xu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Objective

This study aimed to reveal associations between metabolic hormones in cerebral spinal fluid (CSF) and cigarette smoking-induced weight gain and to explore the underlying mechanism.

Methods

A total of 156 adult men were included, comprising active smokers and nonsmokers. In addition to demographic information and body mass index (BMI), plasma levels of ApoA1 and ApoB, high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase in the participants were measured. Moreover, the metabolic hormones adiponectin, fibroblast growth factor 21 (FGF21), ghrelin, leptin, and orexin A, as well as the trace elements iron and zinc in CSF, were assessed.

Results

Compared to nonsmokers, active smokers showed higher BMI, and elevated CSF levels of FGF21, Zn, and Fe, but decreased levels of metabolic hormones adiponectin, ghrelin, leptin, and orexin A. Negative correlations existed between CSF FGF21 and ghrelin, between CSF Zn and ghrelin, as well as between CSF Fe and orexin A in active smokers. Furthermore, elevated CSF FGF21 and Zn predicted ghrelin level decrease in the smokers.

Conclusion

These data relate smoking-induced weight gain to its neurotoxic effect on the neurons that synthesize metabolic hormones such as adiponectin, ghrelin, leptin, or orexin A in the brain, by disrupting mitochondrial function and causing oxidative stress in the neurons.

Open access
Esben Thyssen Vestergaard Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Morten B Krag Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Morten M Poulsen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Steen B Pedersen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Niels Moller Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Jens Otto Lunde Jorgensen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Niels Jessen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Objective

Supraphysiological levels of ghrelin and GH induce insulin resistance. Serum levels of retinol-binding protein-4 (RBP4) correlate inversely with insulin sensitivity in patients with type 2 diabetes. We aimed to determine whether ghrelin and GH affect RBP4 levels in human subjects.

Materials and methods

To study GH-independent effects of ghrelin, seven hypopituitary men undergoing replacement therapy with GH and hydrocortisone were given ghrelin (5 pmol/kg per min) and saline infusions for 300 min in a randomized, double-blind, placebo-controlled, crossover design. Circulating RBP4 levels were measured at baseline and during a hyperinsulinemic–euglycemic clamp on both study days. To study the direct effects of GH, nine healthy men were treated with GH (2 mg at 2200 h) and placebo for 8 days in a randomized, double-blind, placebo-controlled, crossover study. Serum RBP4 levels were measured before and after treatment, and insulin sensitivity was measured by the hyperinsulinemic–euglycemic clamp technique.

Results

Ghrelin acutely decreased peripheral insulin sensitivity. Serum RBP4 concentrations decreased in response to insulin infusion during the saline experiment (mg/l): 43.2±4.3 (baseline) vs 40.4±4.2 (clamp), P<0.001, but this effect was abrogated during ghrelin infusion (mg/l): 42.4±4.5 (baseline) vs 42.9±4.7 (clamp), P=0.73. In healthy subjects, serum RBP4 levels were not affected by GH administration (mg/l): 41.7±4.1 (GH) vs 43.8±4.6 (saline), P=0.09, although GH induced insulin resistance.

Conclusions

i) Serum RBP4 concentrations decrease in response to hyperinsulinemia, ii) ghrelin abrogates the inhibitory effect of insulin on circulating RBP4 concentrations, and iii) ghrelin as well as GH acutely induces insulin resistance in skeletal muscle without significant changes in circulating RBP4 levels.

Open access
Jan Calissendorff Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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Henrik Falhammar Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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Background

Graves’ disease is a common cause of hyperthyroidism. Three therapies have been used for decades: pharmacologic therapy, surgery and radioiodine. In case of adverse events, especially agranulocytosis or hepatotoxicity, pre-treatment with Lugol’s solution containing iodine/potassium iodide to induce euthyroidism before surgery could be advocated, but this has rarely been reported.

Methods

All patients hospitalised due to uncontrolled hyperthyroidism at the Karolinska University Hospital 2005–2015 and treated with Lugol’s solution were included. All electronic files were carefully reviewed manually, with focus on the cause of treatment and admission, demographic data, and effects of iodine on thyroid hormone levels and pulse frequency.

Results

Twenty-seven patients were included. Lugol’s solution had been chosen due to agranulocytosis in 9 (33%), hepatotoxicity in 2 (7%), other side effects in 11 (41%) and poor adherence to medication in 5 (19%). Levels of free T4, free T3 and heart rate decreased significantly after 5–9 days of iodine therapy (free T4 53–20 pmol/L, P = 0.0002; free T3 20–6.5 pmol/L, P = 0.04; heart rate 87–76 beats/min P = 0.0007), whereas TSH remained unchanged. Side effects were noted in 4 (15%) (rash n = 2, rash and vomiting n = 1, swelling of fingers n = 1). Thyroidectomy was performed in 26 patients (96%) and one was treated with radioiodine; all treatments were without serious complications.

Conclusion

Treatment of uncontrolled hyperthyroidism with Lugol’s solution before definitive treatment is safe and it decreases thyroid hormone levels and heart rate. Side effects were limited. Lugol’s solution could be recommended pre-operatively in Graves’ disease with failed medical treatment, especially if side effects to anti-thyroid drugs have occurred.

Open access
Peter D Mark Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Mikkel Andreassen Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Claus L Petersen Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Andreas Kjaer Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Jens Faber Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark
Department of Medicine O, Department of Clinical Physiology and Nuclear Medicine, Department of Clinical Physiology, Faculty of Health Sciences, Center for Functional and Diagnostic Imaging and Research, Centre of Endocrinology and Metabolism, Herlev University Hospital, Herlev Ringvej 75, Herlev DK‐2730, Denmark

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Purpose

The aim of this study was to investigate structure and function of the heart in subclinical hyperthyroidism (SH) before and after obtaining euthyroidism by radioactive iodine treatment, using high precision and observer-independent magnetic resonance imaging (MRI) technology.

Methods

Cardiac MRI was performed before and after euthyroidism was obtained by radioactive iodine treatment in 12 otherwise healthy patients (11 women and one man, mean age 59 years, range 44–71 years) with a nodular goiter and SH, and compared with eight healthy controls investigated at baseline. Cardiac data were expressed as an index, as per body surface area, except for heart rate (HR) and ejection fraction.

Results

Post-treatment cardiac MRI was performed in median 139 days after a normalized serum TSH value had been recorded. During treatment, serum TSH increased from (median (range)) 0.01 (0.01–0.09) to 0.88 (0.27–3.99) mU/l. Patients with untreated SH had increased resting HR (P<0.01) as well as cardiac index (cardiac output as per body surface area) (P<0.01) compared with controls. Obtaining euthyroidism resulted in a significant decrease in left ventricular mass index (LVMI) of 2.7 g/m2 (P=0.034), in HR of 8 bpm (P=0.001), and in cardiac index of 0.24 l/min per m2 (P=0.017).

Conclusions

Normalization of thyroid function by radioactive iodine treatment of SH resulted in significant reductions in clinically important heart parameters such as LVMI, HR, and cardiac index. SH should be regarded as a condition in which aggressive treatment should be considered to protect cardiac function.

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I Azzam Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Tel Aviv, Israel

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S Gilad Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Tel Aviv, Israel

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R Limor Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Tel Aviv, Israel

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N Stern Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Tel Aviv, Israel
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Y Greenman Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Tel Aviv, Israel
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Ghrelin plasma concentration increases in parallel to cortisol after a standardized psychological stress in humans, but the physiological basis of this interaction is unknown. We aimed to elucidate this question by studying the ghrelin response to pharmacological manipulation of the hypothalamic–pituitary–adrenal (HPA) axis. Six lean, healthy male volunteers were examined under four experimental conditions. Blood samples were collected every 30 min for two sequential periods of two hours. Initially, a baseline period was followed by intravenous injection of a synthetic analog of ACTH (250 μg). Subsequently, a single dose of metyrapone was administered at midnight and in the following morning, blood samples were collected for 2 h, followed by an intravenous injection of hydrocortisone (100 mg) with continued sampling. We show that increased cortisol serum levels secondary to ACTH stimulation or hydrocortisone administration are positively associated with plasma ghrelin levels, whereas central stimulation of the HPA axis by blocking cortisol synthesis with metyrapone is associated with decreased plasma ghrelin levels. Collectively, this suggests that HPA-axis-mediated elevations in ghrelin plasma concentration require increased peripheral cortisol levels, independent of central elevation of ACTH and possibly CRH levels.

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Richard P Steeds Department of Cardiology, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK
Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK

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Vandana Sagar Centre for Liver and Gastrointestinal Research, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Shishir Shetty Centre for Liver and Gastrointestinal Research, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Tessa Oelofse Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Harjot Singh Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Raheel Ahmad Department of Cardiology, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Elizabeth Bradley Therapy Services (Dietetics), University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Rachel Moore Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Suzanne Vickrage Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Stacey Smith Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Ivan Yim Department of Cardiothoracic Surgery, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Yasir S Elhassan Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Hema Venkataraman Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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John Ayuk Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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Stephen Rooney Department of Cardiothoracic Surgery, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Tahir Shah Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK
Department of Hepatology and Liver Transplantation, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Carcinoid heart disease (CHD) is a consequence of valvular fibrosis triggered by vasoactive substances released from neuroendocrine tumours, classically in those with metastatic disease and resulting in tricuspid and pulmonary valve failure. CHD affects one in five patients who have carcinoid syndrome (CS). Valve leaflets become thickened, retracted and immobile, resulting most often in regurgitation that causes right ventricular dilatation and ultimately, right heart failure. The development of CHD heralds a significantly worse prognosis than those patients with CS who do not develop valvular disease. Diagnosis requires a low threshold of suspicion in all patients with CS, since symptoms occur late in the disease process and clinical signs are difficult to elicit. As a result, routine screening is recommended using the biomarker, N-terminal pro-natriuretic peptide, and regular echocardiography is then required for diagnosis and follow-up. There is no direct medical therapy for CHD, but the focus of non-surgical care is to control CS symptoms, reduce tumour load and decrease hormone levels. Valve surgery improves long-term outcome for those with severe disease compared to medical management, although peri-operative mortality remains at between 10 and 20% in experienced centres. Therefore, care needs to be multidisciplinary at all stages, with clear discussion with the patient and between teams to ensure optimum outcome for these often-complex patients.

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Alexander Tacey Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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Lewan Parker Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Institute for Physical Activity and Nutrition, Deakin University, Geelong, Victoria, Australia

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Bu B Yeap Medical School, University of Western Australia, and Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, Western Australia, Australia

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John Joseph PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Ee M Lim PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Andrew Garnham Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia

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David L Hare University of Melbourne and the Department of Cardiology, Austin Health, Melbourne, Victoria, Australia

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Tara Brennan-Speranza Department of Physiology and Bosch Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia

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Itamar Levinger Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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The aim of this study was to investigate the effect of a single dose of prednisolone on (A) high-intensity interval cycling performance and (B) post-exercise metabolic, hormonal and haematological responses. Nine young men participated in this double-blind, randomised, cross-over study. The participants completed exercise sessions (4 × 4 min cycling bouts at 90–95% of peak heart rate), 12 h after ingesting prednisolone (20 mg) or placebo. Work load was adjusted to maintain the same relative heart rate between the sessions. Exercise performance was measured as total work performed. Blood samples were taken at rest, immediately post exercise and up to 3 h post exercise. Prednisolone ingestion decreased total work performed by 5% (P < 0.05). Baseline blood glucose was elevated following prednisolone compared to placebo (P < 0.001). Three hours post exercise, blood glucose in the prednisolone trial was reduced to a level equivalent to the baseline concentration in the placebo trial (P > 0.05). Prednisolone suppressed the increase in blood lactate immediately post exercise (P < 0.05). Total white blood cell count was elevated at all time-points with prednisolone (P < 0.01). Androgens and sex hormone-binding globulin were elevated immediately after exercise, irrespective of prednisolone or placebo. In contrast, prednisolone significantly reduced the ratio of testosterone/luteinizing hormone (P < 0.01). Acute prednisolone treatment impairs high-intensity interval cycling performance and alters metabolic and haematological parameters in healthy young men. Exercise may be an effective tool to minimise the effect of prednisolone on blood glucose levels.

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