Search Results
Search for other papers by L Johnsen in
Google Scholar
PubMed
Search for other papers by N B Lyckegaard in
Google Scholar
PubMed
Search for other papers by P Khanal in
Google Scholar
PubMed
Search for other papers by B Quistorff in
Google Scholar
PubMed
Search for other papers by K Raun in
Google Scholar
PubMed
Search for other papers by M O Nielsen in
Google Scholar
PubMed
Objective
We aimed to test, whether fetal under- or overnutrition differentially program the thyroid axis with lasting effects on energy metabolism, and if early-life postnatal overnutrition modulates implications of prenatal programming.
Design
Twin-pregnant sheep (n = 36) were either adequately (NORM), under- (LOW; 50% of NORM) or overnourished (HIGH; 150% of energy and 110% of protein requirements) in the last-trimester of gestation. From 3 days-of-age to 6 months-of-age, twin lambs received a conventional (CONV) or an obesogenic, high-carbohydrate high-fat (HCHF) diet. Subgroups were slaughtered at 6-months-of-age. Remaining lambs were fed a low-fat diet until 2½ years-of-age (adulthood).
Methods
Serum hormone levels were determined at 6 months- and 2½ years-of-age. At 2½ years-of-age, feed intake capacity (intake over 4-h following 72-h fasting) was determined, and an intravenous thyroxine tolerance test (iTTT) was performed, including measurements of heart rate, rectal temperature and energy expenditure (EE).
Results
In the iTTT, the LOW and nutritionally mismatched NORM:HCHF and HIGH:CONV sheep increased serum T3, T3:T4 and T3:TSH less than NORM:CONV, whereas TSH was decreased less in HIGH, NORM:HCHF and LOW:HCHF. Early postnatal exposure to the HCHF diet decreased basal adult EE in NORM and HIGH, but not LOW, and increased adult feed intake capacity in NORM and LOW, but not HIGH.
Conclusions: The iTTT revealed a differential programming of central and peripheral HPT axis function in response to late fetal malnutrition and an early postnatal obesogenic diet, with long-term implications for adult HPT axis adaptability and associated consequences for adiposity risk.
Search for other papers by Paweł Komarnicki in
Google Scholar
PubMed
Search for other papers by Paweł Gut in
Google Scholar
PubMed
Search for other papers by Jan Musiałkiewicz in
Google Scholar
PubMed
Search for other papers by Maja Cieślewicz in
Google Scholar
PubMed
Search for other papers by Adam Maciejewski in
Google Scholar
PubMed
Search for other papers by Prachi Patel in
Google Scholar
PubMed
Search for other papers by George Mastorakos in
Google Scholar
PubMed
Search for other papers by Marek Ruchała in
Google Scholar
PubMed
Introduction
Neuroendocrine tumors (NETs) are rare neoplasms that occur in various locations throughout the body. Despite their usually benign character, they might manifest with distant metastases. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) has previously been described as a useful biomarker in diagnosing carcinoid heart disease (CHD), a common advanced NETs manifestation. We observed plasma concentrations of NT-proBNP in metastatic midgut NETs over a 4-year period.
Objectives
We aimed to explore NT-proBNP concentrations in states of varying levels of cell proliferation and disease status. Our goal was to investigate NT-proBNP’s role in predicting disease progression in relation to previous research and up-to-date scientific guidelines.
Patients and methods
We performed a retrospective multivariate analysis of NT-proBNP concentrations in 41 midgut NETs patients treated with somatostatin analogs, all with liver metastases. NT-proBNP concentrations were measured in every patient across 16 evenly distanced time points over a 48-month period and were compared to variables such as sex, age, grading, Ki-67, primary tumor location, and CT findings.
Results
NT-proBNP concentrations correlated positively with higher liver tumor burden, higher grading, high Ki-67 levels, and with progressive disease in CT. There were no differences in NT-proBNP levels with regard to primary location (ileum vs jejunum), sex, and age.
Conclusion
We conclude that NT-proBNP is a useful analyte for monitoring NETs progression, due to its increased concentration in scenarios implying increased cellular proliferation. These long-term follow-up results align with previous findings and suggest an additional role for NT-proBNP in diagnostic algorithms, beyond a CHD biomarker.
Search for other papers by Yusaku Mori in
Google Scholar
PubMed
Maebashi Hirosegawa Clinic, Maebashi, Gunma, Japan
Search for other papers by Hiroyuki Shimizu in
Google Scholar
PubMed
Search for other papers by Hideki Kushima in
Google Scholar
PubMed
Search for other papers by Tomomi Saito in
Google Scholar
PubMed
Search for other papers by Munenori Hiromura in
Google Scholar
PubMed
Search for other papers by Michishige Terasaki in
Google Scholar
PubMed
Search for other papers by Masakazu Koshibu in
Google Scholar
PubMed
Search for other papers by Hirokazu Ohtaki in
Google Scholar
PubMed
Search for other papers by Tsutomu Hirano in
Google Scholar
PubMed
Nesfatin-1 is a novel anorexic peptide hormone that also exerts cardiovascular protective effects in rodent models. However, nesfatin-1 treatment at high doses also exerts vasopressor effects, which potentially limits its therapeutic application. Here, we evaluated the vasoprotective and vasopressor effects of nesfatin-1 at different doses in mouse models. Wild-type mice and those with the transgene nucleobindin-2, a precursor of nesfatin-1, were employed. Wild-type mice were randomly assigned to treatment with vehicle or nesfatin-1 at 0.2, 2.0 or 10 μg/kg/day (Nes-0.2, Nes-2, Nes-10, respectively). Subsequently, mice underwent femoral artery wire injury to induce arterial remodeling. After 4 weeks, injured arteries were collected for morphometric analysis. Compared with vehicle, nesfatin-1 treatments at 2.0 and 10 μg/kg/day decreased body weights and elevated plasma nesfatin-1 levels with no changes in systolic blood pressure. Furthermore, these treatments reduced neointimal hyperplasia without inducing undesirable remodeling in injured arteries. However, nesfatin-1 treatment at 0.2 μg/kg/day was insufficient to elevate plasma nesfatin-1 levels and showed no vascular effects. In nucleobindin-2-transgenic mice, blood pressure was slightly higher but neointimal area was lower than those observed in littermate controls. In cultured human vascular endothelial cells, nesfatin-1 concentration-dependently increased nitric oxide production. Additionally, nesfatin-1 increased AMP-activated protein kinase phosphorylation, which was abolished by inhibiting liver kinase B1. We thus demonstrated that nesfatin-1 treatment at appropriate doses suppressed arterial remodeling without affecting blood pressure. Our findings indicate that nesfatin-1 can be a therapeutic target for improved treatment of peripheral artery disease.
Search for other papers by Angelo Maria Patti in
Google Scholar
PubMed
Search for other papers by Kalliopi Pafili in
Google Scholar
PubMed
Search for other papers by Nikolaos Papanas in
Google Scholar
PubMed
Search for other papers by Manfredi Rizzo in
Google Scholar
PubMed
Hormonal changes during pregnancy can trigger gestational diabetes (GDM), which is constantly increasing. Its main characteristic is pronounced insulin resistance, but it appears to be a multifactorial process involving several metabolic factors; taken together, the latter leads to silent or clinically evident cardiovascular (CV) events. Insulin resistance and central adiposity are of crucial importance in the development of metabolic syndrome, and they appear to correlate with CV risk factors, including hypertension and atherogenic dyslipidaemia. Hypertensive disease of pregnancy (HDP) is more likely to be an accompanying co-morbidity in pregnancies complicated with GDM. There is still inconsistent evidence as to whether or not co-existent GDM and HDP have a synergistic effects on postpartum risk of cardiometabolic disease; however, this synergism is becoming more accepted since both these conditions may promote endothelial inflammation and early atherosclerosis. Regardless of the presence or absence of the synergism between GDM and HDP, these conditions need to be dealt early enough, in order to reduce CV morbidity and to improve health outcomes for both women and their offspring.
Department of Endocrinology, Austin Health, Melbourne, Australia
Division of Endocrinology, Diabetes and Metabolism, Northwell, Great Neck, New York, USA
Search for other papers by Yee-Ming M Cheung in
Google Scholar
PubMed
Search for other papers by Rudolf Hoermann in
Google Scholar
PubMed
Search for other papers by Karen Van in
Google Scholar
PubMed
Search for other papers by Damian Wu in
Google Scholar
PubMed
Search for other papers by Jenny Healy in
Google Scholar
PubMed
Search for other papers by Bella Halim in
Google Scholar
PubMed
Search for other papers by Manjri Raval in
Google Scholar
PubMed
Search for other papers by Maria McGill in
Google Scholar
PubMed
Department of Cardiology, Austin Health, Melbourne Australia
Search for other papers by Ali Al-Fiadh in
Google Scholar
PubMed
Search for other papers by Michael Chao in
Google Scholar
PubMed
Search for other papers by Shane White in
Google Scholar
PubMed
Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Australia
Search for other papers by Belinda Yeo in
Google Scholar
PubMed
Department of Endocrinology, Austin Health, Melbourne, Australia
Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Department of Endocrinology, Austin Health, Melbourne, Australia
Search for other papers by Mathis Grossmann in
Google Scholar
PubMed
Purpose
We previously demonstrated that 12 months of aromatase inhibitor (AI) treatment was not associated with a difference in body composition or other markers of cardiometabolic health when compared to controls. Here we report on the pre-planned extension of the study. The pre-specified primary hypothesis was that AI therapy for 24 months would lead to increased visceral adipose tissue (VAT) area when compared to controls.
Methods
We completed a 12-month extension to our prospective 12-month cohort study of 52 women commencing AI treatment (median age 64.5 years) and 52 women with breast pathology not requiring endocrine therapy (63.5 years). Our primary outcome of interest was VAT area. Secondary and exploratory outcomes included other measures of body composition, hepatic steatosis, measures of atherosclerosis and vascular reactivity. Using mixed models and the addition of a fourth time point, we increased the number of study observations by 79 and were able to rigorously determine the treatment effect.
Results
Among study completers (AI = 39, controls = 40), VAT area was comparable between groups over 24 months, the mean-adjusted difference was −1.54 cm2 (95% CI: −14.9; 11.9, P = 0.79). Both groups demonstrated parallel and continuous increases in VAT area over the observation period that did not diverge or change between groups. No statistically significant difference in our secondary and exploratory outcomes was observed between groups.
Conclusions
While these findings provide reassurance that short-to-medium-term exposure to AI therapy is not associated with metabolically adverse changes when compared to controls, risk evolution should be less focussed on the AI-associated effect and more on the general development of cardiovascular risk over time.
Search for other papers by Isabel M Abreu in
Google Scholar
PubMed
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
Search for other papers by Eva Lau in
Google Scholar
PubMed
Search for other papers by Bernardo de Sousa Pinto in
Google Scholar
PubMed
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
Search for other papers by Davide Carvalho in
Google Scholar
PubMed
Previous studies suggested that subclinical hypothyroidism has a detrimental effect on cardiovascular risk factors, and that its effective treatment may have a beneficial impact on overall health. The main purpose of this review and meta-analysis was to assess whether subclinical hypothyroidism treatment is of clinical relevance, based on cardiovascular risk parameters correction. A systemic research of the literature using MEDLINE tool was performed to identify the relevant studies. Only placebo-controlled randomized control trials were included. A quantitative analysis was also performed. This systematic review and meta-analysis of randomized placebo-controlled trials assess the different impact of levothyroxine vs placebo treatment. A significant decrease in serum thyroid-stimulating hormone and total and low-density lipoprotein cholesterol was obtained with levothyroxine therapy (66, 9 and 14%, respectively) and, although modest, this could be significant in terms of reduction of the incidence of coronary artery disease. Other significant results of lipid parameters were not obtained. This systematic review provides a strong evidence-based data in favour of specific changes and beneficial effects of levothyroxine treatment.
Search for other papers by Charissa van Zwol-Janssens in
Google Scholar
PubMed
Search for other papers by Aglaia Hage in
Google Scholar
PubMed
Search for other papers by Kim van der Ham in
Google Scholar
PubMed
Search for other papers by Birgitta K Velthuis in
Google Scholar
PubMed
Search for other papers by Ricardo P J Budde in
Google Scholar
PubMed
Search for other papers by Maria P H Koster in
Google Scholar
PubMed
Search for other papers by Arie Franx in
Google Scholar
PubMed
Search for other papers by Bart C J M Fauser in
Google Scholar
PubMed
Search for other papers by Eric Boersma in
Google Scholar
PubMed
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands
Search for other papers by Daniel Bos in
Google Scholar
PubMed
Search for other papers by Joop S E Laven in
Google Scholar
PubMed
Search for other papers by Yvonne V Louwers in
Google Scholar
PubMed
Search for other papers by the CREW consortium in
Google Scholar
PubMed
Besides age, estrogen exposure plays a crucial role in changes in bone density (BD) in women. Premature ovarian insufficiency (POI) and polycystic ovary syndrome (PCOS) are conditions in reproductive-aged women in which the exposure to estrogen is substantially different. Women with a history of preeclampsia (PE) are expected to have normal estrogen exposure. Within the CREw-IMAGO study, we investigated if trabecular BD is different in these women because of differences in the duration of estrogen exposure. Trabecular BD was measured in thoracic vertebrae on coronary CT scans. Women with a reduced estrogen exposure (POI) have a lower BD compared to women with an intermediate exposure (PE) (mean difference (MD) −26.8, 95% CI −37.2 to −16.3). Women with a prolonged estrogen exposure (PCOS) have the highest BD (MD 15.0, 95% CI 4.3–25.7). These results support the hypothesis that the duration of estrogen exposure in these women is associated with trabecular BD.
Significance statement
Our results suggest that middle-aged women with PCOS have a higher BD and women with POI have a lower BD. We hypothesized that this is due to either a prolonged estrogen exposure, as seen in women with PCOS, or a reduced estrogen exposure, as in women with POI. In the counseling of women with reproductive disorders on long-term health issues, coronary CT provides a unique opportunity to assess both coronary artery calcium score for cardiovascular screening as well as trabecular BD.
Search for other papers by Eng-Loon Tng in
Google Scholar
PubMed
Search for other papers by Yee Sian Tiong in
Google Scholar
PubMed
Search for other papers by Aye Thida Aung in
Google Scholar
PubMed
Search for other papers by Nicole Ya Yuan Chong in
Google Scholar
PubMed
Search for other papers by Zhemin Wang in
Google Scholar
PubMed
Background
Evidence on the efficacy and safety of anticoagulation in preventing stroke and thromboembolic events in people with thyrotoxic atrial fibrillation is scarce.
Objective
We evaluated the efficacy and safety of anticoagulation in people with thyrotoxic atrial fibrillation.
Methods
Our study protocol was published in the International Prospective Register of Systematic Reviews (registration no. CRD42020222782). Four databases and two systematic review registers were searched through 25 November 2020 for interventional and observational studies comparing anticoagulation therapy with active comparators, placebo, or no treatment in people with thyrotoxic atrial fibrillation. Random-effects meta-analysis and sensitivity analysis were performed. Quality of evidence was described using the GRADE framework.
Results
In the study, 23,145 records were retrieved. One randomized controlled trial and eight cohort studies were ultimately included. Effect estimates on the efficacy and safety of anticoagulation were extracted. Meta-analysis using the inverse variance and random-effects methods was conducted on four cohort studies with 3443 participants and 277 events. Anticoagulation in people with thyrotoxic atrial fibrillation reduced the risk of ischemic stroke and systemic thromboembolism by 3% (95% CI: 1–6%). Warfarin may prevent ischemic stroke in people with thyrotoxic atrial fibrillation if the CHA2DS2-VASc score exceeds 1 and when atrial fibrillation persists beyond 7 days. Direct oral anticoagulants may be associated with fewer bleeding events than warfarin.
Conclusions
Anticoagulation prevents ischemic stroke and systemic thromboembolism in people with thyrotoxic atrial fibrillation. Direct oral anticoagulants may be associated with fewer bleeding events.
Search for other papers by Robert A Hart in
Google Scholar
PubMed
Search for other papers by Robin C Dobos in
Google Scholar
PubMed
Search for other papers by Linda L Agnew in
Google Scholar
PubMed
Search for other papers by Neil A Smart in
Google Scholar
PubMed
Search for other papers by James R McFarlane in
Google Scholar
PubMed
Pharmacokinetics of leptin in mammals has not been studied in detail and only one study has examined more than one time point in non-mutant mice and this was in a female mice. This is the first study to describe leptin distribution over a detailed time course in normal male mice. A physiologic dose (12 ng) of radiolabelled leptin was injected into adult male mice via the lateral tail vein and tissues were dissected out and measured for radioactivity over a time course of up to two hours. Major targets were the digestive tract, kidneys, skin and lungs. The brain was not a major target, and 0.15% of the total dose was recovered from the brain 5 min after administration. Major differences appear to exist in the distribution of leptin between the male and female mice, indicating a high degree of sexual dimorphism. Although the half-lives were similar between male and female mice, almost twice the proportion of leptin was recovered from the digestive tract of male mice in comparison to that reported previously for females. This would seem to indicate a major difference in leptin distribution and possibly function between males and females.
Search for other papers by Kristin Viste in
Google Scholar
PubMed
Hormone Laboratory, Department of Medicine, Department of Clinical Science, Department of Radiology, Haukeland University Hospital, 5021 Bergen, Norway
Search for other papers by Marianne A Grytaas in
Google Scholar
PubMed
Search for other papers by Melissa D Jørstad in
Google Scholar
PubMed
Search for other papers by Dag E Jøssang in
Google Scholar
PubMed
Search for other papers by Eivind N Høyden in
Google Scholar
PubMed
Search for other papers by Solveig S Fotland in
Google Scholar
PubMed
Search for other papers by Dag K Jensen in
Google Scholar
PubMed
Hormone Laboratory, Department of Medicine, Department of Clinical Science, Department of Radiology, Haukeland University Hospital, 5021 Bergen, Norway
Search for other papers by Kristian Løvås in
Google Scholar
PubMed
Search for other papers by Hrafnkell Thordarson in
Google Scholar
PubMed
Search for other papers by Bjørg Almås in
Google Scholar
PubMed
Hormone Laboratory, Department of Medicine, Department of Clinical Science, Department of Radiology, Haukeland University Hospital, 5021 Bergen, Norway
Search for other papers by Gunnar Mellgren in
Google Scholar
PubMed
Primary aldosteronism (PA) is a common cause of secondary hypertension and is caused by unilateral or bilateral adrenal disease. Treatment options depend on whether the disease is lateralized or not, which is preferably evaluated with selective adrenal venous sampling (AVS). This procedure is technically challenging, and obtaining representative samples from the adrenal veins can prove difficult. Unsuccessful AVS procedures often require reexamination. Analysis of cortisol during the procedure may enhance the success rate. We invited 21 consecutive patients to participate in a study with intra-procedural point of care cortisol analysis. When this assay showed nonrepresentative sampling, new samples were drawn after redirection of the catheter. The study patients were compared using the 21 previous procedures. The intra-procedural cortisol assay increased the success rate from 10/21 patients in the historical cohort to 17/21 patients in the study group. In four of the 17 successful procedures, repeated samples needed to be drawn. Successful sampling at first attempt improved from the first seven to the last seven study patients. Point of care cortisol analysis during AVS improves success rate and reduces the need for reexaminations, in accordance with previous studies. Successful AVS is crucial when deciding which patients with PA will benefit from surgical treatment.
