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Yee-Ming M Cheung Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia
Division of Endocrinology, Diabetes and Metabolism, Northwell, Great Neck, New York, USA

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Rudolf Hoermann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Karen Van Department of Endocrinology, Austin Health, Melbourne, Australia

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Damian Wu Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Jenny Healy Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Bella Halim Department of Endocrinology, Austin Health, Melbourne, Australia

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Manjri Raval Department of Endocrinology, Austin Health, Melbourne, Australia

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Maria McGill Department of Radiology, Austin Health, Melbourne, Australia

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Ali Al-Fiadh Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Cardiology, Austin Health, Melbourne Australia

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Michael Chao Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

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Shane White Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

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Belinda Yeo Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia
Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Australia

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Jeffrey D Zajac Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

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Mathis Grossmann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

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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.

Open access
Bjarke R Medici Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Birte Nygaard Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jeppe L la Cour Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark

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Martin Krakauer Department of Clinical Physiology and Nuclear Medicine, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark

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Andreas Brønden Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark

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Mette P Sonne Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark

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Jens J Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jens F Rehfeld Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Tina Vilsbøll Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark

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Jens Faber Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Filip K Knop Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark

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Context

In individuals with hypothyroidism and overweight, levothyroxine substitution therapy is often expected to cause weight loss due to its effect on resting energy expenditure. However, despite levothyroxine-induced enhancement of resting energy expenditure, fat mass loss is rarely seen after levothyroxine substitution therapy. The mechanism behind this conundrum is unknown.

Aim

The aim of the study was to assess the effect of levothyroxine therapy on hunger sensations and ad libitum food intake in individuals with hypothyroidism.

Design and setting

Prospective cohort study of 18 newly diagnosed hypothyroid women (thyroid-stimulating hormone (TSH) >10 mU/L). Participants were investigated at diagnosis, after normalization of TSH (<4.0 mU/L), and after 6 months of successful treatment. Eighteen age and body mass index-matched healthy controls were also included.

Intervention

Hypothyroid individuals were treated with levothyroxine according to European Thyroid Association guidelines.

Main outcomes

Changes in hunger sensation were assessed using visual analog scales (cm) before and during a standardized mixed meal test, and food intake was measured during a subsequent ad libitum meal (g).

Results

After 6 months of levothyroxine therapy, mean resting energy expenditure was increased by 144 kcal/day (10%) (P < 0.001). Weight loss was comprised of 0.8 kg fat-free mass while fat mass remained unchanged. Fasting hunger sensation increased from a mean of 4.5 (s.d. 2.2) cm to 5.5 (s.d. 2.2) cm (P = 0.047). The numerical increase in ad libitum meal intake did not reach statistical significance.

Conclusion

Our data suggest that levothyroxine-induced hunger may be a culprit in the lack of fat mass loss from levothyroxine therapy.

Open access
Molly L Tanenbaum Division of Endocrinology, Gerontology, and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA

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Persis V Commissariat Section on Clinical, Behavioral, and Outcomes Research, Joslin Diabetes Center, Boston, Massachusetts, USA

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Diabetes technology continues to advance, with more individuals with type 1 diabetes (T1D) adopting insulin pumps, continuous glucose monitoring (CGM), and automated insulin delivery (AID) systems that integrate real-time glucose data with an algorithm to assist with insulin dosing decisions. These technologies are linked with benefits to glycemic outcomes (e.g. increased time in target range), diabetes management behaviors, and quality of life. However, current devices and systems are not without barriers and hassles for the user. The intent of this review is to describe the personal challenges and reactions that users experience when interacting with current diabetes technologies, which can affect their acceptance and motivation to engage with their devices. This review will discuss user experiences and strategies to address three main areas: (i) the emotional burden of utilizing a wearable device; (ii) the perceived and experienced negative social consequences of device use; and (iii) the practical challenges of wearing devices.

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Heng Yeh Department of Emergency Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan
College of Medicine, Chang Gung University, Taoyuan, Taiwan

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Hsuan Yeh College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Chun-Cheng Chiang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ju-Ching Yen College of Medicine, China Medical University, Taichung, Taiwan

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I-Kuan Wang College of Medicine, China Medical University, Taichung, Taiwan
Department of Nephrology, China Medical University Hospital, Taichung, Taiwan

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Shou-Hsuan Liu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Chia Lee College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Hao Weng College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Wen-Hung Huang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ching-Wei Hsu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Tzung-Hai Yen College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Secondary hyperparathyroidism (SHPT) is a common complication of end-stage kidney disease (ESKD). Hungry bone syndrome (HBS) occurs frequently in patients on maintenance dialysis receiving parathyroidectomy for refractory SHPT. However, there is scanty study investigating the clinical risk factors that predict postoperative HBS, and its outcome in peritoneal dialysis (PD) patients. We conducted a single-center retrospective study to analyze 66 PD patients who had undergone parathyroidectomy for secondary hyperparathyroidism at Chang Gung Memorial Hospital between 2009 and 2019. The patients were stratified into two groups based on the presence (n=47) or absence (n=19) of HBS after parathyroidectomy. Subtotal parathyroidectomy was the most common surgery performed (74.2%), followed by total parathyroidectomy with autoimplantation (25.8%). Pathological examination of all surgical specimens revealed parathyroid hyperplasia (100%). Patients with HBS had lower levels of postoperative nadir corrected calcium, higher alkaline phosphate (ALP), and higher potassium levels compared with patients without HBS (all P<0.05). A multivariate logistic regression model confirmed that lower preoperative serum calcium level (OR 0.354, 95% CI 0.133–0.940, P=0.037), higher ALP (OR 1.026, 95% CI 1.008–1.044, P=0.004), and higher potassium level (OR 6.894, 95% CI 1.806–26.317, P=0.005) were associated with HBS after parathyroidectomy. Patients were followed for 58.2±30.8 months after the surgery. There was no significant difference between HBS and non-HBS groups in persistence (P=0.496) or recurrence (P=1.000) of hyperparathyroidism. The overall mortality rate was 10.6% with no significant difference found between both groups (P=0.099). We concluded that HBS is a common complication (71.2%) of parathyroidectomy for SHPT and should be managed appropriately.

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Alexandra Kiess Department of Pediatric Cardiology, Faculty of Medicine, Heart Center Leipzig, University of Leipzig, Strümpellstraße, Leipzig, Germany
Department of Child and Adolescent Medicine, Section of Pediatric Cardiology, University Hospital Jena, Am Klinikum, Jena, Germany

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Jessica Green Alder Hey Children's NHS Foundation Trust, Pediatric Intensive Care Unit, Eaton Road Liverpool, Great Britain

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Anja Willenberg Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics (ILM), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Uta Ceglarek Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics (ILM), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Ingo Dähnert Department of Pediatric Cardiology, Faculty of Medicine, Heart Center Leipzig, University of Leipzig, Strümpellstraße, Leipzig, Germany

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Wieland Kiess LIFE Leipzig Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Strasse, Leipzig, Germany
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Mandy Vogel LIFE Leipzig Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Strasse, Leipzig, Germany
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Background and objectives

As part of the LIFE Child study, we previously described the associations between N-terminal-pro-hormone brain natriuretic peptide (NT-proBNP) and hs-troponin T (hs-TnT) levels and an individual’s sex, age and pubertal status, as well as with body mass index (BMI) and serum lipid levels. For NT-proBNP, we found inverse associations with advancing puberty, increasing BMI and serum lipid levels. These findings led us to further question the putative influences of the developing individual’s metabolic and growth status as represented by levels of insulin-like growth factor-1 (IGF-1) and IGF-1-binding protein-3 (IGF-BP3) as well as hemoglobin A1c (HbA1c) and Cystatin C (CysC).

Material and methods

Serum values, medical history and anthropometric data provided by 2522 children aged 0.25–18 years were collected and analyzed as per study protocol.

Results

A strong negative association between NT-proBNP values and IGF-1, IGF-BP3 and HbA1c levels was identified. For IGF-BP3, this interaction was modulated by sex and age, for HbA1c only by age. For hs-TnT, a positive association was found with IGF-BP3, IGF-1 and CysC. The association between hs-TnT and IGF-1 was sex dependent. The association between CysC and hs-TnT was stronger in girls, but the interaction with age was only seen in boys. Between hs-TnT and HbA1c, the association was significantly negative and modulated by age.

Conclusion

Based on our large pediatric cohort, we could identify age- and sex-dependent interactions between the metabolic status represented by IGF-1, IGF-BP3, CysC and HbA1c levels and the cardiac markers NT-proBNP and hs-TnT.

Open access
Nelma Veronica Marques Neuroendocrinology Research Center, Endocrinology Section, Medical School and Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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Luiz Eduardo Armondi Wildemberg Neuroendocrinology Research Center, Endocrinology Section, Medical School and Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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Monica R Gadelha Neuroendocrinology Research Center, Endocrinology Section, Medical School and Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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Pasireotide long-acting release is effective in achieving biochemical control and reducing tumour volume in patients with acromegaly inadequately controlled by first-line therapy. As part of a long-term, real-world study at our centre, 20 of 50 patients receiving pasireotide benefited from a reduction in pasireotide dose. Pasireotide reduced insulin-like growth factor 1 (IGF1) levels to below the upper limit of the normal range, with some patients responding within 1−3 months of treatment (n = 11) and others after ≥4 months (n = 9). Following pasireotide dose reduction, IGF1 levels showed a mild increase but remained within the normal range after a median of 39 months in the early responders and 17 months in the late responders. Glucose and glycated haemoglobin levels decreased following dose reduction. Identifying patients who may benefit from a reduction in pasireotide dose warrants further research as it may improve the management of pasireotide-associated hyperglycaemia in susceptible patients.

Significance statement

Patients with acromegaly often need medical therapy for extended periods of time, and pasireotide is an effective, long-term treatment option. However, pasireotide may increase blood glucose levels in some patients, such as those with pre-existing diabetes. In this single-centre study, we show that following dose reduction of pasireotide over time, patients with acromegaly maintained their biochemical response (IGF1 < ULN) and had improved glycaemic control. As such, dose reductions may be an effective, personalised treatment approach for managing some patients receiving long-term pasireotide therapy and could allow patients to achieve early and long-term biochemical control while minimising adverse drug effects.

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Yang Yu Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Hairong Hao Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Linghui Kong Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Jie Zhang Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Feng Bai Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Fei Guo Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Pan Wei Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Rui Chen Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Wen Hu Department of Endocrinology and Metabolism, Huai’an Hospital Affiliated to Xuzhou Medical University and Huai’an Second People’s Hospital, Huai’an, Jiangsu, China

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Previous studies have shown that the elevated levels of circulating branched-chain amino acids (BCAAs) are associated with the development of insulin resistance and its complications, including obesity, type 2 diabetes, cardiovascular disease and some cancers. However, animal models that can mimic the metabolic state of chronically elevated BCAAs in humans are rare. Therefore, the aim of this study was to establish the above animal model and analyse the metabolic changes associated with high BCAA levels. Sixteen 8-week-old Sprague–Dawley (SD) rats were randomly divided into two groups and given either a high fructose diet or a normal diet. BCAA levels as well as blood glucose and lipid levels were measured at different time points of feeding. The mRNA expression levels of two key enzymes of BCAA catabolism, ACAD (acyl-CoA dehydrogenase) and BCKDH (branched-chain α-keto acid dehydrogenase), were measured by qPCR, and the protein expression levels of these two enzymes were analysed by immunohistochemistry. Finally, the metabolite expression differences between the two groups were analysed by Q300 metabolomics technology. Our study confirms that defects in the catabolic pathways of BCAAs lead to increased levels of circulating BCAAs, resulting in disorders of glucose and lipid metabolism characterized by insulin resistance by affecting metabolic pathways associated with amino acids and bile acids.

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Paweł Komarnicki Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Paweł Gut Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Jan Musiałkiewicz Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Maja Cieślewicz Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Adam Maciejewski Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Prachi Patel Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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George Mastorakos Unit of Endocrinology, Diabetes Mellitus and Metabolism, Aretaieion University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Marek Ruchała Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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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.

Open access
Paul-Martin Holterhus Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Alexandra Kulle Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Anne-Marie Till Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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Caroline Stille Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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Tabea Lamprecht Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Simon Vieth Department of Pediatrics I, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian-Albrechts-University, CAU, Kiel, Germany

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Melchior Lauten Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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Glucocorticoids represent a key element in the treatment of pediatric acute lymphoblastic leukemia (ALL) and lead to adrenal suppression. We aimed to assess the differential response profile of adrenal steroids in children with ALL during BFM (Berlin–Frankfurt–Münster) induction treatment. Therefore, we performed liquid chromatography tandem–mass spectrometry (LC–MS/MS)-based steroid profiling of up to seven consecutive leftover morning serum samples derived from 11 patients (pts) with ALL before (day 0) and during induction therapy at days 1–5, 6–12, 13–26, 27–29, 30–35 and 36–40. 17-hydroxyprogesterone (17OHP), 11-deoxycortisol (11S), cortisol, 11-deoxycorticosterone (DOC), corticosterone and aldosterone were determined in parallel. Subsequently, steroid concentrations were normalized by multiples of median (MOM) to adequately consider pediatric age- and sex-specific reference ranges. MOM-cortisol and its precursors MOM–11S and MOM–17OHP were significantly suppressed by glucocorticoid treatment until day 29 (P < 8.06 × 10−10, P < 5.102 × 10−5, P < 0.0076, respectively). Cortisol recovered in one of four pts at days 27–29 and in two of five pts at days 36–40. Among the mineralocorticoids, corticosterone was significantly suppressed (P < 3.115 × 10−6). Aldosterone and DOC showed no significant changes when comparing day 0 to the treatment time points. However, two ALL patients with ICU treatment due to the sepsis showed significantly lower MOM–DOC (P = 0.006436) during that time and almost always the lowest aldosterone compared to all other time points. Suppression of mineralocorticoid precursors under high-dose glucocorticoid therapy suggests a functional cross talk of central glucocorticoid regulation and adrenal mineralocorticoid synthesis. Our data should stimulate prospective investigation to assess potential clinical relevance.

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Shaomin Shi Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

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Xinghua Chen Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China

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Wen Yu Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China

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Xiaolan Ke Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

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Tean Ma Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

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Protection of podocytes is one of the important means to delay the progression of diabetic nephropathy (DN), and glucagon-like peptide-1 (GLP-1) has been shown to have a protective effect on the kidney in DN models, but whether it has a protective effect on podocytes and the potential mechanisms of action remain largely unknown. In the present study, we established a type 2 diabetes mellitus (T2DM) mouse model by high-fat diet feeding combined with streptozotocin (STZ) induction and administered the intervention for 14 weeks. We found that liraglutide significantly ameliorated podocyte injury in DN mice. Mechanistically, we detected glucagon-like peptide-1 receptor (GLP-1R) protein expression levels in kidney tissues by immunohistochemical staining, immunofluorescence staining, and western blotting and found that podocytes could express GLP-1R and liraglutide treatment could restore GLP-1R expression in the kidney tissues of DN mice. Furthermore, we found that NLRP3-induced inflammation and pyroptosis were positively correlated with podocyte injury in DN mice, and liraglutide inhibited the expression of NLRP3-induced inflammation and pyroptosis-related proteins. Our results suggest that liraglutide protects DN mouse podocytes by regulating GLP-1R in renal tissues and by regulating NLRP3-induced inflammation and pyroptosis.

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