Search Results
Search for other papers by Cheryl M Isherwood in
Google Scholar
PubMed
Search for other papers by M Denise Robertson in
Google Scholar
PubMed
Search for other papers by Debra J Skene in
Google Scholar
PubMed
Search for other papers by Jonathan D Johnston in
Google Scholar
PubMed
Obesity is a major cause of type 2 diabetes. Transition from obesity to type 2 diabetes manifests in the dysregulation of hormones controlling glucose homeostasis and inflammation. As metabolism is a dynamic process that changes across 24 h, we assessed diurnal rhythmicity in a panel of 10 diabetes-related hormones. Plasma hormones were analysed every 2 h over 24 h in a controlled laboratory study with hourly isocaloric drinks during wake. To separate effects of body mass from type 2 diabetes, we recruited three groups of middle-aged men: an overweight (OW) group with type 2 diabetes and two control groups (lean and OW). Average daily concentrations of glucose, triacylglycerol and all the hormones except visfatin were significantly higher in the OW group compared to the lean group (P < 0.001). In type 2 diabetes, glucose, insulin, C-peptide, glucose-dependent insulinotropic peptide and glucagon-like peptide-1 increased further (P < 0.05), whereas triacylglycerol, ghrelin and plasminogen activator inhibitor-1 concentrations were significantly lower compared to the OW group (P < 0.001). Insulin, C-peptide, glucose-dependent insulinotropic peptide and leptin exhibited significant diurnal rhythms in all study groups (P < 0.05). Other hormones were only rhythmic in 1 or 2 groups. In every group, hormones associated with glucose regulation (insulin, C-peptide, glucose-dependent insulinotropic peptide, ghrelin and plasminogen activator inhibitor-1), triacylglycerol and glucose peaked in the afternoon, whereas glucagon and hormones associated with appetite and inflammation peaked at night. Thus being OW with or without type 2 diabetes significantly affected hormone concentrations but did not affect the timing of the hormonal rhythms.
Leicester Diabetes Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Search for other papers by Benjamin D Maylor in
Google Scholar
PubMed
Search for other papers by Julia K Zakrzewski-Fruer in
Google Scholar
PubMed
Search for other papers by Charlie J Orton in
Google Scholar
PubMed
Centre for Physical Activity in Health and Disease, Brunel University London, Uxbridge, UK
Division of Sport, Health and Exercise Sciences, Department of Life Sciences, Brunel University London, Uxbridge, UK
Search for other papers by Daniel P Bailey in
Google Scholar
PubMed
A single exercise session can affect appetite-regulating hormones and suppress appetite. The effects of short, regular physical activity breaks across the day on appetite are unclear. This study investigated the effects of breaking up sitting with high-intensity physical activity vs a single bout of moderate-intensity exercise and prolonged sitting on appetite control. In this randomised crossover trial, 14 sedentary, inactive adults (7 women) completed 3, 8-h experimental conditions: (i) prolonged sitting (SIT); (ii) 30 min of moderate-intensity exercise followed by prolonged sitting (EX-SIT), and (iii) sitting with 2 min 32 s of high-intensity physical activity every hour (SIT-ACT). Physical activity energy expenditure was matched between EX-SIT and SIT-ACT. Subjective appetite was measured every 30 min with acylated ghrelin and total peptide-YY (PYY) measured hourly in response to two standardised test meals. An ad libitum buffet meal was provided at the end of each condition. Based on linear mixed model analysis, total area under the curve for satisfaction was 16% higher (P = 0.021) and overall appetite was 11% lower during SIT-ACT vs EX-SIT (P = 0.018), with no differences between SIT-ACT and SIT. Time series analysis indicated that SIT-ACT reduced subjective appetite during the majority of the post-lunch period compared with SIT and EX-SIT, with some of these effects reversed earlier in the afternoon (P < 0.05). Total PYY and acylated ghrelin did not differ between conditions. Relative energy intake was 760 kJ lower during SIT-ACT vs SIT (P = 0.024). High-intensity physical activity breaks may be effective in acutely suppressing appetite; yet, appetite-regulating hormones may not explain such responses.
Search for other papers by Yueyuan Yang in
Google Scholar
PubMed
Search for other papers by Tingting Yu in
Google Scholar
PubMed
Search for other papers by Zhili Niu in
Google Scholar
PubMed
Search for other papers by Ling Gao in
Google Scholar
PubMed
Objective
Uridine might be a common link between pathological pathways in diabetes and cardiovascular diseases. This study aimed to investigate the predictive value of plasma uridine for type 2 diabetes (T2D) and T2D with atherosclerosis.
Methods
Individuals with T2D and healthy controls (n = 218) were randomly enrolled in a cross-sectional study. Patients with T2D were divided into two groups based on carotid ultrasound: patients with carotid atherosclerosis (CA) (group DCA) and patients without CA (group D). Plasma uridine was determined using HPLC-MS/MS. Correlation and logistic regression analyses were used to analyze the results.
Results
Fasting and postprandial uridine were significantly increased in patients with T2D compared with healthy individuals. Logistic regression suggested that fasting and postprandial uridine were independent risk factors for T2D. The receiver operating characteristic (ROC) curve showed that fasting uridine had a predictive value on T2D (95% CI, 0.686–0.863, sensitivity 74.3%, specificity 71.8%). Fasting uridine was positively correlated with LDL-c, FBG, and PBG and negatively correlated with fasting C-peptide (CP-0h) and HOMA-IS. The change in postprandial uridine from fasting baseline (Δuridine) was smaller in T2D patients with CA compared with those without (0.80 (0.04–2.46) vs 2.01 (0.49–3.15), P = 0.010). Δuridine was also associated with T2D with CA and negatively correlated with BMI, CP-0h, and HOMA-IR.
Conclusion
Fasting uridine has potential as a predictor of diabetes. Δuridine is closely associated with carotid atherosclerosis in patients with T2D.
Search for other papers by Karoline Winckler in
Google Scholar
PubMed
Department of Cardiology, Department of Research, Institute of Clinical Studies, Clinical Research Unit, Department of Paediatrics, Department of Medicine, Department of Physiology and Nuclear Medicine, Institute of Clinical Medicine, Nephrology and Endocrinology
Department of Cardiology, Department of Research, Institute of Clinical Studies, Clinical Research Unit, Department of Paediatrics, Department of Medicine, Department of Physiology and Nuclear Medicine, Institute of Clinical Medicine, Nephrology and Endocrinology
Search for other papers by Lise Tarnow in
Google Scholar
PubMed
Department of Cardiology, Department of Research, Institute of Clinical Studies, Clinical Research Unit, Department of Paediatrics, Department of Medicine, Department of Physiology and Nuclear Medicine, Institute of Clinical Medicine, Nephrology and Endocrinology
Search for other papers by Louise Lundby-Christensen in
Google Scholar
PubMed
Department of Cardiology, Department of Research, Institute of Clinical Studies, Clinical Research Unit, Department of Paediatrics, Department of Medicine, Department of Physiology and Nuclear Medicine, Institute of Clinical Medicine, Nephrology and Endocrinology
Search for other papers by Thomas P Almdal in
Google Scholar
PubMed
Search for other papers by Niels Wiinberg in
Google Scholar
PubMed
Department of Cardiology, Department of Research, Institute of Clinical Studies, Clinical Research Unit, Department of Paediatrics, Department of Medicine, Department of Physiology and Nuclear Medicine, Institute of Clinical Medicine, Nephrology and Endocrinology
Search for other papers by Pia Eiken in
Google Scholar
PubMed
Search for other papers by Trine W Boesgaard in
Google Scholar
PubMed
Search for other papers by the CIMT trial group in
Google Scholar
PubMed
Despite aggressive treatment of cardiovascular disease (CVD) risk factors individuals with type 2 diabetes (T2D) still have increased risk of cardiovascular morbidity and mortality. The primary aim of this study was to examine the cross-sectional association between total (25-hydroxy vitamin D (25(OH)D)) and risk of CVD in patients with T2D. Secondary objective was to examine the association between 25(OH)D and bone health. A Danish cohort of patients with T2D participating in a randomised clinical trial were analysed. In total 415 patients (68% men, age 60±9 years (mean±s.d.), duration of diabetes 12±6 years), including 294 patients (71%) treated with insulin. Carotid intima–media thickness (IMT) and arterial stiffness (carotid artery distensibility coefficient (DC) and Young's elastic modulus (YEM)) were measured by ultrasound scan as indicators of CVD. Bone health was assessed by bone mineral density and trabecular bone score measured by dual energy X-ray absorptiometry. In this cohort, 214 patients (52%) were vitamin D deficient (25(OH)D <50 nmol/l). Carotid IMT was 0.793±0.137 mm, DC was 0.0030±0.001 mmHg, YEM was 2354±1038 mmHg and 13 (3%) of the patients were diagnosed with osteoporosis. A 25(OH)D level was not associated with carotid IMT or arterial stiffness (P>0.3) or bone health (P>0.6) after adjustment for CVD risk factors. In conclusion, 25(OH)D status was not associated with carotid IMT, arterial stiffness or bone health in this cohort of patients with T2D. To explore these associations and the association with other biomarkers further, multicentre studies with large numbers of patients are required.
Search for other papers by Maxime Duval in
Google Scholar
PubMed
Search for other papers by Kalyane Bach-Ngohou in
Google Scholar
PubMed
Search for other papers by Damien Masson in
Google Scholar
PubMed
Search for other papers by Camille Guimard in
Google Scholar
PubMed
Search for other papers by Philippe Le Conte in
Google Scholar
PubMed
Department of Emergency Medicine, CHU Nantes, Nantes, France
Search for other papers by David Trewick in
Google Scholar
PubMed
Objective
Severe hypocalcemia (Ca <1.9 mmol/L) is often considered an emergency because of a potential risk of cardiac arrest or seizures. However, there is little evidence to support this. The aim of our study was to assess whether severe hypocalcemia was associated with immediately life-threatening cardiac arrhythmias or neurological complications.
Methods
A retrospective observational study was carried out over a 2-year period in the Adult Emergency Department (ED) of Nantes University Hospital. All patients who had a protein-corrected calcium concentration measure were eligible for inclusion. Patients with multiple myeloma were excluded. The primary outcome was the number of life-threatening cardiac arrhythmias and/or neurological complications during the stay in the ED.
Results
A total of 41,823 patients had protein-corrected calcium (pcCa) concentrations measured, 155 had severe hypocalcemia, 22 were excluded because of myeloma leaving 133 for analysis. Median pcCa concentration was 1.73 mmol/L (1.57–1.84). Seventeen (12.8%) patients presented a life-threatening condition, 14 (10.5%) neurological and 3 (2.2%) cardiac during ED stay. However, these complications could be explained by the presence of underlying co-morbidities and or electrolyte disturbances other than hypocalcemia. Overall, 24 (18%) patients died in hospital. Vitamin D deficiency, chronic kidney disease and hypoparathyroidism were the most frequently found causes of hypocalcemia.
Conclusion
Thirteen percent of patients with severe hypocalcemia presented a life-threatening cardiac or neurological complication on the ED. However, a perfectly valid alternative cause could account for these complications. Further research is warranted to define the precise role of hypocalcemia.
Search for other papers by Zhou-Qing Kang in
Google Scholar
PubMed
Search for other papers by Jia-Ling Huo in
Google Scholar
PubMed
Search for other papers by Xiao-Jie Zhai in
Google Scholar
PubMed
Background
The optimal glycemic target during the perioperative period is still controversial. We aimed to explore the effects of tight glycemic control (TGC) on surgical mortality and morbidity.
Methods
PubMed, EMBASE and CENTRAL were searched from January 1, 1946 to February 28, 2018. Appropriate trails comparing the postoperative outcomes (mortality, hypoglycemic events, acute kidney injury, etc.) between different levels of TGC and liberal glycemic control were identified. Quality assessments were performed with the Jadad scale combined with the allocation concealment evaluation. Pooled relative risk (RR) and 95% CI were calculated using random effects models. Heterogeneity was detected by the I 2 test.
Results
Twenty-six trials involving a total of 9315 patients were included in the final analysis. The overall mortality did not differ between tight and liberal glycemic control (RR, 0.92; 95% CI, 0.78–1.07; I 2 = 20.1%). Among subgroup analyses, obvious decreased risks of mortality were found in the short-term mortality, non-diabetic conditions, cardiac surgery conditions and compared to the very liberal glycemic target. Furthermore, TGC was associated with decreased risks for acute kidney injury, sepsis, surgical site infection, atrial fibrillation and increased risks of hypoglycemia and severe hypoglycemia.
Conclusions
Compared to liberal control, perioperative TGC (the upper level of glucose goal ≤150 mg/dL) was associated with significant reduction of short-term mortality, cardic surgery mortality, non-diabetic patients mortality and some postoperative complications. In spite of increased risks of hypoglycemic events, perioperative TGC will benefits patients when it is done carefully.
Search for other papers by Elin Kahlert in
Google Scholar
PubMed
Endokrinologikum Goettingen, Goettingen, Germany
Search for other papers by Martina Blaschke in
Google Scholar
PubMed
Search for other papers by Knut Brockmann in
Google Scholar
PubMed
Search for other papers by Clemens Freiberg in
Google Scholar
PubMed
Search for other papers by Onno E Janssen in
Google Scholar
PubMed
Search for other papers by Nikolaus Stahnke in
Google Scholar
PubMed
Search for other papers by Domenika Strik in
Google Scholar
PubMed
Search for other papers by Martin Merkel in
Google Scholar
PubMed
Search for other papers by Alexander Mann in
Google Scholar
PubMed
Search for other papers by Klaus-Peter Liesenkötter in
Google Scholar
PubMed
Endokrinologikum Goettingen, Goettingen, Germany
Search for other papers by Heide Siggelkow in
Google Scholar
PubMed
Objective
Turner syndrome (TS) is characterized by the complete or partial loss of the second sex chromosome and associated with a wide range of clinical manifestations. We aimed to assess the medical care of adult patients with TS in Germany.
Design
Retrospective multicenter observational study.
Methods
Data were collected from medical records of 258 women with TS treated between 2001 and 2017 in five non-university endocrinologic centers in Germany.
Results
Mean age was 29.8 ± 11.6 years, mean height 152 ± 7.7 cm, and mean BMI 26.6 ± 6.3 kg/m2. The karyotype was known in 50% of patients. Information on cholesterol state, liver enzymes, and thyroid status was available in 81–98% of women with TS; autoimmune thyroiditis was diagnosed in 37%. Echocardiography was performed in 42% and cardiac MRI in 8.5%, resulting in a diagnosis of cardiovascular disorder in 28%. Data on growth hormone therapy were available for 40 patients (15%) and data concerning menarche in 157 patients (61%).
Conclusion
In 258 women with TS, retrospective analysis of healthcare data indicated that medical management was focused on endocrine manifestations. Further significant clinical features including cardiovascular disease, renal malformation, liver involvement, autoimmune diseases, hearing loss, and osteoporosis were only marginally if at all considered. Based on this evaluation and in accordance with recent guidelines, we compiled a documentation form facilitating the transition from pediatric to adult care and further medical management of TS patients. The foundation of Turner Centers in March 2019 will improve the treatment of TS women in Germany.
Search for other papers by Satoshi Higuchi in
Google Scholar
PubMed
Search for other papers by Hideki Ota in
Google Scholar
PubMed
Search for other papers by Takuya Ueda in
Google Scholar
PubMed
Search for other papers by Yuta Tezuka in
Google Scholar
PubMed
Search for other papers by Kei Omata in
Google Scholar
PubMed
Search for other papers by Yoshikiyo Ono in
Google Scholar
PubMed
Search for other papers by Ryo Morimoto in
Google Scholar
PubMed
Search for other papers by Masataka Kudo in
Google Scholar
PubMed
Division of Clinical Hypertension, Endocrinology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan
Search for other papers by Fumitoshi Satoh in
Google Scholar
PubMed
Search for other papers by Kei Takase in
Google Scholar
PubMed
Objective
Regional differences in cardiac magnetic resonance, which can reveal catecholamine-induced myocardial injury in patients with pheochromocytoma, have not yet been assessed using 3T magnetic resonance imaging. We evaluated these differences using myocardial T1-mapping and strain analysis.
Design and Methods
We retrospectively reviewed 16 patients newly diagnosed with catecholamine-producing tumors (CPT group) and 16 patients with essential hypertension (EH group), who underwent cardiac magnetic resonance imaging between May 2016 and March 2018. We acquired 3T magnetic resonance cine and native T1-mapping images and performed feature-tracking-based strain analysis in the former.
Results
Global cardiac function, morphology, global strain and peak strain rate were similar, but end-diastolic wall thickness differed between groups (CPT vs EH: 10.5 ± 1.7 vs 12.6 ± 2.8 mm; P < 0.05). Basal, but not apical, circumferential strain was significantly higher in the CPT than the EH group (19.4 ± 3.2 vs 16.8 ± 3.6 %; P < 0.05). Native T1 values were significantly higher in CPT than in EH patients, in both the basal septum (1307 ± 48 vs 1241 ± 45 ms; P < 0.01) and the apical septum (1377 ± 59 vs 1265 ± 58 ms; P < 0.01) mid-walls. In the CPT, but not in the EH group, native T1 values in the apical wall were significantly higher than those in the basal wall (P < 0.01).
Conclusion
3T magnetic resonance-based T1-mapping can sensitively detect subclinical catecholamine-induced myocardial injury; the influence of catecholamines may be greater in the apical than in the basal wall.
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Marianne Aa Grytaas in
Google Scholar
PubMed
Search for other papers by Kjersti Sellevåg in
Google Scholar
PubMed
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Hrafnkell B Thordarson in
Google Scholar
PubMed
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Eystein S Husebye in
Google Scholar
PubMed
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Kristian Løvås in
Google Scholar
PubMed
Department of Biomedicine, University of Bergen, Bergen, Norway
Search for other papers by Terje H Larsen in
Google Scholar
PubMed
Background
Primary aldosteronism (PA) is associated with increased cardiovascular morbidity, presumably due to left ventricular (LV) hypertrophy and fibrosis. However, the degree of fibrosis has not been extensively studied. Cardiac magnetic resonance imaging (CMR) contrast enhancement and novel sensitive T1 mapping to estimate increased extracellular volume (ECV) are available to measure the extent of fibrosis.
Objectives
To assess LV mass and fibrosis before and after treatment of PA using CMR with contrast enhancement and T1 mapping.
Methods
Fifteen patients with newly diagnosed PA (PA1) and 24 age- and sex-matched healthy subjects (HS) were studied by CMR with contrast enhancement. Repeated imaging with a new scanner with T1 mapping was performed in 14 of the PA1 and 20 of the HS median 18 months after specific PA treatment and in additional 16 newly diagnosed PA patients (PA2).
Results
PA1 had higher baseline LV mass index than HS (69 (53–91) vs 51 (40–72) g/m2; P < 0.001), which decreased significantly after treatment (58 (40–86) g/m2; P < 0.001 vs baseline), more with adrenalectomy (n = 8; −9 g/m2; P = 0.003) than with medical treatment (n = 6; −5 g/m2; P = 0.075). No baseline difference was found in contrast enhancement between PA1 and HS. T1 mapping showed no increase in ECV as a myocardial fibrosis marker in PA. Moreover, ECV was lower in the untreated PA2 than HS 10 min post-contrast, and in both PA groups compared with HS 20 min post-contrast.
Conclusion
Specific treatment rapidly reduced LV mass in PA. Increased myocardial fibrosis was not found and may not represent a common clinical problem.
Search for other papers by Rossella Cannarella in
Google Scholar
PubMed
Search for other papers by Teresa Mattina in
Google Scholar
PubMed
Search for other papers by Rosita A Condorelli in
Google Scholar
PubMed
Search for other papers by Laura M Mongioì in
Google Scholar
PubMed
Search for other papers by Giuseppe Pandini in
Google Scholar
PubMed
Search for other papers by Sandro La Vignera in
Google Scholar
PubMed
Search for other papers by Aldo E Calogero in
Google Scholar
PubMed
Insulin-like growth factor 1 receptor (IGF1R), mapping on the 15q26.3 chromosome, is required for normal embryonic and postnatal growth. The aim of the present study was to evaluate the IGF1R gene expression and function in three unrelated patients with chromosome 15 structural abnormalities. We report two male patients with the smallest 15q26.3 chromosome duplication described so far, and a female patient with ring chromosome 15 syndrome. Patient one, with a 568 kb pure duplication, had overgrowth, developmental delay, mental and psychomotor retardation, obesity, cryptorchidism, borderline low testis volume, severe oligoasthenoteratozoospermia and gynecomastia. We found a 1.8-fold increase in the IGF1R mRNA and a 1.3-fold increase in the IGF1R protein expression (P < 0.05). Patient two, with a 650 kb impure duplication, showed overgrowth, developmental delay, mild mental retardation, precocious puberty, low testicular volume and severe oligoasthenoteratozoospermia. The IGF1R mRNA and protein expression was similar to that of the control. Patient three, with a 46,XX r(15) (p10q26.2) karyotype, displayed intrauterine growth retardation, developmental delay, mental and psychomotor retardation. We found a <0.5-fold decrease in the IGF1R mRNA expression and an undetectable IGF1R activity. After reviewing the previously 96 published cases of chromosome 15q duplication, we found that neurological disorders, congenital cardiac defects, typical facial traits and gonadal abnormalities are the prominent features in patients with chromosome 15q duplication. Interestingly, patients with 15q deletion syndrome display similar features. We speculate that both the increased and decreased IGF1R gene expression may play a role in the etiology of neurological and gonadal disorders.
