Search Results

You are looking at 1 - 10 of 10 items for :

  • Abstract: Arteries x
  • Abstract: Atherosclerosis x
  • Abstract: Circulation x
  • Abstract: Ghrelin x
  • Abstract: Stroke x
  • Abstract: Heart x
  • Abstract: cardiac* x
  • Abstract: Myocardial x
  • Metabolic Syndrome and Diabetes x
Clear All Modify Search
Sigrid Bjerge Gribsholt Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark

Search for other papers by Sigrid Bjerge Gribsholt in
Google Scholar
PubMed
Close
,
Morten Schmidt Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Morten Schmidt in
Google Scholar
PubMed
Close
,
Eskild Bendix Kristiansen Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark

Search for other papers by Eskild Bendix Kristiansen in
Google Scholar
PubMed
Close
,
Bjørn Richelsen Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

Search for other papers by Bjørn Richelsen in
Google Scholar
PubMed
Close
, and
Henrik Toft Sørensen Department of Clinical Epidemiology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

Search for other papers by Henrik Toft Sørensen in
Google Scholar
PubMed
Close

Objective

The aim was to examine the association between hospital-diagnosed overweight/obesity and incident CVD according to the time period of the overweight/obesity diagnosis.

Design

This is a cohort study.

Methods

From Danish national health registries, we identified all residents with a first-time hospital-based overweight/obesity diagnosis code, 1977–2018 (n = 195,221), and an age and sex-matched general population comparison cohort (n = 1,952,210). We computed adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) using Cox regression. We adjusted for comorbidities and educational level and applied 10 years of follow-up.

Results

The overall incidence rate was 10.1 (95% CI 10.0–10.1) per 1000 person-years for the comparison cohort and 25.1 (95% CI 24.8–25.4) per 1000 person-years for the overweight/obesity cohort, corresponding to an aHR of 2.5 (95% CI 2.4–2.5). The aHR was elevated for all subtypes of CVD: heart failure: 3.9 (95% CI 3.7–4.1), bradyarrhythmia: 2.9 (95% CI 2.7–3.1), angina pectoris: 2.7 (95% CI 2.7–2.8), atrial fibrillation or flutter: 2.6 (95% CI 2.5–2.6), acute myocardial infarction: 2.4 (95% CI 2.3–2.4), revascularization procedure: 2.4 (95% CI 2.2–2.5), valvular heart disease: 1.7 (95% CI 1.6–1.8), ischemic stroke: 1.6 (95% CI 1.4–1.7), transient ischemic attack: 1.6 (95% CI 1.5–1.7), and cardiovascular death: 1.6 (95% CI 1.5–1.6). The 1–10-year aHR of any CVD associated with an overweight/obesity diagnosis decreased from 2.8 (95% CI 2.7–2.9) in 1977–1987 to 1.8 (95% CI 1.8–1.9) in 2008–2018.

Conclusion

Patients with hospital-diagnosed overweight/obesity had high rates of ischemic heart disease, heart failure, structural heart disease, arrhythmia, stroke, and death, although the strength of the association decreased in recent years.

Significance statement

Obesity is linked to metabolic abnormalities that predispose individuals to an increased risk of subtypes of CVD. In this population-based nationwide 40-year cohort study, we found that of 195,221 patients with an overweight/obesity diagnosis, more than 31,000 (15.9%) were admitted to hospital within 10 years because of CVD; corresponding to a 2.5-fold greater relative risk of any CVD associated with overweight/obesity than in the general population. We observed an increased risk for most CVD subtypes, including ischemic heart disease, heart failure, structural heart disease, arrhythmia, stroke, and cardiovascular death, although the strength of the association decreased in recent years. Our study emphasizes the importance of improved clinical handling of obesity and underscores the need to prevent associated complications to alleviate the burden of obesity.

Open access
Chaiho Jeong Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Chaiho Jeong in
Google Scholar
PubMed
Close
,
Bongseong Kim Department of Medical Statistics, Soongsil University of Korea, Seoul, Republic of Korea

Search for other papers by Bongseong Kim in
Google Scholar
PubMed
Close
,
Jinyoung Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Jinyoung Kim in
Google Scholar
PubMed
Close
,
Hansang Baek Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Hansang Baek in
Google Scholar
PubMed
Close
,
Mee Kyoung Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Mee Kyoung Kim in
Google Scholar
PubMed
Close
,
Tae-Seo Sohn Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Tae-Seo Sohn in
Google Scholar
PubMed
Close
,
Ki-Hyun Baek Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Ki-Hyun Baek in
Google Scholar
PubMed
Close
,
Ki-Ho Song Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Ki-Ho Song in
Google Scholar
PubMed
Close
,
Hyun-Shik Son Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Hyun-Shik Son in
Google Scholar
PubMed
Close
,
Kyungdo Han Department of Medical Statistics, Soongsil University of Korea, Seoul, Republic of Korea

Search for other papers by Kyungdo Han in
Google Scholar
PubMed
Close
, and
Hyuk-Sang Kwon Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

Search for other papers by Hyuk-Sang Kwon in
Google Scholar
PubMed
Close

Objective

Real-world-based population data about the optimal low-density lipoprotein cholesterol (LDL-C) level for preventing cardiovascular disease in very high-risk populations is scarce.

Methods

From 2009 to 2012, 26,922 people aged ≥ 40 years with type 2 diabetes mellitus (T2DM) who had a history of percutaneous coronary intervention (PCI) were analyzed. Data from the Korean National Health Insurance System were used. They were followed up to the date of a cardiovascular event or the time to death, or until December 31, 2018. Endpoints were recurrent PCI, newly stroke or heart failure, cardiovascular death, and all-cause death. Participants were divided into the following categories according to LDL-C level: <55 mg/dL, 55–69 mg/dL, 70–99 mg/dL, 100–129 mg/dL, 130–159 mg/dL, and ≥ 160 mg/dL.

Results

Compared to LDL-C < 55 mg/dL, the hazard ratios (HR) for re-PCI and stroke increased linearly with increasing LDL-C level in the population < 65 years. However, in ≥ 65 years old, HRs for re-PCI and stroke in LDL-C = 55–69 mg/dL were 0.97 (95% CI: 0.85–1.11) and 0.96 (95% CI: 0.79–2.23), respectively. The optimal range with the lowest HR for heart failure and all-cause mortality were LDL-C = 70–99 mg/dL and LDL-C = 55–69 mg/dL, respectively, in all age groups (HR: 0.99, 95% CI: 0.91–1.08 and HR: 0.91, 95% CI: 0.81–1.01).

Conclusion

LDL-C level below 55 mg/dL appears to be optimal in T2DM patients with established cardiovascular disease aged < 65 years, while an LDL-C level of 55–69 mg/dL may be optimal for preventing recurrent PCI and stroke in patients over 65 years old.

Open access
Svjatoslavs Kistkins Pauls Stradiņš Clinical University Hospital, Riga, Latvia

Search for other papers by Svjatoslavs Kistkins in
Google Scholar
PubMed
Close
,
Othmar Moser Division of Exercise Physiology and Metabolism, Institute of Sport Science, University of Bayreuth, Bayreuth, Germany

Search for other papers by Othmar Moser in
Google Scholar
PubMed
Close
,
Vitālijs Ankudovičs Pauls Stradiņš Clinical University Hospital, Riga, Latvia

Search for other papers by Vitālijs Ankudovičs in
Google Scholar
PubMed
Close
,
Dmitrijs Blizņuks Institute of Smart Computing Technologies, Riga Technical University, Riga, Latvia

Search for other papers by Dmitrijs Blizņuks in
Google Scholar
PubMed
Close
,
Timurs Mihailovs Institute of Smart Computing Technologies, Riga Technical University, Riga, Latvia

Search for other papers by Timurs Mihailovs in
Google Scholar
PubMed
Close
,
Sergejs Lobanovs Pauls Stradiņš Clinical University Hospital, Riga, Latvia

Search for other papers by Sergejs Lobanovs in
Google Scholar
PubMed
Close
,
Harald Sourij Trials Unit for Interdisciplinary Metabolic Medicine, Division of Endocrinology and Diabetolgoy, Medical University of Graz, Graz, Austria

Search for other papers by Harald Sourij in
Google Scholar
PubMed
Close
,
Andreas F H Pfeiffer Department of Endocrinology and Metabolic Medicine, Campus Benjamin Franklin, Charité University Medicine, Hindenburgdamm, Berlin, Germany

Search for other papers by Andreas F H Pfeiffer in
Google Scholar
PubMed
Close
, and
Valdis Pīrāgs Pauls Stradiņš Clinical University Hospital, Riga, Latvia
Faculty of Medicine, University of Latvia, Riga, Latvia

Search for other papers by Valdis Pīrāgs in
Google Scholar
PubMed
Close

The increasing prevalence of ‘diabesity’, a combination of type 2 diabetes and obesity, poses a significant global health challenge. Unhealthy lifestyle factors, including poor diet, sedentary behaviour, and high stress levels, combined with genetic and epigenetic factors, contribute to the diabesity epidemic. Diabesity leads to various significant complications such as cardiovascular diseases, stroke, and certain cancers. Incretin-based therapies, such as GLP-1 receptor agonists and dual hormone therapies, have shown promising results in improving glycaemic control and inducing weight loss. However, these therapies also come with certain disadvantages, including potential withdrawal effects. This review aims to provide insights into the cross-interactions of insulin, glucagon, and GLP-1, revealing the complex hormonal dynamics during fasting and postprandial states, impacting glucose homeostasis, energy expenditure, and other metabolic functions. Understanding these hormonal interactions may offer novel hypotheses in the development of ‘anti-diabesity’ treatment strategies. The article also explores the question of the antagonism of insulin and glucagon, providing insights into the potential synergy and hormonal overlaps between these hormones.

Open access
Cheryl M Isherwood Section of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom

Search for other papers by Cheryl M Isherwood in
Google Scholar
PubMed
Close
,
M Denise Robertson Section of Metabolic Medicine, Food and Macronutrients, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom

Search for other papers by M Denise Robertson in
Google Scholar
PubMed
Close
,
Debra J Skene Section of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom

Search for other papers by Debra J Skene in
Google Scholar
PubMed
Close
, and
Jonathan D Johnston Section of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom

Search for other papers by Jonathan D Johnston in
Google Scholar
PubMed
Close

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.

Open access
Benjamin D Maylor Institute for Sport and Physical Activity Research, School of Sport Science and Physical Activity, University of Bedfordshire, Bedford, UK
Leicester Diabetes Centre, University of Leicester, Leicester General Hospital, Leicester, UK

Search for other papers by Benjamin D Maylor in
Google Scholar
PubMed
Close
,
Julia K Zakrzewski-Fruer Institute for Sport and Physical Activity Research, School of Sport Science and Physical Activity, University of Bedfordshire, Bedford, UK

Search for other papers by Julia K Zakrzewski-Fruer in
Google Scholar
PubMed
Close
,
Charlie J Orton Institute for Sport and Physical Activity Research, School of Sport Science and Physical Activity, University of Bedfordshire, Bedford, UK

Search for other papers by Charlie J Orton in
Google Scholar
PubMed
Close
, and
Daniel P Bailey Institute for Sport and Physical Activity Research, School of Sport Science and Physical Activity, University of Bedfordshire, Bedford, UK
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
Close

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.

Open access
Ann-Cathrin Koschker Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany
Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany

Search for other papers by Ann-Cathrin Koschker in
Google Scholar
PubMed
Close
,
Bodo Warrings Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany
Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Bodo Warrings in
Google Scholar
PubMed
Close
,
Caroline Morbach Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany
Division of Cardiology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Caroline Morbach in
Google Scholar
PubMed
Close
,
Florian Seyfried Department of General, Visceral, Transplant, Vascular, and Pediatric Surgery, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Florian Seyfried in
Google Scholar
PubMed
Close
,
Nicole Rickert Department of Radiology, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Nicole Rickert in
Google Scholar
PubMed
Close
,
Pius Jung Division of Pneumology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Pius Jung in
Google Scholar
PubMed
Close
,
Andreas Geier Division of Hepatology, Department of Internal Medicine II, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Andreas Geier in
Google Scholar
PubMed
Close
,
Ulrich Dischinger Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Ulrich Dischinger in
Google Scholar
PubMed
Close
,
Maike Krauthausen Department of General Practice, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Maike Krauthausen in
Google Scholar
PubMed
Close
,
Martin J Herrmann Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Martin J Herrmann in
Google Scholar
PubMed
Close
,
Christine Stier Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany
Department of General, Visceral, Transplant, Vascular, and Pediatric Surgery, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Christine Stier in
Google Scholar
PubMed
Close
,
Stefan Frantz Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany
Division of Cardiology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Stefan Frantz in
Google Scholar
PubMed
Close
,
Uwe Malzahn Center for Clinical Trials, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Uwe Malzahn in
Google Scholar
PubMed
Close
,
Stefan Störk Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany
Division of Cardiology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany

Search for other papers by Stefan Störk in
Google Scholar
PubMed
Close
,
Martin Fassnacht Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany
Comprehensive Heart Failure Center, University & University Hospital Würzburg, Würzburg, Germany

Search for other papers by Martin Fassnacht in
Google Scholar
PubMed
Close
, and
the WAS Study Group
Search for other papers by the WAS Study Group in
Google Scholar
PubMed
Close
the WAS Study Group

Obesity is a rapidly emerging health problem and an established risk factor for cardiovascular diseases. Bariatric surgery profoundly reduces body weight and mitigates sequelae of obesity. The open, randomized controlled Würzburg Adipositas Studie (WAS) trial compares the effects of Roux-en-Y gastric bypass (RYGB) vs psychotherapy-supported lifestyle modification in morbidly obese patients. The co-primary endpoint addresses 1-year changes in cardiovascular function (peak VO2 during cardiopulmonary exercise testing) and the quality of life (QoL) (Short-Form-36 physical functioning scale). Prior to randomization, all included patients underwent a multimodal anti-obesity treatment for 6–12 months. Thereafter, the patients were randomized and followed through month 12 to collect the primary endpoints. Afterwards, patients in the lifestyle group could opt for surgery, and final visit was scheduled for all patients 24 months after randomization. Sample size calculation suggested to enroll 90 patients in order to arrive at minimally 22 patients per group evaluable for the primary endpoint. Secondary objectives were to quantify changes in body weight, left ventricular hypertrophy, systolic and diastolic function (by echocardiography and cardiac MRI), functional brain MRI, psychometric scales, and endothelial and metabolic function. WAS enrolled 93 patients (72 women, median age 38 years, BMI 47.5 kg/m2) exhibiting a relevantly compromised exercise capacity (median peakVO2 18.3 mL/min/kg) and the QoL (median physical functioning scale 50). WAS is the first randomized controlled trial focusing on the effects of RYGB on cardiovascular function beyond hypertension. In addition, it will provide a wealth of high-quality data on the cerebral, psychiatric, hepatic, and metabolic function in obese patients after RYGB.

Open access
Merlin C Thomas Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia

Search for other papers by Merlin C Thomas in
Google Scholar
PubMed
Close
,
Brendon L Neuen The George Institute for Global Health, Sydney, NSW, Australia

Search for other papers by Brendon L Neuen in
Google Scholar
PubMed
Close
,
Stephen M Twigg The University of Sydney School of Medicine, Sydney, NSW, Australia
Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, NSW, Australia

Search for other papers by Stephen M Twigg in
Google Scholar
PubMed
Close
,
Mark E Cooper Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia

Search for other papers by Mark E Cooper in
Google Scholar
PubMed
Close
, and
Sunil V Badve The George Institute for Global Health, Sydney, NSW, Australia
Department of Renal Medicine, St George Hospital, Sydney, NSW, Australia
Faculty of Medicine and Health, University of New South Wales, Sydney, NSW, Australia

Search for other papers by Sunil V Badve in
Google Scholar
PubMed
Close

Sodium‐glucose co-transporter 2 (SGLT2) inhibitors have recently emerged as an effective means to protect kidney function in people with type 2 diabetes and chronic kidney disease (CKD). In this review, we explore the role of SGLT2 inhibition in these individuals. SGLT2 inhibitors specifically act to inhibit sodium and glucose reabsorption in the early proximal tubule of the renal nephron. Although originally developed as glucose-lowering agents through their ability to induce glycosuria, it became apparent in cardiovascular outcome trials that the trajectory of kidney function decline was significantly slowed and the incidence of serious falls in kidney function was reduced in participants receiving an SGLT2 inhibitor. These observations have recently led to specific outcome trials in participants with CKD, including DAPA-CKD, CREDENCE and EMPA-KIDNEY, and real-world studies, like CVD-REAL-3, that have confirmed the observation of kidney benefits in this setting. In response, recent KDIGO Guidelines have recommended the use of SGLT2 inhibitors as first-line therapy in patients with CKD, alongside statins, renin–angiotensin–aldosterone system inhibitors and multifactorial risk factor management as indicated. However, SGLT2 inhibitors remain significantly underutilized in the setting of CKD. Indeed, an inertia paradox exists, with patients with more severe disease less likely to receive an SGLT2 inhibitor. Concerns regarding safety appear unfounded, as acute kidney injury, hyperkalaemia, major acute cardiovascular events and cardiac death in patients with CKD appear to be lower following SGLT2 inhibition. The first-in-class indication of dapagliflozin for CKD may begin a new approach to managing kidney disease in type 2 diabetes.

Open access
Wang-shu Liu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Wang-shu Liu in
Google Scholar
PubMed
Close
,
Ling-yan Hua Department of Ophthalmology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Ling-yan Hua in
Google Scholar
PubMed
Close
,
Su-xiang Zhu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Su-xiang Zhu in
Google Scholar
PubMed
Close
,
Feng Xu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Feng Xu in
Google Scholar
PubMed
Close
,
Xue-qin Wang Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Xue-qin Wang in
Google Scholar
PubMed
Close
,
Chun-feng Lu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Chun-feng Lu in
Google Scholar
PubMed
Close
,
Jian-bin Su Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Jian-bin Su in
Google Scholar
PubMed
Close
, and
Feng Qi Emergency Intensive Care Unit, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

Search for other papers by Feng Qi in
Google Scholar
PubMed
Close

Background

The aim of the study was to explore whether plasma stromal cell-derived factor 1 (SDF-1) levels are associated with the EZSCAN score and its derived indicators in patients with type 2 diabetes (T2D).

Methods

From July 2020 to December 2020, a total of 253 patients with T2D were consecutively recruited. Serum SDF-1 levels were measured by sandwich ELISA. EZSCAN test was applied to evaluate the sudomotor function of each patient, and based on the results, EZSCAN score, cardiac autonomic neuropathy risk score (CANRS) and cardiovascular risk score (CVDRS) were calculated by particular algorithms. In addition, other relevant clinical data were also collected.

Results

With increasing tertiles of serum SDF-1 levels, the CANRS and CVDRS significantly increased (both Pfor trend <0.001), while the EZSCAN score significantly decreased (Pfor trend <0.001). Moreover, serum SDF-1 levels were significantly and positively correlated with the CANRS and CVDRS (r = 0.496 and 0.510, respectively, both P  < 0.001), and negatively correlated with the EZSCAN score (r = −0.391, P  < 0.001). Furthermore, multivariate linear regression analyses were constructed, and after adjusting for other clinical covariates, serum SDF-1 levels were independently responsible for EZSCAN score (β = −0.273, t = −3.679, P  < 0.001), CANRS (β = 0.334, t = 5.110, P  < 0.001) and CVDRS (β = 0.191, t = 4.983, P  = 0.003).

Conclusions

SDF-1 levels in serum were independently associated with the EZSCAN score and its derived indicators, such as CANRS and CVDRS in patients with T2D.

Open access
Yueyuan Yang Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Yueyuan Yang in
Google Scholar
PubMed
Close
,
Tingting Yu Department of Radiology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Tingting Yu in
Google Scholar
PubMed
Close
,
Zhili Niu Department of Clinical Laboratory, Institute of translational medicine, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Zhili Niu in
Google Scholar
PubMed
Close
, and
Ling Gao Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Ling Gao in
Google Scholar
PubMed
Close

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.

Open access
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

Search for other papers by Yee-Ming M Cheung in
Google Scholar
PubMed
Close
,
Rudolf Hoermann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

Search for other papers by Rudolf Hoermann in
Google Scholar
PubMed
Close
,
Karen Van Department of Endocrinology, Austin Health, Melbourne, Australia

Search for other papers by Karen Van in
Google Scholar
PubMed
Close
,
Damian Wu Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

Search for other papers by Damian Wu in
Google Scholar
PubMed
Close
,
Jenny Healy Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

Search for other papers by Jenny Healy in
Google Scholar
PubMed
Close
,
Bella Halim Department of Endocrinology, Austin Health, Melbourne, Australia

Search for other papers by Bella Halim in
Google Scholar
PubMed
Close
,
Manjri Raval Department of Endocrinology, Austin Health, Melbourne, Australia

Search for other papers by Manjri Raval in
Google Scholar
PubMed
Close
,
Maria McGill Department of Radiology, Austin Health, Melbourne, Australia

Search for other papers by Maria McGill in
Google Scholar
PubMed
Close
,
Ali Al-Fiadh Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Cardiology, Austin Health, Melbourne Australia

Search for other papers by Ali Al-Fiadh in
Google Scholar
PubMed
Close
,
Michael Chao Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

Search for other papers by Michael Chao in
Google Scholar
PubMed
Close
,
Shane White Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

Search for other papers by Shane White in
Google Scholar
PubMed
Close
,
Belinda Yeo Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia
Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Australia

Search for other papers by Belinda Yeo in
Google Scholar
PubMed
Close
,
Jeffrey D Zajac Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Close
, and
Mathis Grossmann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

Search for other papers by Mathis Grossmann in
Google Scholar
PubMed
Close

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