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  • Östgren, Carl Johan, et al. (författare)
  • Atrial fibrillation and its association with type 2 diabetes and hypertension in a Swedish community.
  • 2004
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 6:5, s. 367-374
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To explore the prevalence of atrial fibrillation in patients with hypertension and type 2 diabetes and to identify possible mechanisms for the development of atrial fibrillation. Methods: A community-based, cross-sectional observational study was conducted in the primary health care in Skara, Sweden, and 1739 subjects (798 men, 941 women) were surveyed. Patients were categorized as those with hypertension only (n = 597); those with both hypertension and type 2 diabetes (n = 171), and those with type 2 diabetes only (n = 147). In the reference population, 824 normotensive subjects without diabetes were identified and used as controls. Participants were examined for cardiovascular risk factors including fasting blood glucose, serum insulin, blood pressure, lipids and anthropometric measures. Resting electrocardiogram (ECG) was recorded and Minnesota-coded. Insulin resistance was measured by the homeostasis model assessment (HOMA). Results: Age-adjusted prevalence of atrial fibrillation was 2% in patients with hypertension only, 6% in patients with both hypertension and type 2 diabetes, 4% in patients with type 2 diabetes only and 2% in controls, respectively. Age and sex adjusted odds ratios (OR) (95% CI) were; hypertension 0.7 (0.30-1.5), combined hypertension and type 2 diabetes 3.3 (1.6-6.7), and type 2 diabetes 2.0 (0.9-4.7). The association with combined hypertension and type 2 diabetes remained significant when adjusted for cardiovascular disease (CVD) risk factors and body mass index (BMI), was attenuated with adjustment for ischemic ECG; 2.4 (1.1-5.0) and lost significance with adjustment for insulin resistance; 1.3 (0.5-3.1). Conclusions: Atrial fibrillation is associated with the combined occurrence of type 2 diabetes and hypertension. Insulin resistance may be a common underlying mechanism.
  • Accili, D., et al. (författare)
  • What ails the beta-cell?
  • 2010
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 12, s. 1-3
  • Tidskriftsartikel (övrigt vetenskapligt)
  • Adiels, Martin, 1976, et al. (författare)
  • Role of apolipoprotein C-III overproduction in diabetic dyslipidaemia
  • 2019
  • Ingår i: Diabetes, obesity and metabolism. - 1462-8902. ; 21:8, s. 1861-1870
  • Tidskriftsartikel (refereegranskat)abstract
    • - Aims: To investigate how apolipoprotein C-III (apoC-III) metabolism is altered in subjects with type 2 diabetes, whether the perturbed plasma triglyceride concentrations in this condition are determined primarily by the secretion rate or the removal rate of apoC-III, and whether improvement of glycaemic control using the glucagon-like peptide-1 analogue liraglutide for 16 weeks modifies apoC-III dynamics. Materials and Methods: Postprandial apoC-III kinetics were assessed after a bolus injection of [5,5,5- 2 H 3 ]leucine using ultrasensitive mass spectrometry techniques. We compared apoC-III kinetics in two situations: in subjects with type 2 diabetes before and after liraglutide therapy, and in type 2 diabetic subjects with matched body mass index (BMI) non-diabetic subjects. Liver fat content, subcutaneous abdominal and intra-abdominal fat were determined using proton magnetic resonance spectroscopy. Results: Improved glycaemic control by liraglutide therapy for 16 weeks significantly reduced apoC-III secretion rate (561 ± 198 vs. 652 ± 196 mg/d, P = 0.03) and apoC-III levels (10.0 ± 3.8 vs. 11.7 ± 4.3 mg/dL, P = 0.035) in subjects with type 2 diabetes. Change in apoC-III secretion rate was significantly associated with the improvement in indices of glucose control (r = 0.67; P = 0.009) and change in triglyceride area under the curve (r = 0.59; P = 0.025). In line with this, the apoC-III secretion rate was higher in subjects with type 2 diabetes compared with BMI-matched non-diabetic subjects (676 ± 208 vs. 505 ± 174 mg/d, P = 0.042). Conclusions: The results reveal that the secretion rate of apoC-III is associated with elevation of triglyceride-rich lipoproteins in subjects with type 2 diabetes, potentially through the influence of glucose homeostasis on the production of apoC-III. © 2019 John Wiley & Sons Ltd
  • Ahrén, Bo, et al. (författare)
  • Clinical evidence and mechanistic basis for vildagliptin's action when added to metformin.
  • 2011
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 13:3, s. 193-203
  • Tidskriftsartikel (refereegranskat)abstract
    • Several new oral antidiabetic agents, known as 'gliptins' or 'enzyme dipeptidyl peptidase-IV (DPP-4) inhibitors', have been developed for the treatment of type 2 diabetes and a key clinical use of the gliptins is in combination with metformin. There are important differences in the kinetics of the interaction of different gliptins with the catalytic site of DPP-4, which may lead to varying pharmacokinetics, pharmacodynamics and dosing regimens. Therefore, individual gliptins need to be characterized and here we discuss the extensively studied DPP-4 inhibitor vildagliptin, which has binding characteristics that ensure inhibition of the enzyme beyond the presence of detectable drug levels in plasma. As vildagliptin has been used most often at doses of 50 mg once or twice daily, in combination with metformin, this review focuses on these dose regimens. All clinical trials employing vildagliptin (50 mg once or twice daily) as an add-on therapy to metformin (identified by MEDLINE search using keywords vildagliptin and metformin or known by authors to be in press) are reviewed, as is current knowledge of the mechanism of action of vildagliptin. Vildagliptin added to a stable dose of metformin elicits a dose-related decrease in both HbA1c and fasting plasma glucose. The additional efficacy seen with 50 mg twice daily [ΔHbA1c ∼- 1.1% (-12.1 mmol/mol)] relative to 50 mg once daily [ΔHbA1c ∼- 0.7% (-7.7 mmol/mol)] is attributable to an overnight effect of the evening dose of vildagliptin, with prolonged DPP-4 inhibition and elevated fasting levels of the intact and insulinotropic form of glucagon-like peptide-1 (GLP-1). Vildagliptin's therapeutic actions are primarily mediated by GLP-1 and metformin enhances vildagliptin's effect to raise plasma levels of intact GLP-1. Vildagliptin is weight-neutral and has a very low hypoglycaemic potential, explained by its remarkable ability to enhance both α-cell and β-cell sensitivity to glucose. Therefore, vildagliptin offers a clinically important outcome when added to metformin with a twice daily dose regimen, taking advantage of its tight binding and slow dissociation characteristics that lead to a sustained overnight effect.
  • Ahrén, Bo, et al. (författare)
  • Mechanisms of Action of the DPP-4 Inhibitor Vildagliptin in Man.
  • 2011
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 13:9, s. 775-783
  • Forskningsöversikt (refereegranskat)abstract
    • Inhibition of dipeptidyl peptidase-4 (DPP-4) by vildagliptin prevents degradation of glucagon-like peptide-1 (GLP-1) and reduces glycemia in type 2 diabetes, with low risk for hypoglycemia and no weight gain. Vildagliptin binds covalently to the catalytic site of DPP-4, eliciting prolonged enzyme inhibition. This raises intact GLP-1 levels, both after meal ingestion and in the fasting state. Vildagliptin has been shown to stimulate insulin secretion and to inhibit glucagon secretion in a glucose-dependent manner. At hypoglycemic levels, the counterregulatory glucagon response is enhanced relative to baseline by vildagliptin. Vildagliptin also inhibits hepatic glucose production, mainly through changes in islet hormone secretion, and improves insulin sensitivity, as determined with a variety of methods. These effects underlie the improved glycemia with low risk for hypoglycemia. Vildagliptin also suppresses postprandial triglyceride-rich lipoprotein levels after ingestion of a fat-rich meal and reduces fasting lipolysis, suggesting inhibition of fat absorption and reduced triglyceride stores in non-fat tissues. The large body of knowledge on vildagliptin regarding enzyme binding, incretin and islet hormone secretion and glucose and lipid metabolism is summarized, with discussion of the integrated mechanisms and comparison with other DPP-4 inhibitors and GLP-1 receptor activators, where appropriate.
  • Ahrén, Bo, et al. (författare)
  • Pronounced Reduction Of Postprandial Glucagon By Lixisenatide: A Meta-Analysis Of Randomized Clinical Trials.
  • 2014
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 16:9, s. 861-868
  • Tidskriftsartikel (refereegranskat)abstract
    • Glucagon-like peptide-1 (GLP-1) receptor agonists improve islet function and delay gastric emptying in patients with type 2 diabetes mellitus (T2DM). This meta-analysis aimed to investigate the effects of the once-daily prandial GLP-1 receptor agonist lixisenatide on postprandial plasma glucose (PPG), glucagon and insulin levels.
  • Ahrén, Bo, et al. (författare)
  • Semaglutide induces weight loss in subjects with type 2 diabetes regardless of baseline BMI or gastrointestinal adverse events in the SUSTAIN 1 to 5 trials
  • 2018
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 20:9, s. 2210-2219
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: To assess the effect of baseline body mass index (BMI) and the occurrence of nausea and/or vomiting on weight loss induced by semalgutide, a once-weekly glucagon-like peptide 1 analogue for the treatment of type 2 diabetes. Semaglutide demonstrated superior reductions in HbA1c and superior weight loss (by 2.3-6.3 kg) versus different comparators across the SUSTAIN 1 to 5 trials; the contributing factors to weight loss are not established. Materials and Methods: Subjects with inadequately controlled type 2 diabetes (drug-naïve or on background treatment) were randomized to subcutaneous semaglutide 0.5 mg (excluding SUSTAIN 3), 1.0 mg (all trials), or comparator (placebo, sitagliptin, exenatide extended release or insulin glargine). Subjects were subdivided by baseline BMI and reporting (yes/no) of any nausea and/or vomiting. Change from baseline in body weight was assessed within each trial and subgroup. A mediation analysis separated weight loss into direct or indirect (mediated by nausea or vomiting) effects. Results: Clinically relevant weight-loss differences were observed across all BMI subgroups, with a trend towards higher absolute weight loss with higher baseline BMI. Overall, 15.2% to 24.0% and 21.5% to 27.2% of subjects experienced nausea or vomiting with semaglutide 0.5 and 1.0 mg, respectively, versus 6.0% to 14.1% with comparators. Only 0.07 to 0.5 kg of the treatment difference between semaglutide and comparators was mediated by nausea or vomiting (indirect effects). Conclusions: In SUSTAIN 1 to 5, semaglutide-induced weight loss was consistently greater versus comparators, regardless of baseline BMI. The contribution of nausea or vomiting to this weight loss was minor.
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