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Journal Cover Diabetes & Metabolism
  [SJR: 1.252]   [H-I: 70]   [65 followers]  Follow
    
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   ISSN (Print) 1262-3636
   Published by Elsevier Homepage  [3043 journals]
  • Dipeptidyl peptidase-4 inhibitors and risk of arthralgia: A systematic
           review and meta-analysis
    • Abstract: Publication date: Available online 1 August 2017
      Source:Diabetes & Metabolism
      Author(s): P. Men, N. He, C. Song, S. Zhai
      Background The US Food and Drug Administration has warned that treatment with dipeptidyl peptidase (DPP)-4 inhibitors may promote serious arthralgia. However, the clinical evidence for this is relatively lacking. Objective For this reason, a systematic review and meta-analysis of randomized controlled trials (RCTs) were carried out to determine the relationship between DPP-4 inhibitors and risk of arthralgia, and also to investigate any potential risk factors. Methods An extensive electronic search for RCTs comparing DPP-4 inhibitors with any comparators was performed up to July 2016. Outcomes of interest were overall and serious arthralgia. Summary risk ratios (RRs) with 95% confidence intervals (CIs) were calculated. Results A total of 67 RCTs (involving 79,110 patients) was ultimately included. Pooled results showed that DPP-4 inhibitors were associated with a slightly but significantly increased risk of overall arthralgia (RR: 1.13, 95% CI: 1.04–1.22; P =0.003) and a non-significant increased risk of serious arthralgia (RR: 1.44, 95% CI: 0.83–2.51; P =0.20). Also, subgroup analyses showed that add-on/combination therapy and longer diabetes duration (>5years) were possible factors associated with the increased risk of overall arthralgia. Conclusion These findings suggest that DPP-4 inhibitors can increase the risk of arthralgia. Thus, the benefits of glycaemic control must be weighed against the risk of arthralgia when prescribing DPP-4 inhibitors. Further studies are now needed to identify and confirm these risk factors.

      PubDate: 2017-08-14T11:40:48Z
       
  • Exercise and ectopic fat in type 2 diabetes: A systematic review and
           meta-analysis
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): A. Sabag, K.L. Way, S.E. Keating, R.N. Sultana, H.T. O’Connor, M.K. Baker, V.H. Chuter, J. George, N.A. Johnson
      Ectopic adipose tissue surrounding the intra-abdominal organs (visceral fat) and located in the liver, heart, pancreas and muscle, is linked to cardio-metabolic complications commonly experienced in type 2 diabetes. A systematic review and meta-analysis was performed to determine the effect of exercise on ectopic fat in adults with type 2 diabetes. Relevant databases were searched to February 2016. Included were randomised controlled studies, which implemented≥4 weeks of aerobic and/or resistance exercise and quantified ectopic fat via magnetic resonance imaging, computed tomography, proton magnetic resonance spectroscopy or muscle biopsy before and after intervention. Risk of bias and study quality was assessed using Egger's funnel plot test and modified Downs and Black checklist, respectively. Of the 10,750 studies retrieved, 24 were included involving 1383 participants. No studies were found assessing the interaction between exercise and cardiac or pancreas fat. One study assessed the effect of exercise on intramyocellular triglyceride concentration. There was a significant pooled effect size for the meta-analysis comparing exercise vs. control on visceral adiposity (ES=−0.21, 95% CI: −0.37 to −0.05; P =0.010) and a near-significant pooled effect size for liver steatosis reduction with exercise (ES=−0.28, 95% CI: −0.57 to 0.01; P =0.054). Aerobic exercise (ES=−0.23, 95% CI: −0.44 to −0.03; P =0.025) but not resistance training exercise (ES=−0.13, 95% CI: −0.37 to 0.12; P =0.307) was effective for reducing visceral fat in overweight/obese adults with type 2 diabetes. These data suggest that exercise effectively reduces visceral and perhaps liver adipose tissue and that aerobic exercise should be a key feature of exercise programs aimed at reducing visceral fat in obesity-related type 2 diabetes. Further studies are required to assess the relative efficacy of exercise modality on liver fat reduction and the effect of exercise on pancreas, heart, and intramyocellular fat in type 2 diabetes and to clarify the effect of exercise on ectopic fat independent of weight loss.

      PubDate: 2017-08-14T11:40:48Z
       
  • All-cause mortality in patients with diabetes under glucagon-like
           peptide-1 agonists: A population-based, open cohort study
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): K.A. Toulis, W. Hanif, P. Saravanan, B.H. Willis, T. Marshall, B. Kumarendran, K. Gokhale, S. Ghosh, K.K. Cheng, P. Narendran, G.N. Thomas, K. Nirantharakumar
      Aim The glucagon-like peptide-1 receptor agonist (GLP1a) liraglutide has been described to benefit patients with type 2 diabetes mellitus (T2DM) at high cardiovascular risk. However, there are still uncertainties relating to these cardiovascular benefits: whether they also apply to an unselected diabetic population that includes low-risk patients, represent a class-effect, and could be observed in a real-world setting. Methods We conducted a population-based, retrospective open cohort study using data derived from The Health Improvement Network database between Jan 2008 to Sept 2015. Patients with T2DM exposed to GLP1a (n =8345) were compared to age, gender, body mass index, duration of T2DM and smoking status-matched patients with T2DM unexposed to GLP1a (n =16,541). Results Patients with diabetes receiving GLP1a were significantly less likely to die from any cause compared to matched control patients with diabetes (adjusted incidence rate ratio [aIRR]: 0.64, 95% CI: 0.56–0.74, P-value<0.0001). Similar findings were observed in low-risk patients (aIRR: 0.64, 95% CI: 0.53–0.76, P -value=0.0001). No significant difference in the risk of incident CVD was detected in the low-risk patients (aIRR: 0.93, 95% CI: 0.83–1.12). Subgroup analyses suggested that effect is persistent in the elderly or across glycated haemoglobin categories. Conclusions GLP1a treatment in a real-world setting may confer additional mortality benefit in patients with T2DM irrespective of their baseline CVD risk, age or baseline glycated haemoglobin and was sustained over the observation period.

      PubDate: 2017-08-14T11:40:48Z
       
  • Management of diabetes patients during the year prior to initiation of
           dialysis in France
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): P. Tuppin, A. Cuerq, S. Torre, C. Couchoud, A. Fagot-Campagna
      Aim This study looked at the management of diabetes patients during the year prior to the initiation of dialysis. Methods For this observational study, data were extracted from the National Health Insurance database for general-scheme beneficiaries (77% of the French population). Diabetes patients were identified by at least three reimbursements for antidiabetic drugs in 2012, while the initiation of dialysis was identified by specific refunds in 2013. Results Of the 6412 patients initiating dialysis, 37% (n =2378) had diabetes (men: 61%, median age: 71 years, haemodialysis: 92%). Six months prior to dialysis, 68% had filled at least one prescription for insulin, 38% for other antidiabetics (25% glinides, 8% sulphonylureas, 8% metformin, 6% DPP-4 inhibitors), 69% for three or more classes of antihypertensive drugs and 55% for erythropoiesis-stimulating agents. Within 12 months to 1 month of dialysis, 81% were hospitalized, 28% with a main diagnosis of kidney disease. No nephrologist referral or hospitalization was identified at 6–0 months before dialysis in 6% of patients or in 24% at 12–7 months. One in five patients with diabetes consulted a private endocrinologist within 6 months of dialysis. An arteriovenous fistula was created 1 month before haemodialysis in 43% of patients. Conclusion The quality of preparation for dialysis was variable despite frequent hospitalizations. These data illustrate the need to mobilize patients with diabetes, and for healthcare professionals to more effectively anticipate and coordinate dialysis.

      PubDate: 2017-08-14T11:40:48Z
       
  • Comparison of hepatocellular carcinoma risk between patients treated with
           glimepiride and gliclazide
    • Abstract: Publication date: Available online 1 August 2017
      Source:Diabetes & Metabolism
      Author(s): J.-Y. Lee, G. Kim, Y.-H. Lee, B.-W. Lee, B.-S. Cha, C.M. Nam, E.S. Kang


      PubDate: 2017-08-04T10:40:43Z
       
  • Serum soluble TREM2 is a potential novel biomarker of cognitive impairment
           in Japanese non-obese patients with diabetes
    • Abstract: Publication date: Available online 31 July 2017
      Source:Diabetes & Metabolism
      Author(s): M. Tanaka, H. Yamakage, S. Masuda, T. Inoue, R. Ohue-Kitano, R. Araki, Y. Matoba, M. Saito, T. Nagaoka, K. Yonezawa, T. Tanaka, M. Suzuki, M. Sawamura, M. Nishimura, S. Odori, H. Wada, K. Kotani, T. Kusakabe, A. Shimatsu, K. Hasegawa, N. Satoh-Asahara


      PubDate: 2017-08-04T10:40:43Z
       
  • Heart rate variability in fetuses of type 1 diabetes pregnancies
    • Abstract: Publication date: Available online 31 July 2017
      Source:Diabetes & Metabolism
      Author(s): Y. Hamoud, J. de Jonckheere, A. Vambergue, V. Houfflin-Debarge, L. Storme, M. Flocteil, P. Deruelle, C. Garabedian


      PubDate: 2017-08-04T10:40:43Z
       
  • Clinical inertia and its impact on treatment intensification in people
           with type 2 diabetes mellitus
    • Abstract: Publication date: Available online 25 July 2017
      Source:Diabetes & Metabolism
      Author(s): G. Reach, V. Pechtner, R. Gentilella, A. Corcos, A. Ceriello
      Many people with type 2 diabetes mellitus (T2DM) fail to achieve glycaemic control promptly after diagnosis and do not receive timely treatment intensification. This may be in part due to ‘clinical inertia’, defined as the failure of healthcare providers to initiate or intensify therapy when indicated. Physician-, patient- and healthcare-system-related factors all contribute to clinical inertia. However, decisions that appear to be clinical inertia may, in fact, be only ‘apparent’ clinical inertia and may reflect good clinical practice on behalf of the physician for a specific patient. Delay in treatment intensification can happen at all stages of treatment for people with T2DM, including prescription of lifestyle changes after diagnosis, introduction of pharmacological therapy, use of combination therapy where needed and initiation of insulin. Clinical inertia may contribute to people with T2DM living with suboptimal glycaemic control for many years, with dramatic consequences for the patient in terms of quality of life, morbidity and mortality, and for public health because of the huge costs associated with uncontrolled T2DM. Because multiple factors can lead to clinical inertia, potential solutions most likely require a combination of approaches involving fundamental changes in medical care. These could include the adoption of a person-centred model of care to account for the complex considerations influencing treatment decisions by patients and physicians. Better patient education about the progressive nature of T2DM and the risks inherent in long-term poor glycaemic control may also reinforce the need for regular treatment reviews, with intensification when required.

      PubDate: 2017-07-26T10:20:49Z
       
  • Association of handgrip strength with B-type natriuretic peptide levels
           and cardiovascular events in patients with type 2 diabetes
    • Abstract: Publication date: Available online 24 July 2017
      Source:Diabetes & Metabolism
      Author(s): H. Hamasaki


      PubDate: 2017-07-26T10:20:49Z
       
  • Brain atrophy in ageing: Estimating effects of blood glucose levels vs.
           other type 2 diabetes effects
    • Abstract: Publication date: Available online 21 July 2017
      Source:Diabetes & Metabolism
      Author(s): E.I. Walsh, M. Shaw, P. Sachdev, K.J. Anstey, N. Cherbuin


      PubDate: 2017-07-26T10:20:49Z
       
  • Antenatal antipsychotic exposure induces multigenerational and
           gender-specific programming of adiposity and glucose tolerance in adult
           mouse offspring
    • Abstract: Publication date: Available online 17 July 2017
      Source:Diabetes & Metabolism
      Author(s): E. Courty, P. Gobalakichenane, M. Garcia, A. Muscat, C. Kazakian, T. Ledent, M. Moldes, B. Blondeau, D. Mitanchez, M. Buyse, B. Fève
      Second-generation antipsychotics (SGAs) are well known for their metabolic side effects in humans, including obesity and diabetes. These compounds are maintained during pregnancy to prevent the relapse of psychoses, but they readily diffuse across the placenta to the fetus, as documented with the widely-prescribed drug olanzapine (OLZ). However, observational studies have provided conflicting results on the potential impact of SGAs on fetal growth and body weight, and their effects on metabolic regulation in the offspring. For this reason, our study has tested whether antenatal exposure of CD1 mice to OLZ influenced metabolic outcomes in the offspring of the first (F1) and second (F2) generations. In F1 mice, OLZ antenatal treatment caused a decrease in neonatal body weight in both genders, an effect that persisted throughout life only in male animals. Interestingly, F1 female mice also displayed altered glucose homoeostasis. F2 mice, generated by mating normal males with F1 female mice exposed to OLZ during antenatal life, exhibited higher neonatal body weights which persisted only in F2 female animals. This was associated with expansion of fat mass and a concordant pattern of adipose tissue gene expression. Moreover, male and female F2 mice were glucose-intolerant. Thus, our study has demonstrated that antenatal OLZ exposure induces multigenerational and gender-specific programming of glucose tolerance in the offspring mice as adults, and points to the need for careful monitoring of children exposed to SGAs during pregnancy.

      PubDate: 2017-07-19T02:11:28Z
       
  • Severe hypoglycaemia is a major predictor of incident diabetic retinopathy
           in Japanese patients with type 2 diabetes
    • Abstract: Publication date: Available online 15 July 2017
      Source:Diabetes & Metabolism
      Author(s): S. Tanaka, R. Kawasaki, S. Tanaka-Mizuno, S. Iimuro, S. Matsunaga, T. Moriya, S. Ishibashi, S. Katayama, Y. Ohashi, Y. Akanuma, H. Sone, H. Yamashita
      Aim Hypoglycaemia is a common complication in diabetes patients. However, its relationship with retinopathy has not been well documented in patients with type 2 diabetes (T2D). This study aimed to investigate the associations between hypoglycaemia and the incidence and progression of diabetic retinopathy (DR). Methods In this longitudinal cohort study, which was part of the Japan Diabetes Complications Study (JDCS), adult patients with T2D were recruited at 59 diabetes clinics across Japan. Their history of hypoglycaemia was assessed by standardized self-reported questionnaires. Severe hypoglycaemia was defined as having at least one episode with coma requiring an outpatients visit or hospitalization. Adjusted hazard ratios (HRs) for incidence and progression of DR over 8 years of follow-up were determined. Results Of 1221 patients without DR, 127 (10.4%) had experienced non-severe hypoglycaemia within the previous year, whereas 10 (0.8%) reported severe hypoglycaemia episodes. During the 8-year follow-up involving 8492 person-years, 329 patients developed DR. In 410 patients with prevalent DR, the adjusted HRs for incident DR were 4.35 (95% CI: 1.98–9.56; P <0.01) and, for progression of DR, 2.29 (95% CI: 0.45–11.78; P =0.32) with severe hypoglycaemia. Conclusion Having a history of severe hypoglycaemia was one of the strongest predictors of incident DR in patients with T2D, with a fourfold increased risk. Identifying patients with greater risks of DR based on their history of hypoglycaemia may help to personalize risk evaluation in patients with diabetes.

      PubDate: 2017-07-19T02:11:28Z
       
  • The brown-fat-secreted adipokine neuregulin 4 is decreased in gestational
           diabetes mellitus
    • Abstract: Publication date: Available online 11 July 2017
      Source:Diabetes & Metabolism
      Author(s): S. Kralisch, A. Hoffmann, J. Kratzsch, M. Blüher, M. Stumvoll, M. Fasshauer, T. Ebert
      Aims Neuregulin 4 has recently been recognized as a novel adipokine secreted by brown adipose tissue (BAT), with beneficial effects on murine insulin resistance and hepatic steatosis. Yet, thus far, neither regulation of neuregulin 4 in gestational diabetes mellitus (GDM) nor its longitudinal changes in the peripartum period have been elucidated. Methods Circulating neuregulin 4 levels were measured by ELISA in 74 women with GDM and 74 healthy, gestational-age-matched controls. Also, neuregulin 4 was quantified during pregnancy and compared with postpartum levels in a follow-up study of 25 women with previous GDM and 25 healthy control women. Results Women with GDM had lower median serum levels of the novel BAT-secreted adipokine neuregulin 4 (3.0μg/L) compared with healthy (non-GDM) pregnant controls (3.5μg/L; P =0.020), and the area under the glucose curve (AUCGlucose) was an independent and negative predictor of circulating neuregulin 4 (P =0.033). Also, median postpartum serum concentrations of neuregulin 4 (3.2μg/L) were not significantly different from prepartum levels (2.8μg/L; P =0.328). In addition, neuregulin 4 was positively and independently associated with irisin (P =0.009), but not other BAT-secreted adipokines. Conclusion/interpretation Women with GDM have significantly lower circulating neuregulin 4 levels compared with healthy pregnant controls, and the AUCGlucose is negatively and independently associated with neuregulin 4 during pregnancy. Neuregulin 4 is positively correlated with irisin during pregnancy, as well as in a longitudinal fashion. Future studies are now needed to better elucidate the precise pathomechanisms of the regulation of BAT-secreted adipokines during pregnancy.

      PubDate: 2017-07-19T02:11:28Z
       
  • The impact of triglycerides on glucose tolerance: Lipotoxicity revisited
    • Abstract: Publication date: Available online 8 July 2017
      Source:Diabetes & Metabolism
      Author(s): M. Seghieri, D. Tricò, A. Natali
      Elevated plasma triglycerides (TGs) are early key features of conditions associated with a dysregulation in glucose metabolism and may predict the development of type 2 diabetes (T2D) over time. Although the acute ingestion of lipid, either mixed with or shortly before the meal, is neutral or slightly beneficial on glucose tolerance, a short-term increase in plasma TGs induced by either an i.v. lipid infusion or a high-fat diet produces a deterioration of glucose control. Accordingly, chronic lowering of plasma TGs by fibrates improves glucose homeostasis and may also prevent T2D. The chronic effects of the elevation of dietary lipid intake are less clear, particularly in humans, being the quality of fat probably more important than total fat intake. Although on the bases of the available experimental and clinical evidence it cannot be easily disentangled, with respect to elevated non-esterified fatty acids (NEFA) the relative contribution of elevated TGs to glucose homeostasis disregulation seems to be greater and also more plausible. In conclusion, although the association between elevated plasma TGs and impaired glucose tolerance is commonly considered not causative or merely a consequence of NEFA-mediated lipotoxicity, the available data suggest that TGs per se may directly contribute to disorders of glucose metabolism.

      PubDate: 2017-07-10T01:27:52Z
       
  • Carbamylation is a competitor of glycation for protein modification in
           vivo
    • Abstract: Publication date: Available online 8 July 2017
      Source:Diabetes & Metabolism
      Author(s): C. Nicolas, S. Jaisson, L. Gorisse, F.J. Tessier, C. Niquet-Léridon, P. Jacolot, C. Pietrement, P. Gillery
      Aim Chronic kidney disease (CKD) and diabetes mellitus are two diseases that accelerate protein molecular ageing through carbamylation and glycation reactions, characterized by the binding of urea-derived isocyanic acid and of sugars on proteins, respectively. These two reactions target the same protein amino groups and, thus, compete with each other. Such competition may arise especially in diabetic patients with nephropathy. This study aimed to evaluate their potential competitive effects in vitro and under conditions reproducing CKD and/or diabetes in vivo. Methods Albumin was incubated in vitro with glucose, urea or cyanate. Carbamylation in vivo was enhanced in normal and diabetic (db/db) mice by either subtotal nephrectomy or cyanate consumption. Homocitrulline, carbamylated haemoglobin and furosine were measured by LC–MS/MS, fructosamine by colorimetric assay and HbA1c by immunological assay. Results Reciprocal inhibition between carbamylation and glycation was observed during albumin incubations in vitro. Besides, 5 weeks after induction of CKD in vivo, plasma homocitrulline concentrations were similar in both diabetic and non-diabetic mice, whereas fructosamine and HbA1c were decreased (−23% and −42%, respectively) in diabetic mice with CKD compared with only diabetic ones. Fructosamine and HbA1c were also decreased in cyanate-spiked water-drinking mice compared with plain water-drinking diabetic mice. Conclusion Carbamylation competes with glycation in vivo, especially under conditions of high glycation. Thus, the classic markers of glycaemic control should be interpreted with caution in diabetic patients with CKD because of this competitive effect.

      PubDate: 2017-07-10T01:27:52Z
       
  • Low serum C-reactive protein levels predict 90-day mortality in
           hypoglycaemic patients
    • Abstract: Publication date: Available online 4 July 2017
      Source:Diabetes & Metabolism
      Author(s): A. Bonaventura, F. Gallo, F. Carbone, G. Sacchi, L. Liberale, F. Dallegri, D. Maggi, F. Montecucco, R. Cordera


      PubDate: 2017-07-10T01:27:52Z
       
  • Pioglitazone and lung cancer risk in Taiwanese patients with type 2
           diabetes
    • Abstract: Publication date: Available online 3 July 2017
      Source:Diabetes & Metabolism
      Author(s): C.-H. Tseng


      PubDate: 2017-07-10T01:27:52Z
       
  • Identification of urine metabolites associated with 5-year changes in
           biomarkers of glucose homoeostasis
    • Abstract: Publication date: Available online 29 June 2017
      Source:Diabetes & Metabolism
      Author(s): N. Friedrich, T. Skaaby, M. Pietzner, K. Budde, B.H. Thuesen, M. Nauck, A. Linneberg
      Aim Metabolomics provides information on pathogenetic mechanisms and targets for interventions, and may improve risk stratification. During the last decade, metabolomics studies were used to gain deeper insight into the pathogenesis of diabetes mellitus. However, longitudinal metabolomics studies of possible subclinical states of disturbed glucose metabolism are limited. Therefore, the aim of this study was to analyze the associations between baseline urinary metabolites and 5-year changes in continuous markers of glucose homoeostasis, including fasting glucose, HbA1c and homoeostasis model assessment of insulin resistance (HOMA-IR) index values. Methods Urine metabolites in 3986 participants at both baseline and 5-year follow-up of the population-based Inter99 study were analyzed by 1H-NMR spectroscopy. Linear regression and analyses of covariance models were used to detect associations between urine metabolites and 5-year changes in markers of glucose homoeostasis. Results Higher baseline levels of urinary alanine, betaine, N,N-dimethylglycine (DMG), creatinine and trimethylamine were associated with an increase in HbA1c from baseline to follow-up. In contrast, formic acid and trigonelline levels were associated with a decrease in HbA1c over time. Analyses of 5-year changes in fasting glucose and HOMA-IR index showed similar findings, with high baseline levels of lactic acid, beta-d-glucose, creatinine, alanine and 1-methylnicotinamide associated with increases in both parameters. Conclusion Several urine metabolites were found to be associated with detrimental longitudinal changes in biomarkers of glucose homoeostasis. The identified metabolites point to mechanisms involving betaine and coffee metabolism as well as the possible influence of the gut microbiome.

      PubDate: 2017-07-01T02:24:07Z
       
  • Family history of type 1 and type 2 diabetes and risk of latent autoimmune
           diabetes in adults (LADA)
    • Abstract: Publication date: Available online 29 June 2017
      Source:Diabetes & Metabolism
      Author(s): R. Hjort, L. Alfredsson, T. Andersson, P.-O. Carlsson, V. Grill, L. Groop, M. Martinell, B. Rasouli, P. Storm, T. Tuomi, S. Carlsson
      Background A family history of diabetes (FHD) is a strong predictor of diabetes risk, yet has rarely been investigated in latent autoimmune diabetes in adults (LADA). This study therefore investigated the risk of LADA and type 2 diabetes (T2D) in relation to FHD, taking into account the type of diabetes in relatives. Methods Data from a population-based study were used, including incident cases of LADA [glutamic acid decarboxylase antibody (GADA)-positive, n =378] and T2D (GADA-negative, n =1199), and their matched controls (n =1484). First-degree relatives with disease onset at age<40 years and taking insulin treatment were classified as type 1 diabetes (T1D) or, if otherwise, as T2D. Odds ratios (ORs) were adjusted for age, gender, BMI, education and smoking. Cases were genotyped for high- and low-risk HLA genotypes. Results Both FHD–T1D (OR: 5.8; 95% CI: 3.2–10.3) and FHD–T2D (OR: 1.9; 95% CI: 1.5–2.5) were associated with an increased risk of LADA, whereas the risk of T2D was associated with FHD–T2D (OR: 2.7; 95% CI: 2.2–3.3), but not FHD–T1D. In LADA patients, FHD–T1D vs FHD–T2D was associated with higher GADA but lower C-peptide levels, lower prevalence of low-risk HLA genotypes (5.0% vs 28.6%, respectively; P =0.038) and a tendency for higher prevalence of high-risk genotypes (90.0% vs 69.1%, respectively; P =0.0576). Conclusion The risk of LADA is substantially increased with FHD–T1D but also, albeit significantly less so, with FHD–T2D. This supports the idea of LADA as a mix of both T1D and T2D, but suggests that the genes related to T1D have greater impact. LADA patients with FHD–T1D had more T1D-like features, emphasizing the heterogeneity of LADA.

      PubDate: 2017-07-01T02:24:07Z
       
  • High efficacy of screening for diabetes and prediabetes in cardiac
           rehabilitation after an acute coronary syndrome (ACS). The REHABDIAB study
           
    • Abstract: Publication date: Available online 29 June 2017
      Source:Diabetes & Metabolism
      Author(s): B. Vergès, B. Patois-Vergès, K. Goueslard, J. Cottenet, A. Nguyen, S. Tatulashvili, M.-C. Blonde, C. Quantin


      PubDate: 2017-07-01T02:24:07Z
       
  • Effect of GLP-1 receptor agonist on gastrointestinal tract motility and
           residue rates as evaluated by capsule endoscopy
    • Abstract: Publication date: Available online 23 June 2017
      Source:Diabetes & Metabolism
      Author(s): Y. Nakatani, M. Maeda, M. Matsumura, R. Shimizu, N. Banba, Y. Aso, T. Yasu, H. Harasawa
      Aim This study evaluated the effects of a glucagon-like peptide-1 receptor agonist on gastrointestinal (GI) tract motility and residue rates by examining GI transit time and lumen using capsule endoscopy. Material and methods GI motility and lumen were assessed by capsule endoscopy before and after liraglutide administration in 14 patients with type 2 diabetes mellitus (T2DM). Results Gastric transit time in the group with diabetic neuropathy (DN) was 1:12:36±1:04:30h before liraglutide administration and 0:48:40±0:32:52h after administration (nonsignificant difference, P =0.19). Gastric transit time in the non-DN group was 1:01:30±0:52:59h before administration and 2:33:29±1:37:24h after administration (significant increase, P =0.03). Duodenal and small intestine transit time in the DN group was 4:10:34±0:25:54h before and 6:38:42±3:52:42h after administration (not significant, P =0.09) and, in the non-DN group, 3:51:03±0:53:47h before and 6:45:31±2:41:36h after administration (significant increase, P =0.03). The GI residue rate in the DN group was 32.1±24% before administration and 90.0±9.1% after administration (significant increase, P <0.001), and increased in all patients; in the non-DN group, it was 32.1±35.3% before and 78.3±23.9% after administration (significant increase, P <0.001), and also increased in all patients. Conclusion Liraglutide causes delayed gastric emptying and inhibits duodenal and small intestine motility. However, these GI movement-inhibiting effects may be decreased or absent in patients with DN-associated dysautonomia.

      PubDate: 2017-07-01T02:24:07Z
       
  • Combination avelumab and utomilumab immunotherapy can induce diabetic
           ketoacidosis
    • Abstract: Publication date: Available online 23 June 2017
      Source:Diabetes & Metabolism
      Author(s): P.W. Atkins, D.M. Thompson


      PubDate: 2017-07-01T02:24:07Z
       
  • Glycaemic control and hypoglycaemia with insulin glargine 300U/mL versus
           insulin glargine 100U/mL in insulin-naïve people with type 2 diabetes:
           12-month results from the EDITION 3 trial
    • Abstract: Publication date: Available online 13 June 2017
      Source:Diabetes & Metabolism
      Author(s): G.B. Bolli, M.C. Riddle, R.M. Bergenstal, M. Wardecki, H. Goyeau, P.D. Home
      Aim To explore if efficacy and safety findings for insulin glargine 300U/mL (Gla-300) versus insulin glargine 100U/mL (Gla-100), observed over 6 months in insulin-naïve people with type 2 diabetes, are maintained after 12 months. Methods EDITION 3 was a phase 3a, randomized, multicentre, open-label, parallel-group, treat-to-target study of once-daily Gla-300 versus Gla-100 (target fasting self-monitored plasma glucose, 4.4–5.6mmol/L [80–100mg/dL]). Participants completing the initial 6-month treatment phase continued their previously allocated basal insulin. Results Of 878 participants randomized, 337/439 (77%) and 314/439 (72%) assigned to Gla-300 and Gla-100, respectively, completed 12 months of treatment. Improved glycaemic control was sustained until 12 months in both treatment groups, with similar reductions in HbA1c from baseline to month 12 (difference: −0.08 [95% confidence interval (CI): −0.23 to 0.07] % or −0.9 [−2.5 to 0.8] mmol/mol). Relative risk of experiencing≥1 confirmed (≤3.9mmol/L [≤70mg/dL]) or severe hypoglycaemic event with Gla-300 versus Gla-100 was 0.86 (95% CI: 0.69 to 1.07) at night and 0.92 (0.82 to 1.03) at any time of day. For events with a glycaemic threshold of<3.0mmol/L (<54mg/dL) these numbers were 0.76 (0.49 to 1.19) and 0.66 (0.50 to 0.88). A similar pattern was seen for documented symptomatic events. No between-group differences in adverse events were identified. Conclusion Over 12 months, Gla-300 treatment was as effective as Gla-100 in reducing HbA1c in insulin-naïve people with type 2 diabetes, with lower overall risk of hypoglycaemia at the<3.0mmol/L threshold.

      PubDate: 2017-06-15T13:00:48Z
       
  • Higher parathyroid hormone levels are associated with increased
           below-the-knee arterial calcification in type 2 diabetes
    • Abstract: Publication date: Available online 8 June 2017
      Source:Diabetes & Metabolism
      Author(s): A. Mary, A. Hartemann, M. Brazier, C.E. Aubert, S. Kemel, J.E. Salem, P. Cluzel, S. Liabeuf, Z. Massy, R. Mentaverri, O. Bourron, S. Kamel


      PubDate: 2017-06-11T22:13:43Z
       
  • Different insulin concentrations in resuspended vs. unsuspended NPH
           insulin: Practical aspects of subcutaneous injection in patients with
           diabetes
    • Abstract: Publication date: Available online 7 June 2017
      Source:Diabetes & Metabolism
      Author(s): P. Lucidi, F. Porcellati, A. Marinelli Andreoli, P. Candeloro, P. Cioli, G.B. Bolli, C.G. Fanelli
      Aims This study measured the insulin concentration (Ins[C]) of NPH insulin in vials and cartridges from different companies after either resuspension (R+) or not (R−; in the clear/cloudy phases of unsuspended NPH). Methods Measurements included Ins[C] in NPH(R+) and in the clear/cloudy phases of NPH(R−), and the time needed to resuspend NPH and time for NPH(R+) to separate again into clear/cloudy parts. Results In vials of NPH(R+) (assumed to be 100%), Ins[C] in the clear phase of NPH(R−) was<1%, but 230±41% and 234±54% in the cloudy phases of Novo Nordisk and Eli Lilly NPH, respectively. Likewise, in pen cartridges, Ins[C] in the clear phase of NPH(R−) was<1%, but 182±33%, 204±22% and 229±62% in the cloudy phases of Novo, Lilly and Sanofi NPH. Time needed to resuspend NPH (spent in tipping) in vials was brief with both Novo (5±1s) and Lilly NPH (6±1s), but longer with all pen cartridges (50±8s, 40±6s and 30±4s from Novo, Lilly and Sanofi, respectively; P =0.022). Time required for 50% separation into cloudy and clear parts of NPH was longer with Novo (60±7min) vs. Lilly (18±3min) in vials (P =0.021), and affected by temperature, but not by the different diameter sizes of the vials. With pen cartridges, separation into clear and cloudy parts was significantly faster than in vials (P <0.01). Conclusion Ins[C] in NPH preparations varies depending on their resuspension or not. Thus, subcutaneous injection of the same number of units of NPH in patients with diabetes may deliver different amounts of insulin depending on its prior NPH resuspension.

      PubDate: 2017-06-11T22:13:43Z
       
  • Plasma trans-palmitoleic acid is associated with cardio-metabolic risk
           factors in youth with type 1 diabetes
    • Abstract: Publication date: Available online 2 June 2017
      Source:Diabetes & Metabolism
      Author(s): N.S. The, I.B. King, S.C. Couch, J.L. Crandell, D. Dabelea, A.D. Liese, E.J. Mayer-Davis


      PubDate: 2017-06-06T21:30:15Z
       
  • Effects of anti-somatostatin agents on glucose metabolism
    • Abstract: Publication date: Available online 1 June 2017
      Source:Diabetes & Metabolism
      Author(s): B. Vergès
      The anti-somatostatin agents used to treat acromegaly, Cushing's disease and neuroendocrine tumours also have hyperglycaemic effects. This is particularly true for pasireotide. Hyperglycaemic events are seen in 57–73% of patients with Cushing's treated with pasireotide, with a need to initiate antidiabetic treatment in about 50% of these patients. In acromegaly, treatment with pasireotide induces hyperglycaemia in 29–61% of patients. Pasireotide-induced hyperglycemia occurs early, within the first 3 months of treatment, due to a decrease in insulin secretion secondary to a fall in secretion of GLP-1 and GIP, and potentially also due to a direct inhibitory effect of pasireotide on beta cells. Close monitoring of blood glucose is mandatory in all patients during the first 3 months of treatment with pasireotide. Where necessary, antidiabetic treatment should be initiated, preferably with a DPP-4 inhibitor or a GLP-1 receptor agonist, both of which have proven efficacy in the control of hyperglycaemia induced by pasireotide.

      PubDate: 2017-06-06T21:30:15Z
       
  • The type 2 diabetes susceptibility TCF7L2 gene variants affect
           postprandial glucose and fat utilization in non-diabetic subjects
    • Abstract: Publication date: Available online 31 May 2017
      Source:Diabetes & Metabolism
      Author(s): E. Adamska, A. Kretowski, J. Goscik, A. Citko, W. Bauer, M. Waszczeniuk, K. Maliszewska, M. Paczkowska-Abdulsalam, M. Niemira, L. Szczerbinski, M. Ciborowski, M. Gorska


      PubDate: 2017-06-01T20:43:20Z
       
  • A decrease in glutamic acid decarboxylase autoantibody levels with
           sitagliptin use in patients with latent autoimmune diabetes in adults
    • Abstract: Publication date: Available online 29 May 2017
      Source:Diabetes & Metabolism
      Author(s): H. Yanai


      PubDate: 2017-06-01T20:43:20Z
       
  • Predictors of cardiovascular risk among patients with type 1 diabetes: A
           critical analysis of the metabolic syndrome and its components
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): V. Gingras, C. Leroux, A. Fortin, L. Legault, R. Rabasa-Lhoret
      Patients with type 1 diabetes (T1D) are at increased risk for cardiovascular diseases. The metabolic syndrome (MetS), a complex disorder defined by a cluster of interconnected factors including abdominal obesity, hypertension, dyslipidaemia and insulin resistance, has been proposed to identify patients with T1D at high cardiovascular risk. The MetS has been identified in 8–45% of patients with T1D, depending on the definition and cohort studied. However, clinicians and researchers face several issues with the criteria for MetS in patients with T1D, therefore questioning its value in routine care. For example, three criteria can lead to overestimation of MetS prevalence; the impaired fasting glucose criterion is irrelevant as it is automatically fulfilled; and the widespread use of antihypertensive and lipid-lowering medications for cardiac and renal preventative purposes can contribute to overestimations of the prevalence of raised blood pressure and elevated triglycerides. In cross-sectional studies, the MetS has been associated mostly with an increased risk of microvascular complications whereas, in prospective cohorts, the predictive value of MetS for micro- and macrovascular outcomes has been inconsistent. While identifying diabetes patients at increased risk for cardiovascular complications and early mortality is crucial from a prevention standpoint, for patients with T1D, the current definition of MetS may not be the most suitable tool. The aims of the present report are to review the applicability and limitations of the MetS in patients with T1D, and to discuss alternative avenues to identify high-risk patients.

      PubDate: 2017-05-27T20:28:25Z
       
  • Long-term risk of stroke in type 2 diabetes patients with diabetic
           ketoacidosis: A population-based, propensity score-matched, longitudinal
           follow-up study
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): Y.-L. Chen, S.-F. Weng, C.-Y. Yang, J.-J. Wang, K.-J. Tien
      Aim To investigate the long-term risk of stroke in type 2 diabetes (T2D) patients with previous episodes of diabetic ketoacidosis (DKA). Methods This retrospective nationwide population-based cohort study was conducted using Taiwan's National Health Insurance database. Claims data from 2000 to 2002 were extracted for 3572 T2D patients with DKA and 7144 controls matched for age, gender, diabetes complications severity index, frequency of clinical visits and baseline comorbidities. Patients with type 1 diabetes (T1D), identified by glucagon C-peptide stimulation or glutamic acid decarboxylase (GAD) antibody blood tests and possession of a catastrophic illness certificate were excluded. All patients were tracked until a new stroke diagnosis, death or the end of 2011. Results Of the 3572 selected patients, 270 with DKA and 404 of the 7144 controls were diagnosed with a new stroke, giving an incidence rate ratio (IRR) of 1.56 (95% CI: 1.34–1.82; P <0.0001). DKA patients had a higher risk of ischaemic stroke than those without DKA (IRR: 1.62, 95% CI: 1.34–1.96; P <0.0001), and DKA patients with hypertension and hyperlipidaemia were at even greater risk of stroke. Also, DKA patients were at particular risk for stroke during the first half-year following DKA diagnosis. After adjusting for patient characteristics and comorbidities, these patients were 1.55 times more likely to have a stroke than those without DKA (95% CI: 1.332–1.813, P <0.0001). Conclusion T2D patients with previous DKA have a higher risk of stroke, especially ischaemic strokes.

      PubDate: 2017-05-27T20:28:25Z
       
  • An extended fatty liver index to predict non-alcoholic fatty liver disease
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): K. Kantartzis, I. Rettig, H. Staiger, J. Machann, F. Schick, L. Scheja, A. Gastaldelli, E. Bugianesi, A. Peter, M.B. Schulze, A. Fritsche, H.-U. Häring, N. Stefan
      Background In clinical practice, there is a strong interest in non-invasive markers of non-alcoholic fatty liver disease (NAFLD). Our hypothesis was that the fold-change in plasma triglycerides (TG) during a 2-h oral glucose tolerance test (fold-change TGOGTT) in concert with blood glucose and lipid parameters, and the rs738409 C>G single nucleotide polymorphism (SNP) in PNPLA3 might improve the power of the widely used fatty liver index (FLI) to predict NAFLD. Methods The liver fat content of 330 subjects was quantified by 1H-magnetic resonance spectroscopy. Blood parameters were measured during fasting and after a 2-h OGTT. A subgroup of 213 subjects underwent these measurements before and after 9 months of a lifestyle intervention. Results The fold-change TGOGTT was closely associated with liver fat content (r =0.51, P <0.0001), but had less power to predict NAFLD (AUROC=0.75) than the FLI (AUROC=0.79). Not only was the fold-change TGOGTT independently associated with liver fat content and NAFLD, but so also were the 2-h blood glucose level and rs738409 C>G SNP in PNPLA3. In fact, a novel index (extended FLI) generated from these and the usual FLI parameters considerably increased its power to predict NAFLD (AUROC=0.79–0.86). The extended FLI also increased the power to predict changes in liver fat content with a lifestyle intervention (n =213; standardized beta coefficient: 0.23–0.29). Conclusion This study has provided novel data confirming that the OGTT-derived fold-change TGOGTT and 2-h glucose level, together with the rs738409 C>G SNP in PNPLA3, allow calculation of an extended FLI that considerably improves its power to predict NAFLD.

      PubDate: 2017-05-27T20:28:25Z
       
  • Adipose tissue is influenced by hypoxia of obstructive sleep apnea
           syndrome independent of obesity
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): C.E. Thorn, B. Knight, E. Pastel, L.J. McCulloch, B. Patel, A.C. Shore, K. Kos
      Aims Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular risk and diabetes independent of obesity. We investigated whether adipose tissue dysfunction is exacerbated due to increased tissue hypoxia. Methods Adipose tissue (AT) oxygenation was measured with a Clarke-type electrode (pATO2) in 16 men with OSAS before and after 4 months of continuous positive airway pressure therapy (CPAP) and in BMI-matched controls. Oxygenation was simultaneously monitored in arterial blood by pulse oximetry (SaO2); mixed blood in AT microcirculation by reflectance spectroscopy (SATO2) along with blood flow. Markers of hypoxia, adipo- and angiogenesis, inflammation and fibrosis were analysed in AT and serum. Results OSAS subjects were more insulin resistant. Despite lower arterial SaO2 (95.4±1.3% vs. 97.1±1.6%, P =0.013) in subjects with OSAS, there was no difference in the oxygen content of AT microcirculation (61.6±18.4 vs. 72.2±7.0%, P =0.07) or pATO2 (49.2±7.5 vs. 50.4±14.7mmHg, P =0.83) between groups. Resting AT blood flow was higher in OSAS compared to controls (108.5±22.7 vs. 78.9±24.9au, P <0.005) and strongly associated with inflammation markers IL-6 and MCP-1. AT of OSAS subjects showed increased inflammation (TNFA P =0.049) and fibrosis (COL3A1 P =0.02), a trend of higher HIF1A expression (P =0.06) and reduced adipogenesis (PPARG P =0.006). After CPAP, only expression of the lipid deposition marker LPL increased (30%, P =0.047). Conclusions Adipose tissue of awake OSAS subjects appears no more hypoxic than adipose tissue of BMI-matched controls despite daytime hypoxaemia. Increased adipose tissue blood flow may be explained by an increased inflammatory response. We observe features of adipose dysfunction in subjects with OSAS, which attribute to increased cardiometabolic risk associated with this condition.

      PubDate: 2017-05-27T20:28:25Z
       
  • Early age at menarche and gestational diabetes mellitus risk: Results from
           the Healthy Baby Cohort study
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): H. Li, L. Shen, L. Song, B. Liu, X. Zheng, S. Xu, Y. Wang
      Aim Early age at menarche has been reported to increase type 2 diabetes risk, but little is known of its impact on gestational diabetes mellitus (GDM) risk. The aim of this study was to examine the association between age at menarche and plasma glucose levels as well as GDM risk. Methods A total of 6900 pregnant women from the Healthy Baby Cohort Study were included in our analysis. Age at menarche was self-reported and categorized into five groups (9–11, 12, 13, 14 and 15–18 years of age). GDM was diagnosed using the International Association of Diabetes and Pregnancy Study Groups criteria. Comparisons of plasma glucose levels according to age at menarche categories were performed using analysis of covariance. Logistic regression models were used to estimate the association between age at menarche and GDM risk. Results Of our 6900 participants, 1015 (14.7%) were diagnosed with GDM. Mean age at menarche was 13.1±1.2 years. Early age at menarche (9–11 years) was associated with higher fasting, 1-h and 2-h plasma glucose levels (all P <0.05) compared with menarche at age 13 years. Furthermore, early age at menarche was linked to increased GDM risk after adjusting for potential confounders (OR: 1.41, 95% CI: 1.06–1.87). Conclusion Early age at menarche is an independent risk factor for GDM and, as such, may help to identify women at higher GDM risk who would benefit from early preventative strategies.

      PubDate: 2017-05-27T20:28:25Z
       
  • FGF21 deficiency is associated with childhood obesity, insulin resistance
           and hypoadiponectinaemia: The BCAMS Study
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): G. Li, J. Yin, J. Fu, L. Li, S.F.A. Grant, C. Li, M. Li, J. Mi, M. Li, S. Gao
      Objective Fibroblast growth factor 21 (FGF21) exerts beneficial effects on metabolic homoeostasis and has been reported to be regulated by adiponectin, leptin and resistin. However, while an association between increased circulating FGF21 and metabolic disorders has been reported in adults, paediatric-specific data are lacking. Design and methods This study investigated the relationship between FGF21 levels and obesity, insulin resistance (IR), the metabolic syndrome (MetS) and adipokines (adiponectin, leptin and resistin) in a cohort of 3231 Chinese youngsters aged 6–18. Results There were gender- and puberty-related differences in FGF21 levels. Unexpectedly, FGF21 levels were decreased in children with obesity, and negatively correlated with insulin, HOMA-IR and leptin levels after adjusting for age, gender, puberty and lifestyle factors. Moreover, multiple regression analyses showed that serum FGF21 positively predicted adiponectin levels while resistin positively predicted FGF21 levels independent of BMI (P <0.05). Children in the lowest FGF21 quintile were more likely to have IR (OR: 1.85, 95% CI: 1.41–2.42; P =0.002) and MetS (OR: 1.62, 95% CI: 1.14–2.28; P =0.007) than those in the highest quintile. Further adjusting for BMI and/or the three adipokines modified the association of FGF21 with MetS (P >0.10) but not with IR (P <0.01). Conclusion Although the associations between adiponectin, leptin, resistin and metabolic abnormalities in our paediatric population were similar to those in adults, correlations of FGF21 levels with obesity, IR and MetS were the inverse of those found in adults. Our present findings suggest that FGF21 deficiency, rather than resistance, contribute to IR and hypoadiponectinaemia independently of obesity in young people.

      PubDate: 2017-05-27T20:28:25Z
       
  • Impact of glucose tolerance status on the development of coronary artery
           disease among working-age men
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): K. Fujihara, R. Igarashi, M. Yamamoto, M. Ishizawa, Y. Matsubayasi, S. Matsunaga, K. Kato, C. Ito, M. Koishi, N. Yamanaka, S. Kodama, H. Sone
      Aims To examine the impact of glucose tolerance status on the development of coronary artery disease (CAD) in working-age men in Japan. Methods This population-based retrospective cohort study included 111,621 men aged 31–60 years [63,558 with normal glucose tolerance (NGT); 37,126 with prediabetes; 10,937 with diabetes]. The Cox proportional-hazards regression model was used to identify variables related to the incidence of CAD. Results Multivariate analysis showed that, compared with NGT, diabetes increased the risk of CAD by 17.3 times (95% CI: 6.36–47.0) at ages 31–40 years, by 2.74 times (95% CI: 1.85–4.05) at ages 41–50 years and by 2.47 times (95% CI: 1.69–3.59) at ages 51–60 years. The HRs for CAD in men with diabetes aged 31–40 equaled that of men with NGT aged 51–60 [18.2 (7.15–46.4) and 19.4 (8.28–45.4), respectively]. Conclusion The impact of diabetes on CAD was markedly greater in men aged 31–40 years compared with those aged 41–60 years.

      PubDate: 2017-05-27T20:28:25Z
       
  • Glucagon-secretion inhibition using somatostatin: An old hormone for the
           treatment of diabetes-associated pancreatectomy
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): J.-P. Riveline, P. Boudou, B. Blondeau, J.-F. Gautier


      PubDate: 2017-05-27T20:28:25Z
       
  • Oral hygiene behaviours and tooth-loss assessment in patients with
           diabetes: A report from a diabetology centre in Belgium
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): M. Buysschaert, C. Tshongo Muhindo, O. Alexopoulou, D. Rahelic, H. Reychler, V. Preumont


      PubDate: 2017-05-27T20:28:25Z
       
  • One-year metreleptin therapy decreases PCSK9 serum levels in diabetic
           patients with monogenic lipodystrophy syndromes
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): C. Vatier, L. Arnaud, X. Prieur, B. Guyomarch, C. Le May, E. Bigot, M. Pichelin, A. Daguenel, M.-C. Vantyghem, J.-F. Gautier, C. Vigouroux, B. Cariou


      PubDate: 2017-05-27T20:28:25Z
       
  • A prospective study of leucocyte mitochondrial DNA content and deletion in
           association with the metabolic syndrome
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): J.-Y. Kim, J.R. Choi, I.H. Park, J.H. Huh, J.-W. Son, K.W. Kim, K.-S. Park, S.-K. Cha, J.H. Sohn, D.-H. Jung, S.-B. Koh


      PubDate: 2017-05-27T20:28:25Z
       
  • The association between hand grip strength and non-exercise activity
           thermogenesis in patients with type 2 diabetes
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): H. Hamasaki, Y. Kawashima, H. Yanai


      PubDate: 2017-05-27T20:28:25Z
       
  • Serum vitamin A-related metabolite levels are associated with incidence of
           type 2 diabetes
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): M. Kim, S.H. Jee, M. Kim, H.J. Yoo, M. Kang, J. Kim, J.H. Lee


      PubDate: 2017-05-27T20:28:25Z
       
  • Impact of ethnicity and obesity on insulin resistance in two ethnic groups
           at very high risk of type 2 diabetes
    • Abstract: Publication date: June 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 3
      Author(s): S. Hassoun, M. Al-Atrash, M. Alkasim, Z. Dabbous, O. Mujahed, R.A. DeFronzo, A. Jayyousi, M. Zirie, M. Abdul-Ghani


      PubDate: 2017-05-27T20:28:25Z
       
  • ‘Treatment-resistant’ type 2 diabetes: Which definition for
           clinical practice?
    • Abstract: Publication date: Available online 25 May 2017
      Source:Diabetes & Metabolism
      Author(s): A.J. Scheen


      PubDate: 2017-05-27T20:28:25Z
       
  • Comparison of simple indices for measuring insulin resistance that
           integrates adipokines in non-diabetic obese postmenopausal women before
           and after weight loss: A MONET study
    • Abstract: Publication date: Available online 23 May 2017
      Source:Diabetes & Metabolism
      Author(s): C. Vatier, S. Fellahi, A.D. Karelis, M. Brochu, E. Doucet, D. Prud’homme, R. Rabasa-Lhoret, J.-P. Bastard


      PubDate: 2017-05-27T20:28:25Z
       
  • Informal caregiving as a risk factor for type 2 diabetes in individuals
           with favourable and unfavourable psychosocial work environments: A
           longitudinal multi-cohort study
    • Abstract: Publication date: Available online 17 May 2017
      Source:Diabetes & Metabolism
      Author(s): J. Mortensen, A.J. Clark, T. Lange, G.S. Andersen, M. Goldberg, C.H. Ramlau-Hansen, J. Head, M. Kivimäki, I.E.H. Madsen, C. Leineweber, R. Lund, R. Rugulies, M. Zins, H. Westerlund, N.H. Rod
      Aim To examine whether informal caregiving is associated with increased risk of type 2 diabetes (T2D), and whether job strain and social support at work modify the association. Methods Individual participant's data were pooled from three cohort studies—the French GAZEL study, the Swedish Longitudinal Occupational Survey of Health (SLOSH) and the British Whitehall II study—a total of 21,243 study subjects. Informal caregiving was defined as unpaid care for a closely related person. Job strain was assessed using the demand-control model, and questions on co-worker and supervisor support were combined in a measure of social support at work. Incident T2D was ascertained using registry-based, clinically assessed and self-reported data. Results A total of 1058 participants developed T2D during the up to 10 years of follow-up. Neither informal caregiving (OR: 1.09, 95% CI: 0.92–1.30) nor high job strain (OR: 1.04, 95% CI: 0.86–1.26) were associated with T2D risk, whereas low social support at work was a risk factor for T2D (OR: 1.18, 95% CI: 1.02–1.37). Also, informal caregivers who were also exposed to low social support at work were at higher risk of T2D (OR: 1.40, 95% CI: 1.08–1.82) compared with those who were not informal caregivers and had high social support at work (multiplicative test for interaction, P =0.04; additive test for interaction, synergy index=10). Conclusion Informal caregiving was not independently associated with T2D risk. However, low social support at work was a risk factor, and informal caregivers with low social support at work had even higher risks of T2D.

      PubDate: 2017-05-23T11:13:55Z
       
  • Low serum creatinine is a type 2 diabetes risk factor in men and women:
           The Yuport Health Checkup Center cohort study
    • Abstract: Publication date: Available online 17 May 2017
      Source:Diabetes & Metabolism
      Author(s): S. Kashima, K. Inoue, M. Matsumoto, K. Akimoto
      Aim Type 2 diabetes (T2D) is a risk factor for muscle loss and subsequent frailty. The reverse association, however, may also happen. This study examined whether serum creatinine level, an indicator of muscle mass, predicted diabetes development. In addition, a role for body mass index (BMI) as an effect modifier of creatinine levels was evaluated. Methods This cohort study included 9667 subjects without diabetes or hypertension and with normal creatinine levels at baseline. Multiple-adjusted hazard ratios (HRs) for associations between baseline creatinine and diabetes development were estimated using the Cox proportional-hazards model. Stratified analyses based on BMI were also performed. Results During the follow-up period (mean: 5.6 years), 287 (5.5%) men and 115 (2.3%) women developed T2D. HR in men with serum creatinine≤0.7mg/dL compared with 0.9–1.2mg/dL was 1.40 (95% CI: 1.05–1.87) after adjusting for age, BMI, blood pressure and fasting plasma glucose at baseline, whereas the adjusted HR in women with creatinine≤0.5mg/dL compared with 0.7–1.1mg/dL was 1.69 (95% CI: 1.04–2.76). In a subgroup analysis stratified by BMI, interactions between BMI and baseline creatinine levels for T2D were statistically significant in women with the lowest creatinine levels (P =0.08 for interaction). Conclusion Low serum creatinine levels, a surrogate marker of muscle mass, predict T2D development in both genders, even after excluding the effect of diabetic and prediabetic glomerular hyperfiltration. BMI modified the association between creatinine and diabetes development in women.

      PubDate: 2017-05-17T12:43:16Z
       
  • Impact of glucose-lowering therapies on risk of stroke in type 2 diabetes
    • Abstract: Publication date: Available online 15 May 2017
      Source:Diabetes & Metabolism
      Author(s): F. Bonnet, A.J. Scheen
      Patients with type 2 diabetes (T2D) have an increased risk of stroke compared with people without diabetes. However, the effects of glucose-lowering drugs on risk of ischaemic stroke in T2D have been less extensively investigated than in coronary heart disease. Some evidence, including the UKPDS, has suggested a reduced risk of stroke with metformin, although the number of studies is limited. Inhibition of the KATP channels increases ischaemic brain lesions in animals. This is in agreement with a recent meta-analysis showing an increased risk of stroke with sulphonylureas vs. various comparators as both mono- and combination therapy. Pioglitazone can prevent recurrence of stroke in patients with previous stroke, as already shown in PROactive, although results are less clear for first strokes. As for DPP-4 inhibitors, there was a non-significant trend towards benefit for stroke, whereas a possible increased risk of stroke with SGLT2 inhibitors—and in particular, empagliflozin in the EMPA-REG OUTCOME trial—has been suggested and requires clarification. Experimental results support a potential protective effect of GLP-1 receptor agonists against stroke that has, at least in part, been translated to clinical benefits in T2D patients in the LEADER and SUSTAIN-6 trials. Further interventional studies are now warranted to confirm the effects of glucose-lowering agents on risk of stroke in patients with T2D. In summary, the effects of antidiabetic drugs on risk of stroke appear to be heterogeneous, with some therapies (pioglitazone, GLP-1 receptor agonists) conferring possible protection against ischaemic stroke, other classes showing a neutral impact (DPP-4 inhibitors, insulin) and some glucose-lowering agents being associated with an increased risk of stroke (sulphonylureas, possibly SGLT2 inhibitors, high-dose insulin in the presence of insulin resistance).

      PubDate: 2017-05-17T12:43:16Z
       
  • Dapagliflozin modulates glucagon secretion in an SGLT2-independent manner
           in murine alpha cells
    • Abstract: Publication date: Available online 9 May 2017
      Source:Diabetes & Metabolism
      Author(s): A. Solini, G. Sebastiani, L. Nigi, E. Santini, C. Rossi, F. Dotta
      Aim SGLT2 inhibitors reduce renal glucose uptake through an insulin-independent mechanism. They also increase glucagon concentration, although the extent to which this is due to a direct effect on pancreatic alpha cells remains unclear. Methods In the present work, αTC1 cells treated with the SGLT2 inhibitor dapagliflozin (Dapa) were analyzed for glucose transporters, molecular mediators of hormone secretion, glucagon and GLP-1 release, and the effects of somatostatin. Data were validated in murine and human pancreatic islets. Results SLC5A2 (the SGLT2-encoding gene) was nearly undetectable in αTC1 cells, not even by a digital PCR technique using different probes. In contrast, SLC5A1 (the SGLT1-encoding gene) was constitutively abundant in αTC1 cells and in islets, and increased with Dapa. This was associated with greater glucagon release, preceded by increased expression of preproglucagon and HNF4α. Looking at the candidate intracellular signalling pathway, reduced PASK and increased AMPK-α2 expression were also detected. GLUT1 and GLUT2, as well as regulators of glucagon release and alpha-cell phenotype (chromogranin A, paired box 6, proprotein convertase 1/2, synaptophysin), were unaffected by Dapa, as were GLP-1 receptor expression and GLP-1 release. Low glucose did not influence the stimulatory effect of Dapa on glucagon release, but was instead almost fully reverted by SLC5A1 silencing. When the effect of Dapa on AMPK and PASK, emerging regulators of lipid and glucose metabolism, was tested, upregulated AMPK-α2 appeared to be involved in molecular signalling. Conclusion Our study has shown that, in αTC1 cells, Dapa acutely upregulates SGLT1 expression and increases glucagon release through an SGLT1-dependent mechanism, with SGLT2 expression virtually undetectable. These results suggest the involvement of SGLT1 in modulating glucagon increases following SGLT2 inhibition.

      PubDate: 2017-05-13T12:27:58Z
       
 
 
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