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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  [3042 journals]
  • 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
       
  • Fenofibrate decreases plasma ceramide in type 2 diabetes patients: A novel
           marker of CVD?
    • Abstract: Publication date: Available online 9 May 2017
      Source:Diabetes & Metabolism
      Author(s): M. Croyal, Z. Kaabia, L. León, S. Ramin-Mangata, T. Baty, F. Fall, S. Billon-Crossouard, A. Aguesse, T. Hollstein, D.R. Sullivan, E. Nobecourt, G. Lambert, M. Krempf
      Aim The benefit of the lipid-lowering drug fenofibrate on cardiovascular outcomes is controversial. Our aim was to find new circulating markers to identify those patients most likely to benefit from fenofibrate prescription. Methods Analyses were conducted of plasma samples collected from 102 patients with type 2 diabetes, enrolled in the FIELD trial, before and after fenofibrate treatment (200mg/day). Non-targeted and targeted lipid analyses and apolipoprotein measurements were made using mass spectrometry methods. Results Lipidomics revealed a global decrease in ceramide after fenofibrate treatment confirmed by quantitative analysis (−18.2%, P <0.001). These changes were strongly associated with those found for plasma sphingomyelin (r =0.80, P <0.001) and, to a lesser extent, for sphingosine-1-phosphate (r =0.34, P <0.001). Ceramide levels decreased in 73.5% of patients. In addition to the expected lipid changes (decreases in triglycerides, total cholesterol and LDL cholesterol, and increase in HDL cholesterol), fenofibrate also lowered plasma apoC-II (−11.1%, P <0.01), apoC-III (−24.6%; P <0.001), apoB100 (−27.0%, P <0.01) and sphingomyelinase (−7.6%, P <0.001), and increased plasma apoA-II (22.4%, P <0.001) as well as adiponectin (11.4%, P <0.001). No significant association was found between ceramide decrease and these modulations except for total cholesterol (r =0.20, P =0.047) and HDL protein components. At baseline, only elevated sphingolipid levels were significantly associated with ceramide reduction after fenofibrate treatment. Conclusion Fenofibrate lowers plasma ceramide independently of the usual lipid parameters. As ceramide is a strong marker of atherosclerosis, our study underpins the need to further evaluate its contribution to cardiovascular events in fenofibrate-treated patients.

      PubDate: 2017-05-13T12:27:58Z
       
  • 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
       
  • The yin and yang of apolipoprotein CIII
    • Abstract: Publication date: Available online 8 May 2017
      Source:Diabetes & Metabolism
      Author(s): K. Åvall, P.-O. Berggren, L. Juntti-Berggren


      PubDate: 2017-05-13T12:27:58Z
       
  • Acute pancreatitis with dipeptidyl peptidase-4 (DPP4) inhibitor or
           fulminant type 1 diabetes?
    • Abstract: Publication date: Available online 5 May 2017
      Source:Diabetes & Metabolism
      Author(s): C. Amouyal, P. Levy, F. Andreelli, A. Hartemann


      PubDate: 2017-05-07T11:56:10Z
       
  • Psychosocial determinants of non-adherence to antidiabetic drug treatment:
           A prospective cohort study
    • Abstract: Publication date: Available online 5 May 2017
      Source:Diabetes & Metabolism
      Author(s): L. Guénette, A. Zongo, L. Guillaumie, S. Lauzier, L. Blais, J.-P. Grégoire, J. Moisan


      PubDate: 2017-05-07T11:56:10Z
       
  • Canagliflozin as a replacement therapy for patients with type 2 diabetes
           not responding to GLP-1 receptor agonists
    • Abstract: Publication date: Available online 2 May 2017
      Source:Diabetes & Metabolism
      Author(s): M.D. Garcia de Lucas, J.O. Sierra


      PubDate: 2017-05-07T11:56:10Z
       
  • A synopsis of brown adipose tissue imaging modalities for clinical
           research
    • Abstract: Publication date: Available online 25 April 2017
      Source:Diabetes & Metabolism
      Author(s): L. Sun, J. Yan, L. Sun, S.S. Velan, M.K.S. Leow
      Body weight gain results from a chronic excess of energy intake over energy expenditure. Accentuating endogenous energy expenditure has been accorded considerable attention ever since the presence of brown adipose tissue (BAT) in adult humans was recognized, given that BAT is known to increase energy expenditure via thermogenesis. Besides classic BAT, significant strides in our understanding of inducible brown adipocytes have been made regarding its development and function. While it is ideal to study BAT histologically, its relatively inaccessible anatomical locations and the inherent risks associated with biopsy preclude invasive techniques to evaluate BAT on a routine basis. Thus, there has been a surge in interest to employ non-invasive methods to examine BAT. The gold standard of non-invasive detection of BAT activation is 18F-fluorodeoxyglucose positron emission tomography (PET) with computed tomography (CT). However, a major limitation of PET/CT as a tool for human BAT studies is the clinically significant doses of ionizing radiation. More recently, several other imaging methods, including single-photon emission computed tomography (SPECT), magnetic resonance imaging (MRI), infrared thermography (IRT)/thermal imaging and contrast ultrasonography (US) have been developed in hopes that they would allow non-invasive, quantitative measures of BAT mass and activity with lower costs. This review focuses on such methods to detect human BAT activation and white adipose tissue (WAT) browning to prompt the establishment of BAT-centric strategies for augmenting energy expenditure and combatting obesity. Clinical validation of these methods will most likely expand the scope and flexibility of future BAT studies.

      PubDate: 2017-05-02T10:29:18Z
       
  • Importance of alternative-site blood glucose testing in the diagnosis of
           artifactual hypoglycaemia in systemic scleroderma
    • Abstract: Publication date: Available online 4 April 2017
      Source:Diabetes & Metabolism
      Author(s): V. Dubourdieu, H. Mosbah, C. Amouyal, A. Hartemann, F. Andreelli


      PubDate: 2017-05-02T10:29:18Z
       
  • Metformin is associated with a lower risk of colorectal cancer in
           Taiwanese patients with type 2 diabetes: A retrospective cohort analysis
    • Abstract: Publication date: Available online 21 April 2017
      Source:Diabetes & Metabolism
      Author(s): C.-H. Tseng
      Background The association between metformin and colorectal cancer (CRC) has rarely been investigated in Asian populations. Methods This retrospective cohort study included patients with newly diagnosed type 2 diabetes during 1999–2005, recruited from Taiwan's National Health Insurance database. A total of 169,601 patients (original cohort: 153,270 ever-users and 16,331 never-users of metformin) and a subgroup of 1:1 propensity-score-matched pairs of 16,331 ever-users and 16,331 never-users (matched cohort) were followed up to 31 December 2011. Cox regression was constructed with the inverse probability of treatment-weighting, using propensity scores, and was used to estimate hazard ratios (HRs). Results In the original cohort, the incidence of CRC was 242.9 and 480.9 per 100,000 person-years, respectively, in ever- and never-users. The overall HR [0.50, 95% confidence interval (CI): 0.45–0.56] suggested a significantly lower risk in metformin users, while compared with never-users, the HR (95% CI) for the first (<27.1 months), second (27.1–58.1 months) and third (>58.1 months) tertiles of cumulative duration of metformin therapy was 0.86 (0.76–0.98), 0.51 (0.45–0.59) and 0.26 (0.23–0.30), respectively. Analyses in the matched cohort showed similar findings with an overall HR of 0.62 (0.53–0.74), and a tertile analysis HR of 1.02 (0.81–1.28), 0.70 (0.56–0.89) and 0.32 (0.23–0.43), respectively. Re-analyses using more stringent diagnoses of CRC and cumulative duration as a continuous variable have consistently supported a protective effect with metformin use. Conclusion Metformin is associated with a lower frequency of CRC.

      PubDate: 2017-04-25T09:45:54Z
       
  • Glycaemic control and hypoglycaemia with insulin glargine 300 U/mL
           compared with glargine 100 U/mL in Japanese adults with type 2 diabetes
           using basal insulin plus oral anti-hyperglycaemic drugs (EDITION JP 2
           randomised 12-month trial including 6-month extension)
    • Abstract: Publication date: Available online 19 April 2017
      Source:Diabetes & Metabolism
      Author(s): Y. Terauchi, M. Koyama, X. Cheng, M. Sumi, M.C. Riddle, G.B. Bolli, T. Hirose
      Aims To compare insulin glargine 300 U/mL (Gla-300) with glargine 100 U/mL (Gla-100) in Japanese adults with uncontrolled type 2 diabetes on basal insulin and oral anti-hyperglycaemic drugs over 12 months. Methods EDITION JP 2 was a randomised, open-label, phase 3 study. Following a 6-month treatment period, participants continued receiving previously assigned once daily Gla-300 or Gla-100, plus oral anti-hyperglycaemic drugs, in a 6-month extension period. Glycaemic control, hypoglycaemia and adverse events were assessed. Results The 12-month completion rate was 88% for Gla-300 and 96% for Gla-100, with comparable reasons for discontinuation. Mean HbA1c decrease from baseline to month 12 was 0.3% in both groups. Annualised rates of confirmed (≤3.9mmol/L [≤70mg/dL]) or severe hypoglycaemia were lower with Gla-300 than Gla-100 (nocturnal [00:00–05:59h]: rate ratio 0.41; 95% confidence interval: 0.18 to 0.92; anytime [24h]: rate ratio 0.64; 95% confidence interval: 0.44 to 0.94). Cumulative number of hypoglycaemic events was lower with Gla-300 than Gla-100. Adverse event profiles were comparable between treatments. Conclusion Over 12 months, Gla-300-treated participants achieved sustained glycaemic control and experienced less hypoglycaemia, particularly at night, versus Gla-100, supporting 6-month results.

      PubDate: 2017-04-25T09:45:54Z
       
  • Associations between a fetal imprinted gene allele score and late
           pregnancy maternal glucose concentrations
    • Abstract: Publication date: Available online 6 April 2017
      Source:Diabetes & Metabolism
      Author(s): C.J. Petry, K. Mooslehner, P. Prentice, M.G. Hayes, M. Nodzenski, D.M. Scholtens, I.A. Hughes, C.L. Acerini, K.K. Ong, W.L. Lowe, D.B. Dunger
      Aim We hypothesised that some of the genetic risk for gestational diabetes (GDM) is due to the fetal genome affecting maternal glucose concentrations. Previously, we found associations between fetal IGF2 gene variants and maternal glucose concentrations in late pregnancy. Methods In the present study, we tested associations between SNP alleles from 15 fetal imprinted genes and maternal glucose concentrations in late pregnancy in the Cambridge Baby Growth and Wellbeing cohorts (1160 DNA trios). Results Four fetal SNP alleles with the strongest univariate associations: paternally-transmitted IGF2 rs10770125 (P-value=2×10–4) and INS rs2585 (P-value=7×10–4), and maternally-transmitted KCNQ1(OT1) rs231841 (P-value=1×10–3) and KCNQ1(OT1) rs7929804 (P-value=4×10–3), were used to construct a composite fetal imprinted gene allele score which was associated with maternal glucose concentrations (P-value=4.3×10–6, n =981, r2 =2.0%) and GDM prevalence (odds ratio per allele 1.44 (1.15, 1.80), P-value=1×10–3, n =89 cases and 899 controls). Meta-analysis of the associations including data from 1367 Hyperglycaemia and Adverse Pregnancy Outcome Study participants confirmed the paternally-transmitted fetal IGF2/INS SNP associations (rs10770125, P-value=3.2×10–8, rs2585, P-value=3.6×10–5) and the composite fetal imprinted gene allele score association (P-value=1.3×10–8), but not the maternally-transmitted fetal KCNQ1(OT1) associations (rs231841, P-value=0.4; rs7929804, P-value=0.2). Conclusion This study suggests that polymorphic variation in fetal imprinted genes, particularly in the IGF2/INS region, contribute a small but significant part to the risk of raised late pregnancy maternal glucose concentrations.

      PubDate: 2017-04-11T09:28:07Z
       
  • Evolution of subcutaneous adipose tissue fibrosis after bariatric surgery
    • Abstract: Publication date: April 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 2
      Author(s): K. Chabot, M.-S. Gauthier, P.Y. Garneau, R. Rabasa-Lhoret
      Aim Obesity is associated with the development of metabolic complications such as insulin resistance (IR). The mechanisms leading to IR remain unclear. This study aimed to investigate the relationship between adipose tissue fibrosis and IR in obese patients before and after bariatric surgery. Methods Thirty-five obese patients awaiting bariatric surgery (12 with type 2 diabetes) were included in the study. Non-diabetic patients were classified as either insulin-sensitive (n =11) or insulin-resistant (n =12), based on the Matsuda insulin sensitivity index (ISIMatsuda). Homoeostasis model assessment (HOMA-IR) was used for longitudinal evaluation of insulin resistance. Fibrosis was quantified by Masson's trichrome staining on microscopy, and mRNA levels of fibrosis-related genes were examined in subcutaneous (SAT) and visceral adipose tissue (VAT) biopsies collected during and 6 months after bariatric surgery (SAT only). Results Despite their similar age, body mass index and fat mass, SAT fibrosis was significantly higher in diabetic vs insulin-sensitive patients (P <0.05), and associated with IR as assessed by both ISIMatsuda (r =−0.417, P =0.038) and HOMA-IR (r =0.464, P =0.007) at baseline, whereas VAT fibrosis was not. Six months after surgery and significant weight loss, fibrosis levels remained unchanged in SAT, although IR was significantly reduced in all groups (P <0.0001). No correlation was found between SAT fibrosis and IR after surgery. Conclusion Overall, these results show a significant but, most likely, transient association between SAT fibrosis and IR in obese humans.

      PubDate: 2017-04-04T08:54:02Z
       
  • Low adiponectin levels at baseline and decreasing adiponectin levels over
           10 years of follow-up predict risk of the metabolic syndrome
    • Abstract: Publication date: April 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 2
      Author(s): S. Lindberg, J.S. Jensen, M. Bjerre, J. Frystyk, A. Flyvbjerg, J. Jeppesen, R. Mogelvang
      Aim Adiponectin is the most abundant adipokine and may play a key role in the interplay between obesity, inflammation, insulin resistance and the metabolic syndrome (MetS). Thus, this large population-based cohort investigated whether adiponectin at baseline and/or a decrease in adiponectin during follow-up is associated prospectively with the risk of incident MetS. Methods Using a prospective study design, the development of MetS was examined in 1134 healthy participants from the community. Plasma adiponectin was measured at study entry and again after a median follow-up of 9.4 years (IQR: 9.2–9.7). During follow-up, 187 participants developed MetS, and 439 presented with at least two components of MetS. Results During follow-up, adiponectin decreased in participants who developed MetS, whereas adiponectin was increased in those who did not develop MetS (P <0.001). Those with low adiponectin levels (quartile 1) at baseline had an increased risk of developing MetS (OR: 2.92, 2.08–6.97; P <0.001) compared with those with high levels (quartile 4). After adjusting for confounding variables, low adiponectin levels at baseline remained independently associated with MetS (OR: 2.24, 1.11–4.52; P =0.017). Similarly, participants with a decrease in adiponectin during follow-up also had an increased risk of MetS (OR: 2.96, 2.09–4.18; P <0.001). This association persisted after multivariable adjustments, including for baseline adiponectin (OR: 4.37, 2.77–6.97; P <0.001). Finally, adiponectin levels at follow-up were inversely associated with an increase in the number of components of MetS (P <0.001); geometric mean adiponectin levels were 9.5mg/L (95% CI: 9.0–10.0) for participants with no components vs 7.0mg/L (95% CI: 6.3–7.9) for those with four to five components. Conclusions/interpretation Low plasma adiponectin levels at baseline and decreasing adiponectin levels during follow-up are both associated with an increased risk of MetS.

      PubDate: 2017-04-04T08:54:02Z
       
  • Sex hormone levels are not associated with progression of renal disease in
           male patients with T2DM
    • Abstract: Publication date: April 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 2
      Author(s): E. Feigerlová, P.-J. Saulnier, P. Gourdy, R. Roussel, J.-M. Halimi, E. Gand, D. Dardari, B. Guerci, P. Sosner, M. Marre, P. Zaoui, S. Ragot, S. Hadjadj
      Background Greater renal function decline (RFD) in type 2 diabetes (T2DM) has been suggested in men compared with women, and imbalances in estrogen/androgen levels have been associated with cardiovascular disease mortality in elderly men, but it remains unclear whether sex hormone disequilibrium is related to diabetic nephropathy (DN) in men with T2DM. Objective This study examined the relationship between sex steroid concentrations and renal outcomes in male T2DM patients. Population and methods Total testosterone (T), total estradiol (E2), sex hormone-binding globulin (SHBG), and total and calculated free (cf) E2/T ratios were compared in 735 male T2DM patients with (n =513) and without (n =222) DN, using a cross-sectional approach. Also, in a pilot complementary prospective nested case-control cohort, total E2/total T and cfE2/cfT were evaluated according to a hard renal outcome (HRO): end-stage renal disease/doubling of baseline serum creatinine (36 HRO cases, 72 HRO controls) and rate of eGFR decline (68 rapid vs 68 slow RFD). Result With the cross-sectional approach, E2 and cfE2 were higher in DN cases vs DN controls (95.5 vs 86.8pmol/L [P =0.0246] and 2.59 vs 2.36pmol/L [P =0.005], respectively). The difference in E2 persisted on multivariate analysis. In the prospective approach, E2 and T concentrations, and total E2/total T and cfE2/cfT2 ratios did not differ in HRO cases vs controls or in patients with rapid vs slow RFD. Conclusion Although positively related to DN in the cross-sectional analysis, progression of renal disease in male patients with T2DM was not related to either sex hormone levels or aromatase index as reflected by E2/T ratio.

      PubDate: 2017-04-04T08:54:02Z
       
  • Impaired development and dysfunction of endothelial progenitor cells in
           type 2 diabetic mice
    • Abstract: Publication date: April 2017
      Source:Diabetes & Metabolism, Volume 43, Issue 2
      Author(s): S. Tsukada, H. Masuda, S.Y. Jung, J. Yun, S. Kang, D.Y. Kim, J.H. Park, S.T. Ji, S.-M. Kwon, T. Asahara
      Aim Dysfunction of circulating endothelial progenitor cells (EPCs) has been shown to affect the development of microvascular diseases in diabetes patients. The aim of this study was to elucidate the development and mechanical dysfunction of EPCs in type 2 diabetes (T2D). Methods The colony-forming capacity of EPCs and differentiation potential of bone marrow (BM) c-Kit(+)/Sca-I(+) lineage-negative mononuclear cells (KSL) were examined in T2D mice, db/db mice and KKAy mice, using EPC colony-forming assay (EPC-CFA). Results T2D mice had fewer BM stem/progenitor cells, and proliferation of KSL was lowest in the BM of db/db mice. In T2D mice, the frequency of large colony-forming units (CFUs) derived from BM-KSL was highly reduced, indicating dysfunction of differentiation into mature EPCs. Only a small number of BM-derived progenitors [CD34(+) KSL cells], which contribute to the supply of EPCs for postnatal neovascularization, was also found. Furthermore, in terms of their plasticity to transdifferentiate into various cell types, BM-KSL exhibited a greater potential to differentiate into granulocyte macrophages (GMs) than into other cell types. Conclusion T2D affected EPC colony formation and differentiation of stem cells to mature EPCs or haematopoietic cells. These data suggest opposing regulatory mechanisms for differentiation into mature EPCs and GMs in T2D mice.

      PubDate: 2017-04-04T08:54:02Z
       
  • Basal insulin treatment intensification in patients with type 2 diabetes
           mellitus: A comprehensive systematic review of current options
    • Abstract: Publication date: Available online 4 February 2017
      Source:Diabetes & Metabolism
      Author(s): D. Raccah
      Aim As type 2 diabetes mellitus progresses, most patients require treatment with basal insulin in combination with another agent to achieve recommended glycaemic targets. The purpose of this systematic review was to examine the evidence supporting the use of the available add-on treatments [rapid-acting insulin (RAI), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), dipeptidyl peptidase (DPP)-4 inhibitors and sodium–glucose cotransporter-2 (SGLT-2) inhibitors] to basal insulin. Methods MEDLINE, EMBASE and EBSCOhost were searched for English-language articles, and all those captured were original articles (case studies and narrative reviews were omitted). Data on study design, population demographics, interventions and outcomes were tabulated. The extracted outcome data included changes in glycated haemoglobin (HbA1c), fasting plasma glucose (FPG) and postprandial plasma glucose (PPG), as well as body weight and safety data. Results A total of 88 publications were deemed relevant. All treatments reduced HbA1c and FPG. The most pronounced reductions in PPG, an unmet need in patients not controlled by basal insulin, were seen following administration of RAIs and short-acting GLP-1 RAs, although data for this outcome are generally lacking. Body weight benefits were observed with GLP-1 RAs and SGLT-2 inhibitors. However, as only articles in English were included, the result was a possible publication bias, while the diversity of study designs and drug combinations limited comparisons between studies. Conclusion The evidence supports effectiveness of the available add-on treatments to basal insulin. However, other factors, such as potential body-weight increases, convenience/compliance and adverse events, particularly hypoglycaemia, should be considered on a patient-by-patient basis to optimalize treatment outcomes.

      PubDate: 2017-02-05T01:29:20Z
       
  • Effects of reducing blood pressure on renal outcomes in patients with type
           2 diabetes: Focus on SGLT2 inhibitors and EMPA-REG OUTCOME
    • Abstract: Publication date: Available online 30 January 2017
      Source:Diabetes & Metabolism
      Author(s): A.J. Scheen, P. Delanaye
      Empagliflozin, a sodium–glucose cotransporter type 2 (SGLT2) inhibitor, has enabled remarkable reductions in cardiovascular and all-cause mortality as well as in renal outcomes in patients with type 2 diabetes (T2D) and a history of cardiovascular disease in the EMPA-REG OUTCOME. These results have been attributed to haemodynamic rather than metabolic effects, in part due to the osmotic/diuretic action of empagliflozin and the reduction in arterial blood pressure (BP). The present narrative review includes the results of meta-analyses of trials evaluating the effects on renal outcomes of lowering BP in patients with T2D, with a special focus on the influence of baseline and achieved systolic BP, and compares the renal outcome results of the EMPA-REG OUTCOME with those of other major trials with inhibitors of the renin–angiotensin system in patients with T2D and the preliminary findings with other SGLT2 inhibitors, and also evaluates post hoc analyses from the EMPA-REG OUTCOME of special interest as regards the BP-lowering hypothesis and renal function. While systemic BP reduction associated to empagliflozin therapy may have contributed to the renal benefits reported in EMPA-REG OUTCOME, other local mechanisms related to kidney homoeostasis most probably also played a role in the overall protection observed in the trial.

      PubDate: 2017-02-05T01:29:20Z
       
 
 
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