Diabetes (DIABETES )
Diabetes publishes original research about the physiology and pathophysiology of diabetes mellitus. Submitted manuscripts can report any aspect of laboratory, animal, or human research. Emphasis is on investigative reports focusing on areas such as the pathogenesis of diabetes and its complications, normal and pathologic pancreatic islet function and intermediary metabolism, pharmacological mechanisms of drug and hormone action, and biochemical and molecular aspects of normal and abnormal biological processes. Studies in the areas of diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus are not published.
- Impact factor7.90Show impact factor historyHide impact factor history
- 5-year impact8.61
- Cited half-life8.00
- Immediacy index1.54
- Article influence3.03
- WebsiteDiabetes website
- Other titlesDiabetes
- Material typePeriodical, Internet resource
- Document typeJournal / Magazine / Newspaper, Internet Resource
- Archiving status unclear
- Author can archive a post-print version
- On author website, institutional repository or funding body (eg NIH)
- Post-prints must include the set statement (see copyright assignment information)
- Must link to publisher version
- Must be identical to final accepted version
- Authors may make erratum at any time
- Publisher's version/PDF cannot be used
- Classification blue
Publications in this journal
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ABSTRACT: We have investigated the role of heat shock (HS) in preventing insulin resistance induced endothelial dysfunction. To best of our knowledge here we report for the first time that insulin resistance inhibits vascular HSP72 expression. Heat shock treatment (HS, 41°C for 20 min) restored the HSP72 expression. High fat diet (HFD) fed insulin resistant rats show attenuated Ang-(1-7) induced vasodilator effect, eNOS phosphorylation, AMPK phosphorylation and SIRT1 expression. Interestingly, HS prevented this attenuation. We also provide first evidence that HFD fed rats show increased vascular DNMT1 expression and HS prevented this increase. Our data shows that in HFD fed rats HS prevented loss in the expression of Ang-(1-7) receptor Mas and ACE2 responsible for vascular complications. Further, inhibition of eNOS (L-NAME), Mas (A-779) and SIRT1 (Nicotinamide) prevented the favourable effects of HS. This suggests that HS augmented Ang-(1-7) signalling via Mas/eNOS/SIRT1 pathway. Our study, for the first time, suggests that induction of intracellular HSP72 alters DNMT1 expression and may function as epigenetic regulator of SIRT1 and eNOS expression. We propose that induction of HSP72 is a novel approach to prevent insulin resistance induced vascular complications.Diabetes 11/2013;
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ABSTRACT: In patients with diabetes, impaired ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13) proteolysis of highly thrombogenic von Willebrand factor (VWF) multimers may accelerate renal and cardiovascular complications. Restoring physiological VWF handling might contribute to ACE inhibitors' (ACEi) reno- and cardioprotective effects. To assess how Pro618Ala ADAMTS13 variants and related proteolytic activity interact with ACEi therapy in predicting renal and cardiovascular complications, we genotyped 1,163 normoalbuminuric type 2 diabetic patients from BErgamo NEphrologic DIabetes Complications Trial (BENEDICT). Interaction between Pro618Ala and ACEi was significant in predicting both renal and combined renal and cardiovascular events. The risk for renal or combined events versus reference Ala carriers on ACEi progressively increased from Pro/Pro homozygotes on ACEi (hazard ratio 2.80 [95% CI 0.849-9.216] and 1.58 [0.737-3.379], respectively) to Pro/Pro homozygotes on non-ACEi (4.77 [1.484-15.357] and 1.99 [0.944-4.187]) to Ala carriers on non-ACEi (8.50 [2.416-29.962] and 4.00 [1.739-9.207]). In a substudy, serum ADAMTS13 activity was significantly lower in Ala carriers than in Pro/Pro homozygotes and in case subjects with renal, cardiovascular, or combined events than in diabetic control subjects without events. ADAMTS13 activity significantly and negatively correlated with all outcomes. In patients with diabetes, ADAMTS13 618Ala variant associated with less proteolytic activity, higher risk of chronic complications, and better response to ACEi therapy. Screening for Pro618Ala polymorphism may help identify patients with diabetes at highest risk who may benefit the most from early reno- and cardioprotective therapy.Diabetes 10/2013; 62(10):3599-609.
Article: hla three snpsDiabetes 03/2013;
- Diabetes 01/2013;
- Diabetes 01/2013; 62(1):254-60.
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ABSTRACT: Mutations in the gene encoding glucokinase (GCK) cause a mild hereditary form of diabetes termed maturity onset diabetes of the young (MODY) 2 or GCK-MODY. The disease does not progress over time and diabetes complications rarely develop. It has therefore been suggested that GCK-MODY represents a metabolically compensated condition but experimental support for this notion is lacking. Here, we profiled metabolites in serum from patients with MODY 1 (HNF4A), MODY 2 (GCK), MODY 3 (HNF1A), type 2 diabetes, and healthy individuals, to characterize metabolic perturbations caused by specific mutations. Analysis of four GCK-MODY patients revealed a metabolite pattern similar to that of healthy individuals while other forms of diabetes differed markedly in their metabolite profiles. Furthermore, despite elevated glucose concentrations, carriers of GCK mutations showed lower levels of free fatty acids and triglycerides than healthy controls. The metabolite profiling was confirmed by enzymatic assays and replicated in a cohort of 11 GCK-MODY patients. Elevated levels of fatty acids are known to associate with ß-cell dysfunction, insulin resistance and increased incidence of late complications. Our results show that GCK-MODY represents a metabolically normal condition, which may contribute to the lack of late complications and the non-progressive nature of the disease.Diabetes 08/2012;
- Diabetes 06/2012;
- Diabetes 10/2011;
- Diabetes 01/2011; 60:A163.
- Diabetes 06/2010; 59(Suppl1):A397-A397.
Article: Obesity is an FGF21 resistant stateDiabetes 01/2010; 59(6).
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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Bentham Science Publishers
ISSN: 1875-6212, Impact factor: 2.82