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 factor8.29Show impact factor historyHide impact factor history
- WebsiteDiabetes website
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
Publications in this journal
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ABSTRACT: A growing body of research is investigating the potential contribution of mitochondrial function to the etiology of type 2 diabetes. Numerous in vitro, in situ, and in vivo methodologies are available to examine various aspects of mitochondrial function, each requiring an understanding of their principles, advantages, and limitations. This review provides investigators with a critical overview of the strengths, limitations and critical experimental parameters to consider when selecting and conducting studies on mitochondrial function. In vitro (isolated mitochondria) and in situ (permeabilized cells/tissue) approaches provide direct access to the mitochondria, allowing for study of mitochondrial bioenergetics and redox function under defined substrate conditions. Several experimental parameters must be tightly controlled, including assay media, temperature, oxygen concentration, and in the case of permeabilized skeletal muscle, the contractile state of the fibers. Recently developed technology now offers the opportunity to measure oxygen consumption in intact cultured cells. Magnetic resonance spectroscopy provides the most direct way of assessing mitochondrial function in vivo with interpretations based on specific modeling approaches. The continuing rapid evolution of these technologies offers new and exciting opportunities for deciphering the potential role of mitochondrial function in the etiology and treatment of diabetes.Diabetes 04/2013; 62(4):1041-1053.
Article: hla three snpsDiabetes 03/2013;
Article: Corneal confocal microscopy detects early nerve regeneration in diabetic neuropathy after simultaneous pancreas and kidney transplantationDiabetes 01/2013; 62(1):254-60.
Article: Effects of a Single Bout of Interval Hypoxia on Cardio-Respiratory Control in Patients with Type 1 Diabetes MellitusDiabetes 01/2013;
Article: Metabolite profiling reveals normal metabolic control in carriers of mutations in the glucokinase gene (MODY2)[show abstract] [hide abstract]
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;
Article: GLUT2 accumulation in enterocyteapical and intracellular membrane: a study in morbidly obese human subjects and ob/ob and high fat-fed miceDiabetes 10/2011;
Article: Characterization of microRNAs derived from the plasmacytoma variant translocation 1 gene (PVT1) as mediator of diabetic kidney diseaseDiabetes 01/2011; 60:A163.
Article: Chronic Administration of the Glucagon-Like Peptide1 (GLP-1) Analog, Liraglutide, Delays the Onset of Diabetes and Lowers Triglycerides in UCD-T2DM RatsDiabetes 01/2010; 59(9).
Article: Characterization of the plasmacytoma variant translocation 1 gene (PVT1) as mediator of diabetic kidney diseaseDiabetes 01/2010; 59:A1-2.
Diabetes 06/2009; 58:A625.
Article: Breast-Feeding Modifies the Association of PPAR 2 Polymorphism Pro12Ala With Growth in Early Life: The Generation R StudyDiabetes 01/2009; 58(4):992-998.
Article: Exogenous Glucose-Dependent Insulinotropic Polypeptide Worsens Post prandial Hyperglycemia in T ype 2 DiabetesDiabetes 01/2009; 58(6):1342-1349.
Article: Common Variants of Hepatocyte Nuclear Factor 1 Are Associated With Type 2 Diabetes in a Chinese PopulationDiabetes 01/2009; 58(4):1023-1027.
Article: Cell Hyperplasia Induced by Hepatic Insulin Resistance: Role of a Liver-Pancreas Endocrine Axis Through Insulin Receptor A IsoformDiabetes 01/2009; 58(4):820-828.
Article: Inactivation of GSK-3 by Metallothionein Prevents Diabetes-Related Changes in Cardiac Energy Metabolism, Inflammation, Nitrosative Damage, and RemodelingDiabetes 01/2009; 58(6):1391-1402.
Article: Specific Local Cardiovascular Changes of N -(Carboxymethyl)lysine, Vascular Endothelial Growth Factor, and Smad2 in the Developing Embryos Coincide With Maternal Diabetes-Induced Congenital Heart DefectsDiabetes 01/2009; 58(5):1222-1228.
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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