Diabetes (DIABETES)

Publications in this journal

• Article: Methods for Assessing Mitochondrial Function in Diabetes

  C.G.R. Perry, D.A. Kane, I.R. Lanza, P.D. Neufer
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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 snps

  Nguyen, Morahan
  Diabetes 03/2013;
• Article: Corneal confocal microscopy detects early nerve regeneration in diabetic neuropathy after simultaneous pancreas and kidney transplantation

  Tavakoli M, Mitu-Pretorian M, Petropoulos IN, Fadavi H, Asghar O, Alam U, Ponirakis G, Jeziorska M, Marshall A, Efron N, Boulton AJ, Augustine T, Malik RA
  Diabetes 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 Mellitus

  Tobias Duennwald, Luciano Bernardi, Daniel Gordin, Anna Sandelin, Anna Syreeni, Christopher Fogarty, Janne P Kytö, Hannes Gatterer, Markku Lehto, Sohvi Hörkkö
  Diabetes 01/2013;
• Article: Metabolite profiling reveals normal metabolic control in carriers of mutations in the glucokinase gene (MODY2)

  Peter Spégel, Ella Ekholm, Tiinamaija Toumi, Leif Groop, Hindrik Mulder, Karin Filipsson
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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;
• Article: Adoptive Transfer of Immunomodulatory M2 Macrophages Prevents Type 1 Diabetes in NOD Mice.

  Parsa R, Andresen P, Gillett A, Mia S, Zhang XM, Mayans S, Holmberg D, Harris RA
  Diabetes 06/2012;
• Article: GLUT2 accumulation in enterocyteapical and intracellular membrane: a study in morbidly obese human subjects and ob/ob and high fat-fed mice

  Ait-Omar A, Monteiro-Sepulveda M, Poitou C, Le Gall M, Cotillard A, Gilet J, Garbin K, Houllier A, Chateau D
  Diabetes 10/2011;
• Article: Characterization of microRNAs derived from the plasmacytoma variant translocation 1 gene (PVT1) as mediator of diabetic kidney disease

  M. Lucrecia Alvarez
  Diabetes 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 Rats

  B. P. Cummings, K. L. Stanhope, J. L. Graham, D. G. Baskin, S. C. Griffen, C. Nilsson, A. Sams, L. B. Knudsen, K. Raun, P. J. Havel
  Diabetes 01/2010; 59(9).
• Article: Characterization of the plasmacytoma variant translocation 1 gene (PVT1) as mediator of diabetic kidney disease

  M. Lucrecia Alvarez
  Diabetes 01/2010; 59:A1-2.
• Article: GLP-1 Prevents AGEs-Induced Pancreatic Beta Cell Dysfunction

  Alessandra Puddu, Arianna Durante, Daniela Storace, Patrizio Odetti, Giorgio L Viviani
  Diabetes 06/2009; 58:A625.
• Article: Breast-Feeding Modifies the Association of PPAR 2 Polymorphism Pro12Ala With Growth in Early Life: The Generation R Study

  D. O. Mook-Kanamori, E. A. P. Steegers, A. G. Uitterlinden, H. A. Moll, C. M. van Duijn, A. Hofman, V. W. V. Jaddoe
  Diabetes 01/2009; 58(4):992-998.
• Article: Exogenous Glucose-Dependent Insulinotropic Polypeptide Worsens Post prandial Hyperglycemia in T ype 2 Diabetes

  C. W. Chia, O. D. Carlson, W. Kim, Y.-K. Shin, C. P. Charles, H. S. Kim, D. L. Melvin, J. M. Egan
  Diabetes 01/2009; 58(6):1342-1349.
• Article: Common Variants of Hepatocyte Nuclear Factor 1 Are Associated With Type 2 Diabetes in a Chinese Population

  C. Wang, C. Hu, R. Zhang, Y. Bao, X. Ma, J. Lu, W. Qin, X. Shao, J. Xu, H. Lu, K. Xiang, W. Jia
  Diabetes 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 Isoform

  O. Escribano, C. Guillen, C. Nevado, A. Gomez-Hernandez, C. R. Kahn, M. Benito
  Diabetes 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 Remodeling

  Y. Wang, W. Feng, W. Xue, Y. Tan, D. W. Hein, X.-K. Li, L. Cai
  Diabetes 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 Defects

  P. A. M. Roest, D. G. M. Molin, C. G. Schalkwijk, L. van Iperen, P. Wentzel, U. J. Eriksson, A. C. Gittenberger-de Groot
  Diabetes 01/2009; 58(5):1222-1228.