title: Mitochondrial dysfunction and complications associated with diabetes.
abstract: BACKGROUND
  Diabetes is a metabolic syndrome that results in chronically increased blood glucose (hyperglycaemia) due to defects either in insulin secretion consequent to the loss of beta cells in the pancreas (type 1) or to loss of insulin sensitivity in target organs in the presence of normal insulin secretion (type 2). Long term hyperglycaemia can lead to a number of serious health-threatening pathologies, or complications, especially in the kidney, heart, retina and peripheral nervous system.
  
  
  METHODS
  Here we summarise the current literature on the role of the mitochondria in complications associated with diabetes, and the limitations and potential of rodent models to explore new modalities to limit complication severity.
  
  
  CONCLUSIONS
  Prolonged hyperglycaemia results in perturbation of catabolic pathways and in an over-production of ROS by the mitochondria, which in turn may play a role in the development of diabetic complications. Furthermore, current models don't offer a comprehensive recapitulation of these complications.
  
  
  CONCLUSIONS
  The onset of complications associated with type 1 diabetes can be varied, even with tightly controlled blood glucose levels. The potential role of inherited, mild mitochondrial dysfunction in accelerating diabetic complications, both in type 1 and 2 diabetes, remains unexplored. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research.
authors.affiliation: Centre for Eye Research Australia, University of Melbourne, Department of Ophthalmology, Royal Victorian Eye and Ear Hospital, 32 Gisborne Street East, Melbourne, Victoria 3002, Australia; University of Melbourne Department of Medicine, St. Vincent's Hospital, Fitzroy, Melbourne, Victoria 3065, Australia.
authors.forename: Rachel
authors.initials: R
authors.lastname: Blake
authors.affiliation: Centre for Eye Research Australia, University of Melbourne, Department of Ophthalmology, Royal Victorian Eye and Ear Hospital, 32 Gisborne Street East, Melbourne, Victoria 3002, Australia; University of Melbourne Department of Medicine, St. Vincent's Hospital, Fitzroy, Melbourne, Victoria 3065, Australia. Electronic address: i.trounce@unimelb.edu.au.
authors.forename: Ian A
authors.initials: IA
authors.lastname: Trounce
mesh_terms: D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use; D008687:Metformin / Q000494:pharmacology / Q000627:therapeutic use; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D028361:Mitochondrial Diseases / Q000209:etiology* / Q000503:physiopathology
chemical_list: D007328:Insulin; D008687:Metformin
keywords: Complication; Diabetes; Mitochondria; Mouse model; Oxidative phosphorylation; Reactive oxygen species