title: A possible link between hepatic mitochondrial dysfunction   and diet-induced insulin resistance.
abstract: BACKGROUND
  Mitochondria are the main cellular sites devoted to ATP production and lipid oxidation. Therefore, the mitochondrial dysfunction could be an important determinant of cellular fate of circulating lipids, that accumulate in the cytoplasm, if they are not oxidized. The ectopic fat accumulation is associated with the development of insulin resistance, and a link between mitochondrial dysfunction and insulin resistance has been proposed.
  
  
  METHODS
  Recent data on the possible link existing between mitochondrial dysfunction in the liver and diet induced obesity will be summarized, focusing on the three factors that affect the mitochondrial oxidation of metabolic fuels, i.e. organelle number, organelle activity, and energetic efficiency of the mitochondrial machinery in synthesizing ATP. Search in PubMed relevant articles from 2003 to 2014 was conducted, by using query “liver mitochondria and obesity” “hepatic mitochondria and obesity” “liver mitochondria and high fat diet” and “hepatic mitochondria and high fat diet” and including related articles by the same groups.
  
  
  RESULTS
  Several works, by using different physiological approaches, have dealt with alteration in mitochondrial function in obesity and diabetes. Most results show that hepatic mitochondrial function is impaired in models of obesity and insulin resistance induced by high-fat or highfructose feeding.
  
  
  CONCLUSIONS
  Since mitochondria are the main producers of both cellular energy and free radicals, dysfunctional mitochondria could play an important role in the development of insulin resistance and ectopic fat storage in the liver, thus supporting the emerging idea that mitochondrial dysfunction is closely related to the development of obesity, type 2 diabetes mellitus and non-alcoholic steatohepatitis.
authors.forename: Raffaella
authors.initials: R
authors.lastname: Crescenzo
authors.forename: Francesca
authors.initials: F
authors.lastname: Bianco
authors.forename: Arianna
authors.initials: A
authors.lastname: Mazzoli
authors.forename: Antonia
authors.initials: A
authors.lastname: Giacco
authors.forename: Giovanna
authors.initials: G
authors.lastname: Liverini
authors.forename: Susanna
authors.initials: S
authors.lastname: Iossa
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D059305:Diet, High-Fat / Q000009:adverse effects*; D004195:Disease Models, Animal; D005632:Fructose / Q000008:administration & dosage / Q000009:adverse effects*; D006801:Humans; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008930:Mitochondria, Liver / Q000473:pathology*; D065626:Non-alcoholic Fatty Liver Disease / Q000503:physiopathology; D009765:Obesity / Q000503:physiopathology
chemical_list: D005632:Fructose