title: Emerging Concepts in Diabetes: Mitochondrial Dynamics and Glucose Homeostasis.
abstract: BACKGROUND
  Mitochondria form an interconnected and dynamic web that undergoes continuous cycles of fusion and fission events. This phenomenon, known as mitochondrial dynamics, represents a key quality control system to maintain a healthy mitochondrial population but also a mechanism to bioenergetically adapt to the cellular and tissue energetic demands. Consequently, mitochondria can be viewed not only as energy supply organelles but also as energy sensors. It is therefore not surprising that disrupted mitochondrial bioenergetics, concomitantly with alterations in mitochondrial architecture, has been associated with several diseases including metabolic disorders.
  
  
  CONCLUSIONS
  Here, we review current evidences connecting mitochondrial dynamics and bioenergetic alterations with the development of obesity and diabetes-related phenotypes, and how current strategies to alleviate such phenotypes impact on mitochondrial network and function.
authors.affiliation: Diabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona. Spain.
authors.forename: Alicia G
authors.initials: AG
authors.lastname: Gómez-Valadés
authors.affiliation: Biophysics Unit, Department of Physiological Sciences II, IDIBELL-University of Barcelona, Campus de Bellvitge, 08907 L'Hospitalet de Llobregat, Barcelona. Spain.
authors.forename: Alba
authors.initials: A
authors.lastname: Gonzalez-Franquesa
authors.affiliation: Biophysics Unit, Department of Physiological Sciences II, IDIBELL-University of Barcelona, Campus de Bellvitge, 08907 L'Hospitalet de Llobregat, Barcelona. Spain.
authors.forename: Pau
authors.initials: P
authors.lastname: Gama-Perez
authors.affiliation: Diabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centre Esther Koplowitz, C/Rosselló 149-153, 5th floor, 08036 Barcelona. Spain.
authors.forename: Marc
authors.initials: M
authors.lastname: Claret
authors.affiliation: Biophysics Unit, Department of Physiological Sciences II, IDIBELL-University of Barcelona, Campus de Bellvitge, 08907 L'Hospitalet de Llobregat, Barcelona. Spain.
authors.forename: Pablo M
authors.initials: PM
authors.lastname: Garcia-Roves
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001343:Autophagy; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D004734:Energy Metabolism; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D063154:Mitochondrial Dynamics; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009765:Obesity / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D015398:Signal Transduction
chemical_list: D015415:Biomarkers; D001786:Blood Glucose
keywords: Energy metabolism; Type 2 diabetes; fission; fusion; glucose homeostasis; mitochondria; mitochondrial dynamics; obesity