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@ARTICLE{Monaco:139937,
      author       = {Monaco, Cynthia M F and Hughes, Meghan C and Ramos, Sofhia
                      V and Varah, Nina E and Lamberz, Christian and Rahman, Fasih
                      A and McGlory, Chris and Tarnopolsky, Mark A and Krause,
                      Matthew P and Laham, Robert and Hawke, Thomas J and Perry,
                      Christopher G R},
      title        = {{A}ltered mitochondrial bioenergetics and ultrastructure in
                      the skeletal muscle of young adults with type 1 diabetes.},
      journal      = {Diabetologia},
      volume       = {61},
      number       = {6},
      issn         = {0012-186X},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2020-06259},
      pages        = {1411-1423},
      year         = {2018},
      abstract     = {A comprehensive assessment of skeletal muscle
                      ultrastructure and mitochondrial bioenergetics has not been
                      undertaken in individuals with type 1 diabetes. This study
                      aimed to systematically assess skeletal muscle mitochondrial
                      phenotype in young adults with type 1 diabetes.Physically
                      active, young adults (men and women) with type 1 diabetes
                      (HbA1c 63.0 ± 16.0 mmol/mol $[7.9\% ± 1.5\%])$
                      and without type 1 diabetes (control), matched for sex, age,
                      BMI and level of physical activity, were recruited
                      (n = 12/group) to undergo vastus lateralis muscle
                      microbiopsies. Mitochondrial respiration (high-resolution
                      respirometry), site-specific mitochondrial H2O2 emission and
                      Ca2+ retention capacity (CRC) (spectrofluorometry) were
                      assessed using permeabilised myofibre bundles. Electron
                      microscopy and tomography were used to quantify
                      mitochondrial content and investigate muscle ultrastructure.
                      Skeletal muscle microvasculature was assessed by
                      immunofluorescence.Mitochondrial oxidative capacity was
                      significantly lower in participants with type 1 diabetes vs
                      the control group, specifically at Complex II of the
                      electron transport chain, without differences in
                      mitochondrial content between groups. Muscles of those with
                      type 1 diabetes also exhibited increased mitochondrial H2O2
                      emission at Complex III and decreased CRC relative to
                      control individuals. Electron tomography revealed an
                      increase in the size and number of autophagic remnants in
                      the muscles of participants with type 1 diabetes. Despite
                      this, levels of the autophagic regulatory protein,
                      phosphorylated AMP-activated protein kinase
                      (p-AMPKαThr172), and its downstream targets, phosphorylated
                      Unc-51 like autophagy activating kinase 1 (p-ULK1Ser555) and
                      p62, was similar between groups. In addition, no differences
                      in muscle capillary density or platelet aggregation were
                      observed between the groups.Alterations in mitochondrial
                      ultrastructure and bioenergetics are evident within the
                      skeletal muscle of active young adults with type 1 diabetes.
                      It is yet to be elucidated whether more rigorous exercise
                      may help to prevent skeletal muscle metabolic deficiencies
                      in both active and inactive individuals with type 1
                      diabetes.},
      keywords     = {Adult / Body Mass Index / Calcium: chemistry / Diabetes
                      Mellitus, Type 1: metabolism / Diabetes Mellitus, Type 1:
                      pathology / Energy Metabolism / Exercise: physiology /
                      Female / Humans / Hydrogen Peroxide: metabolism / Insulin:
                      metabolism / Male / Microscopy, Electron, Transmission /
                      Microscopy, Fluorescence / Mitochondria: metabolism /
                      Mitochondria: ultrastructure / Muscle, Skeletal: metabolism
                      / Muscle, Skeletal: pathology / Muscle, Skeletal:
                      ultrastructure / Oxygen Consumption / Young Adult / Insulin
                      (NLM Chemicals) / Hydrogen Peroxide (NLM Chemicals) /
                      Calcium (NLM Chemicals)},
      cin          = {AG Alamoudi},
      ddc          = {610},
      cid          = {I:(DE-2719)1013012},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29666899},
      doi          = {10.1007/s00125-018-4602-6},
      url          = {https://pub.dzne.de/record/139937},
}