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000139937 0247_ $$2doi$$a10.1007/s00125-018-4602-6
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000139937 041__ $$aEnglish
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000139937 1001_ $$aMonaco, Cynthia M F$$b0
000139937 245__ $$aAltered mitochondrial bioenergetics and ultrastructure in the skeletal muscle of young adults with type 1 diabetes.
000139937 260__ $$aHeidelberg$$bSpringer$$c2018
000139937 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2018-04-18
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000139937 520__ $$aA 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.
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000139937 650_7 $$2NLM Chemicals$$aInsulin
000139937 650_7 $$0BBX060AN9V$$2NLM Chemicals$$aHydrogen Peroxide
000139937 650_7 $$0SY7Q814VUP$$2NLM Chemicals$$aCalcium
000139937 650_2 $$2MeSH$$aAdult
000139937 650_2 $$2MeSH$$aBody Mass Index
000139937 650_2 $$2MeSH$$aCalcium: chemistry
000139937 650_2 $$2MeSH$$aDiabetes Mellitus, Type 1: metabolism
000139937 650_2 $$2MeSH$$aDiabetes Mellitus, Type 1: pathology
000139937 650_2 $$2MeSH$$aEnergy Metabolism
000139937 650_2 $$2MeSH$$aExercise: physiology
000139937 650_2 $$2MeSH$$aFemale
000139937 650_2 $$2MeSH$$aHumans
000139937 650_2 $$2MeSH$$aHydrogen Peroxide: metabolism
000139937 650_2 $$2MeSH$$aInsulin: metabolism
000139937 650_2 $$2MeSH$$aMale
000139937 650_2 $$2MeSH$$aMicroscopy, Electron, Transmission
000139937 650_2 $$2MeSH$$aMicroscopy, Fluorescence
000139937 650_2 $$2MeSH$$aMitochondria: metabolism
000139937 650_2 $$2MeSH$$aMitochondria: ultrastructure
000139937 650_2 $$2MeSH$$aMuscle, Skeletal: metabolism
000139937 650_2 $$2MeSH$$aMuscle, Skeletal: pathology
000139937 650_2 $$2MeSH$$aMuscle, Skeletal: ultrastructure
000139937 650_2 $$2MeSH$$aOxygen Consumption
000139937 650_2 $$2MeSH$$aYoung Adult
000139937 7001_ $$aHughes, Meghan C$$b1
000139937 7001_ $$aRamos, Sofhia V$$b2
000139937 7001_ $$aVarah, Nina E$$b3
000139937 7001_ $$0P:(DE-2719)2811203$$aLamberz, Christian$$b4$$udzne
000139937 7001_ $$aRahman, Fasih A$$b5
000139937 7001_ $$aMcGlory, Chris$$b6
000139937 7001_ $$aTarnopolsky, Mark A$$b7
000139937 7001_ $$aKrause, Matthew P$$b8
000139937 7001_ $$aLaham, Robert$$b9
000139937 7001_ $$0P:(DE-HGF)0$$aHawke, Thomas J$$b10$$eCorresponding author
000139937 7001_ $$aPerry, Christopher G R$$b11
000139937 77318 $$2Crossref$$3journal-article$$a10.1007/s00125-018-4602-6$$b : Springer Science and Business Media LLC, 2018-04-18$$n6$$p1411-1423$$tDiabetologia$$v61$$x0012-186X$$y2018
000139937 773__ $$0PERI:(DE-600)1458993-X$$a10.1007/s00125-018-4602-6$$gVol. 61, no. 6, p. 1411 - 1423$$n6$$p1411-1423$$q61:6<1411 - 1423$$tDiabetologia$$v61$$x0012-186X$$y2018
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