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WEDNESDAY, April 18, 2018 (HealthDay News) — Physically active young adults with type 1 diabetes have alterations in mitochondrial ultrastructure and bioenergetics within skeletal muscle, according to a study published online April 18 in Diabetologia<\/i>.<\/p>\n
Cynthia M.F. Monaco, from McMaster University in Hamilton, Canada, and colleagues examined skeletal muscle mitochondrial phenotype in 12 physically active, young adults with type 1 diabetes and 12 controls without diabetes matched for sex, age, body mass index, and level of physical activity. Participants underwent vastus lateralis muscle microbiopsies.<\/p>\n
The researchers found that, compared with the control group, participants with type 1 diabetes had significantly lower mitochondrial oxidative capacity, specifically at Complex II of the electron transport chain, with no between-group differences in mitochondrial content. Increased mitochondrial H2<\/sub>O2<\/sub> emission at Complex III and decreased Ca2+<\/sup> retention capacity was seen in muscles of those with type 1 diabetes relative to controls. Participants with type 1 diabetes had an increase in the size and number of autophagic remnants in muscles; however, levels of the autophagic regulatory protein, phosphorylated AMP-activated protein kinase, and its downstream targets were similar between groups.<\/p>\n “Alterations in mitochondrial ultrastructure and bioenergetics are evident within the skeletal muscle of active young adults with type 1 diabetes,” the authors write. “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.”<\/p>\n Abstract\/Full Text (subscription or payment may be required)<\/a><\/p>\n <\/i><\/p>\n