Ghosh 2011 Abstract IOC65

From Bioblast
Ghosh SA, Lertwattanarak R, Richardson AG, Van Remmen H, DeFronzo RA, Musi N (2011) Effect of aging and exercise training on mitochondrial function in skeletal muscle. MiPNet16.03.

Link: MiPNet16.03 IOC65 Abstracts

Ghosh SA, Lertwattanarak R, Richardson AG, Van Remmen H, DeFronzo RA, Musi N (2011)

Event: IOC65

Older subjects have a high risk of developing metabolic abnormalities such as impaired glucose tolerance (IGT) and type 2 diabetes. Decreased mitochondrial function, manifested by reduced ATP synthesis and increased reactive oxygen species (ROS) release in peripheral tissues such as muscle, has been implicated in the pathogenesis of these metabolic abnormalities. Our goals were to examine: (i) whether aging in normal-glucose tolerant (NGT) subjects affects ex vivo ATP and ROS production by isolated muscle mitochondria; (ii) whether older subjects with IGT have mitochondrial dysfunction; and (iii) whether aerobic exercise training can improve mitochondrial function (increase ATP and reduce ROS production) in muscle from older subjects. ATP synthesis was lower in older NGT and older IGT versus younger NGT subjects. Surprisingly, mitochondria from older (NGT and IGT) subjects had a reduction in ROS production compared with younger individuals. ATP and ROS production was similar in older NGT and IGT subjects. Exercise improved mitochondrial function (ATP synthesis) in older NGT, older IGT, and younger individuals. Mitochondrial ROS production also increased after training in all three groups. Proteomic analysis of fraction enriched in mitochondria revealed downregulation of several electron transport chain proteins which was reversed by training. In summary, aging is associated with mitochondrial dysfunction manifested by reduced ATP synthesis, and the severity of mitochondrial dysfunction is similar between NGT and IGT subjects. Despite decreased mitochondrial function (i.e. ATP synthesis), older subjects had a reduction in ROS production. In addition, physical activity reverses the mitochondrial phenotype (proteome and function) observed in old mitochondria.

β€’ Keywords: Aging; Human skeletal muscle; Mitochondria; Exercise; Insulin Resistance

β€’ O2k-Network Lab: US OK Oklahoma City Van Remmen H, US TX San Antonio Musi N

Labels: Pathology: Aging;senescence, Diabetes 

Tissue;cell: Skeletal muscle 

Authors: Sangeeta Ghosh (1), Raweewan Lertwattanarak (1), Arlan G. Richardson(2), Holly Van Remmen(2), Ralph A. DeFronzo(1,3), Nicolas Musi(1, 3, 4)

Affiliations: (1) Diabetes Division, Department of Medicine, University of Texas Health Science Center at San Antonio, Texas. (2) Sam and Ann Barshop Institute for Longevity and Aging Studies. (3) Texas Diabetes Institute, San Antonio, Texas. (4) Geriatric Research, Education, and Clinical Center, Audie L. Murphy VA Hospital, San Antonio Texas.

References: Ghosh S, Lertwattanarak R, Lefort N, Molina-Carrion M, Joya-Galeana J, Bowen BP, de Jesus Garduno-Garcia J, Abdul-Ghani M, Richardson A, DeFronzo RA, Mandarino L, Van Remmen H, Musi N (2011) Reduction in reactive oxygen species production by mitochondria from aging human muscle. Diabetes 60: 2051-2060.

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