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Fructose induces mitochondrial dysfunction and triggers apoptosis in skeletal muscle cells by provoking oxidative stress

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dc.contributor.author Natasha, J
dc.contributor.author Maurya, C K
dc.contributor.author Deepti, A
dc.contributor.author Deepa, R A
dc.contributor.author Prathapan, A
dc.contributor.author Raj, P S
dc.contributor.author Raghu, K G
dc.contributor.author Shasi, V K
dc.contributor.author Akhilesh Kumar, T
dc.date.accessioned 2015-07-20T06:46:22Z
dc.date.available 2015-07-20T06:46:22Z
dc.date.issued 2015
dc.identifier.citation Apoptosis 20(7):930-947;Jul 2015 en_US
dc.identifier.issn 1360-8185
dc.identifier.uri http://ir.niist.res.in:8080/jspui/handle/123456789/1848
dc.description.abstract Mitochondrial dysfunction in skeletal muscle has been implicated in the development of insulin resistance, a major characteristic of type 2 diabetes. There is evidence that oxidative stress results from the increased production of reactive oxygen species and reactive nitrogen species leads to mitochondrial dysfunction, tissue damage, insulin resistance, and other complications observed in type 2 diabetes. It has been suggested that intake of high fructose contributes to insulin resistance and other metabolic disturbances. However, there is limited information about the direct effect of fructose on the mitochondrial function of skeletal muscle, the major metabolic determinant of whole body insulin activity. Here, we assessed the effect of fructose exposure on mitochondria-mediated mechanisms in skeletal muscle cells. Exposure of L6 myotubes to high fructose stimulated the production of mitochondrial reactive oxygen species and nitric oxide (NO), and the expression of inducible NO synthase. Fructose-induced oxidative stress was associated with increased translocation of nuclear factor erythroid 2-related factor-2 to the nucleus, decreases in mitochondrial DNA content and mitochondrial dysfunctions, as evidenced by decreased activities of citrate synthase and mitochondrial dehydrogenases, loss of mitochondrial membrane potential, decreased activity of the mitochondrial respiratory complexes, and impaired mitochondrial energy metabolism. Furthermore, positive Annexin-propidium iodide staining and altered expression of Bcl-2 family members and caspases in L6 myotubes indicated that the cells progressively became apoptotic upon fructose exposure. Taken together, these findings suggest that exposure of skeletal muscle cells to fructose induced oxidative stress that decreased mitochondrial DNA content and triggered mitochondrial dysfunction, which caused apoptosis. en_US
dc.language.iso en en_US
dc.publisher Springer en_US
dc.subject Fructose en_US
dc.subject Skeletal muscle en_US
dc.subject Mitochondrial dysfunction en_US
dc.subject Apoptosis en_US
dc.subject Oxidative stress en_US
dc.title Fructose induces mitochondrial dysfunction and triggers apoptosis in skeletal muscle cells by provoking oxidative stress en_US
dc.type Article en_US

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