Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus.
Skeletal muscle resistance to insulin is related to accumulation of lipid-derived products, but it is not clear whether this accumulation is caused by skeletal muscle mitochondrial dysfunction. Diabetes and obesity are reported to have a selective effect on the function of subsarcolemmal and interfi...
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Public Library of Science (PLoS)
2017-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183978&type=printable |
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| author | Nicola Lai China Kummitha Charles Hoppel |
| author_facet | Nicola Lai China Kummitha Charles Hoppel |
| author_sort | Nicola Lai |
| collection | DOAJ |
| description | Skeletal muscle resistance to insulin is related to accumulation of lipid-derived products, but it is not clear whether this accumulation is caused by skeletal muscle mitochondrial dysfunction. Diabetes and obesity are reported to have a selective effect on the function of subsarcolemmal and interfibrillar mitochondria in insulin-resistant skeletal muscle. The current study investigated the role of the subpopulations of mitochondria in the pathogenesis of insulin resistance in the absence of obesity. A non-obese spontaneous rat model of type 2 diabetes mellitus, (Goto-Kakizaki), was used to evaluate function and biochemical properties in both populations of skeletal muscle mitochondria. In subsarcolemmal mitochondria, minor defects are observed whereas in interfibrillar mitochondria function is preserved. Subsarcolemmal mitochondria defects characterized by a mild decline of oxidative phosphorylation efficiency are related to ATP synthase and structural alterations of inner mitochondria membrane but are considered unimportant because of the absence of defects upstream as shown with polarographic and spectrophometric assays. Fatty acid transport and oxidation is preserved in both population of mitochondria, whereas palmitoyl-CoA increased 25% in interfibrillar mitochondria of diabetic rats. Contrary to popular belief, these data provide compelling evidence that mitochondrial function is unaffected in insulin-resistant skeletal muscle from T2DM non-obese rats. |
| format | Article |
| id | doaj-art-58edd0bfbe4c4e3ea648555a7d84adc1 |
| institution | Kabale University |
| issn | 1932-6203 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
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| series | PLoS ONE |
| spelling | doaj-art-58edd0bfbe4c4e3ea648555a7d84adc12025-01-18T05:31:08ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01128e018397810.1371/journal.pone.0183978Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus.Nicola LaiChina KummithaCharles HoppelSkeletal muscle resistance to insulin is related to accumulation of lipid-derived products, but it is not clear whether this accumulation is caused by skeletal muscle mitochondrial dysfunction. Diabetes and obesity are reported to have a selective effect on the function of subsarcolemmal and interfibrillar mitochondria in insulin-resistant skeletal muscle. The current study investigated the role of the subpopulations of mitochondria in the pathogenesis of insulin resistance in the absence of obesity. A non-obese spontaneous rat model of type 2 diabetes mellitus, (Goto-Kakizaki), was used to evaluate function and biochemical properties in both populations of skeletal muscle mitochondria. In subsarcolemmal mitochondria, minor defects are observed whereas in interfibrillar mitochondria function is preserved. Subsarcolemmal mitochondria defects characterized by a mild decline of oxidative phosphorylation efficiency are related to ATP synthase and structural alterations of inner mitochondria membrane but are considered unimportant because of the absence of defects upstream as shown with polarographic and spectrophometric assays. Fatty acid transport and oxidation is preserved in both population of mitochondria, whereas palmitoyl-CoA increased 25% in interfibrillar mitochondria of diabetic rats. Contrary to popular belief, these data provide compelling evidence that mitochondrial function is unaffected in insulin-resistant skeletal muscle from T2DM non-obese rats.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183978&type=printable |
| spellingShingle | Nicola Lai China Kummitha Charles Hoppel Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. PLoS ONE |
| title | Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. |
| title_full | Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. |
| title_fullStr | Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. |
| title_full_unstemmed | Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. |
| title_short | Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus. |
| title_sort | defects in skeletal muscle subsarcolemmal mitochondria in a non obese model of type 2 diabetes mellitus |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183978&type=printable |
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