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- Pablo Esteban Morales
- Departamento de Tecnología Médica, Facultad de Medicina, Universidad de Chile, Santiago, Chile
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- Jose Luis Bucarey
- CIDIS-AC, Escuela de Medicina, Universidad de Valparaiso, Valparaiso, Chile
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- Alejandra Espinosa
- Departamento de Tecnología Médica, Facultad de Medicina, Universidad de Chile, Santiago, Chile
書誌事項
- 公開日
- 2017
- 権利情報
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- http://creativecommons.org/licenses/by/4.0/
- DOI
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- 10.1155/2017/1789395
- 公開者
- Wiley
この論文をさがす
説明
<jats:p>Skeletal muscle is one of the main regulators of carbohydrate and lipid metabolism in our organism, and therefore, it is highly susceptible to changes in glucose and fatty acid (FA) availability. Skeletal muscle is an extremely complex tissue: its metabolic capacity depends on the type of fibers it is made up of and the level of stimulation it undergoes, such as acute or chronic contraction. Obesity is often associated with increased FA levels, which leads to the accumulation of toxic lipid intermediates, oxidative stress, and autophagy in skeletal fibers. This lipotoxicity is one of the most common causes of insulin resistance (IR). In this scenario, the “isolation” of certain lipids in specific cell compartments, through the action of the specific lipid droplet, perilipin (PLIN) family of proteins, is conceived as a lifeguard compensatory strategy. In this review, we summarize the cellular mechanism underlying lipid mobilization and metabolism inside skeletal muscle, focusing on the function of lipid droplets, the PLIN family of proteins, and how these entities are modified in exercise, obesity, and IR conditions.</jats:p>
収録刊行物
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- Journal of Diabetes Research
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Journal of Diabetes Research 2017 1-10, 2017
Wiley
