AI Article Synopsis
- Skeletal muscle plays a crucial role in regulating carbohydrate and lipid metabolism, making it sensitive to changes in glucose and fatty acid levels.
- Obesity increases fatty acid levels in the body, leading to toxic lipid build-up and oxidative stress, which contribute to insulin resistance.
- The review highlights how lipid droplets and perilipin proteins help manage lipid storage and metabolism in skeletal muscle, especially in response to exercise, obesity, and insulin resistance.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5476901 | PMC |
| http://dx.doi.org/10.1155/2017/1789395 | DOI Listing |
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