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The Potential of Leucine to Regulate Skeletal Muscle Energy Metabolism Under Obesogenic Conditions
Author(s) -
Baum Jamie I,
Inman Thomas G,
Shouse Stephanie A
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.652.9
Subject(s) - skeletal muscle , medicine , endocrinology , insulin resistance , leucine , mitochondrial biogenesis , myogenesis , insulin , glucose uptake , myocyte , biology , chemistry , mitochondrion , biochemistry , amino acid
Skeletal muscle is a major site of metabolic activity. Healthy skeletal muscle plays a key role in the prevention of metabolic disorders such as obesity and diabetes. Skeletal muscle is responsible for a majority of insulin‐stimulated glucose disposal and plays an important role in the pathogenesis of insulin resistance. Obesity may lead to increased intramyocellular lipid deposition, which is correlated with insulin resistance. In addition, mitochondria play a critical role in energy production and impact whole body metabolic homeostasis. Mitochondrial biogenesis and function are altered with insulin resistance. Mitochondrial dysfunction could be due to deregulated nutrient‐sensing by mammalian target of rapamycin (mTOR), an amino acid sensing pathway. Therefore, the objective of this study was to determine if the branched‐chain amino acid leucine improves mitochondrial function and decreases skeletal muscle fat uptake under obese conditions in skeletal muscle using C2C12 myotubes. C2C12 myotubes were either left untreated (control), treated with 0.75 mM palmitate, 5 mM leucine, or 0.75 mM palmitate + 5 mM leucine for 48 hours. Fifteen minutes before harvesting, cells were treated with or without 100 nM insulin for 15 minutes. Data was analyzed using one‐way ANOVA with the Bonferroni procedure for multiple comparisons. P < 0.05 was considered significant. Treatment with leucine decreased lipid deposition in cells also treated with palmitate, with no additional effect of insulin. There was no effect of palmitate or leucine treatment on PC1a or PPARg expression compared to control cells. However, cells treated with palmitate + Leu + insulin had significantly higher ( P < 0.05) PC1a and PPARg expression. There was no treatment effect on Akt phosphorylation compared to controls. These data suggest that leucine has the potential to decrease skeletal muscle fat deposition and improves markers of energy metabolism in obesogenic muscle cells in the presence of insulin. Support or Funding Information Arkansas Biosciences Institute. University of Arkansas Honors College Grant.