The L-type amino acid transporter inhibitor, BCH, inhibits myotube BCAA uptake and mitochondrial function without altering myotube insulin sensitivity during insulin resistance in C2C12 myotubes.

Introduction: Branched-chain amino acids (BCAA) are essential nutrients involved in protein synthesis. BCAA are absorbed via the L-type amino acid transporter (LAT1) in skeletal muscle where the majority of BCAA are metabolized. Higher circulating BCAA levels have been shown to correlate with insulin resistance.

The effect of Semaglutide on mitochondrial function and insulin sensitivity in a myotube model of insulin resistance.

Aims: Semaglutide (SEMA) is a glucagon-like peptide-1 receptor agonist (GLP-1RA) that has recently emerged as a popular pharmacological treatment for type 2 diabetes and insulin resistance due to its weight loss properties. Previous studies have examined the metabolic effects of SEMA using supra-pharmacokinetically (but not pharmacokinetically attainable) concentrations. The aim of the present study was to determine the metabolic effects of pharmacokinetically attainable levels of SEMA on mitochondrial function and metabolism, which are often reduced during insulin resistance.

The Effect of Dexamethasone-Mediated Atrophy on Mitochondrial Function and BCAA Metabolism During Insulin Resistance in C2C12 Myotubes.

: Muscle loss during sarcopenia and atrophy is also commonly associated with age-related insulin resistance. Interestingly, branched-chain amino acids (BCAA) which are known for stimulating muscle protein synthesis are commonly elevated during insulin resistance and sarcopenic obesity. : This study investigated the effects of the interplay between atrophy and insulin resistance on insulin sensitivity, mitochondrial metabolism, and BCAA catabolic capacity in a myotube model of skeletal muscle insulin resistance.