A perspective on interaction between lipid and branched chain amino acids (BCAA) in developing insulin resistance

Abstract

There is a reciprocal relationship between glucose and fatty acid oxidation. Over nutrition or obesity causes perturbation in this reciprocal metabolic interrelationship leading to “metabolic inflexibility” resulting in mitochondrial dysfunction causing insulin resistance. Excess fat intake in obesity results in an inhibition of fatty acid oxidation in the adipose tissue accompanied by increased BCAA catabolism in skeletal muscle. This results in an increase in the levels of acyl carnitines which impair insulin action. It is suggested that serum acyl carnitine levels could therefore be taken as markers of insulin resistance.