Table 2 shows the distributions of genotypes of our subjects on -866 G/A variant of UCP2 gene and -55 C/T variant of UCP3 gene.
In this study, we investigated whether capsaicin ingestion affects cardiac ANS activity and cardiac QT intervals as well as, for the first time to our knowledge, the association between cardiac ANS activity and variants of UCP2 and UCP3 polymorphisms during aerobic exercise in obese males.
Nevertheless, no studies, at least to our knowledge, are performed to investigate the alterations of cardioprotective functions upon the distribution of UCP2 and UCP3 genotypes and capsaicin supplementation during the exercise in obese individuals.
We also suggested that 866 G/A variants of UCP2, but not UCP3 polymorphism may associate with alteration of cardiac ANS activity.
Distribution of genotype defined by the -866 G/A variant of the UCP2 promoter gene and -55 C/T variant of the UCP3 promoter gene in nine obese men.
UCP2 is the only ubiquitous isoform, whereas UCP3 is expressed in skeletal and cardiac muscles and shows 54 to 59% homology of amino acid sequence with UCP1; UCP4 has been found in kidney and central nervous system and UCP5, also called brain mitochondrial carrier protein (BMCP1), has been found in brain cells.
In animal model of heart failure induced by pressure overload induced by constriction of the ascending aorta, the expression of UCP2 and UCP3 is downregulated and an increase of ROS generation is enhanced to induce cardiac cell hypertrophy [38,44].
In addition to FFA, growth factors such as insulin growth factors 1 and 2 (IGF1 and IGF2) and fibroblast growth factor 21 (FGF21), a secreted protein from liver, involved in the control of glucose homeostasis, insulin sensitivity, and ketogenesis were recently found to induce the expression of genes encoding mitochondrial UCP2, UCP3, and superoxide dismutase-2 (SOD2) involved in antioxidative pathways in cardiomyocytes in culture preventing inflammation and hypertrophic process .
The slight uncoupling of the mitochondrial membrane potential by UCP3 or by low concentration of FCCP was demonstrated to be cardioprotective against ischemia/reperfusion (I/R) injury [77,78].
The overexpression of UCP2 and UCP3 under lipotoxicity conditions suggests that UCPs are required to protect cells from the detrimental consequences of excessive fatty acid metabolism or storage.