Possible role of avian uncoupling protein in down‐regulating mitochondrial superoxide overproduction in skeletal muscle of fasted chickens

Abstract

Little is known about the precise physiological roles of the UCP1-homologues (UCP2, UCP3, avian UCP). The confusing aspect regarding the physiological characterization of these UCP variants is that their expression was enhanced in response to fasting, a peculiar result considering that the enhanced expression of these variants occurred in muscle in the fasted state, a basal metabolic state in which energy expenditure would be expected, instead, to be depressed. The aim of this investigation, using skeletal muscle from fasted chickens, was to examine alterations in the expression of gene encoding for avian UCP. We also examined altered transcription of key enzymes relevant to lipid flux across the mitochondrial β-oxidation pathway, and clarified whether up-regulation of avUCP modulates ROS production by mitochondria. avUCP transcription was increased 7.7-fold after a 24 h fast and diminished about 5.0-fold higher than baseline after 48 h of fasting. CPT-I gene expression was enhanced remarkably after 24 h of fasting and was diminished after 48 h, similar to the results seen for avUCP, while members of the β-oxidation pathway, LCAD and 3HADH, were up-regulated after 24 h of fasting, with levels then increasing linearly with time. ROS analysis with LDCL method exhibited the percentage decreases of mitochondrial ROS production following exposure to palmitate, probably via uncoupling, which were 44 and 86 % at time 0 and 24 h of fasting, respectively. This is the first investigation demonstrating possible regulation of mitochondrial ROS via UCP in chicken skeletal muscle in response to fasting.