We have previously shown that animals born from protein-restricted pregnancies are growth retarded at birth. However, these animals rapidly gain weight if normally nourished after birth. These ‘catch-up’ offspring appeared to age sooner than controls and die earlier from renal failure [1]. We have recently reported that mitochondrial dysfunction in the renal cortex of the catch up animals is caused by a deficit of CoQ [2]. Mechanisms of CoQ deficiency in this diet-induced model of premature death are currently unknown but alterations in regulation of CoQ biosynthesis (via the mevalonate pathway) could be implicated. Proxisome proliferators activated receptor α (PPAR α) can influence rates of CoQ synthesis and an activation of PPAR α expression by ‘newly synthesized’ fat has been reported recently [3]. The aim of this study was to investigate levels of expression of PPAR α during the lifetime of offspring who were malnourished in utero. Pregnant Sprague-Dawley female rats were fed either normal (containing 20% protein) or a low protein (8%) diet throughout pregnancy [1]. At birth pups born to mothers fed on low-protein diet were fostered to recently parturient normally nourished control dams. Likewise, litters of control dams were cross-fostered to control dams. All groups were weaned and maintained on 20% normal laboratory chow. Quantification of gene expression of PPAR α and 18S (endogenous control) in the cortex of renal samples from 22 days and 12 month old control and catch up offspring male rats was performed using relative standard curve method and TaqMan probes. All expression data were normalized by 18S mRNA levels. An arbitrary chosen heart cDNA sample was designated as a calibrator and differences in expression was determined by dividing the normalized amount of a target gene by normalized amount of the calibrator. Results were analysed by unpaired t test and expressed as mean ± SEM. At 22 days of age, renal PPAR α mRNA level was markedly higher in catch-up offspring (n=4) than in controls (n=6) (1.62 ± 0.05 vs 1.45 ±0.02, p< 0.05). Expression of PPAR α in kidney cortex decreased with age and those levels at 12 months were significantly lower than at 22 days in both control (0.34 ± 0.02 vs 1.45 ± 0.02,p<0.001) and catch-up animals (0.46 ± 0.01 1.63± 0.05 p<0.001). However, adult catch-up offspring (n=10) still had a higher mRNA level of PPAR α than control animals (n=10)(0.46 ± 0.01 vs 0.34 ± 0.02, p< 0.01). Environmental and temporal alterations in expression of PPAR α may underlie the observed deficit of CoQ in this diet-induced model of reduced longevity.