PPAR mRNA Levels Are Modified by Dietary n-3 Fatty Acid Restriction and Energy Restriction in the Brain and Liver of Growing Rats.

Without dietary sources of n-3 (ω-3) long-chain polyunsaturated fatty acids (LCPUFAs), α-linolenic acid (ALA; 18:3n-3) is the precursor for docosahexaenoic acid (DHA; 22:6n-3). It is not known how energy restriction (ER) affects ALA conversion to DHA. We tested the hypothesis that ER reduces n-3 LCPUFA concentrations in tissues of growing rats fed diets replete with and deficient in ALA. Male Sprague-Dawley rats (23 d old) were provided AIN93G diets (4 wk) made with soybean oil (SO; ALA sufficient) or corn oil (CO; ALA deficient) providing 16% of energy as fat. For each dietary oil, ER rats were individually pair-fed 75% of another rat's ad libitum (AL) intake. Fatty acid (FA) concentrations in brain regions, liver, and plasma were analyzed. Expression of peroxisome proliferator-activated receptors (PPARs), uncoupling proteins (UCPs), and mitochondrial DNA was analyzed in the brain and liver. AL rats consuming CO had a 65% lower concentration of n-3 docosapentaenoic acid (22:5n-3) and a 10% lower DHA concentration in the cerebral cortex and cerebellum than did the SO-AL group. ER did not alter cerebral n-3 LCPUFA status. Liver n-3 LCPUFA concentrations were reduced in rats fed CO compared with SO. ER reduced hepatic linoleic acid (18:2n-6), ALA, and arachidonic acid (20:4n-6) regardless of oil. ER and n-3 FA deficiency had independent effects on the mRNA levels of Pparα, Pparβ/δ, and Pparγ in the liver, cerebral cortex, and cerebellum. ER reduced Ucp3 mRNA by nearly 50% in the cerebral cortex, cerebellum, and liver, and Ucp5 mRNA was 30% lower in the cerebellum of rats receiving the CO diet. Small perturbations in PUFA concentration and ER modify the mRNA levels of Ppar and Ucp in the juvenile rat brain. More research is needed to identify the long-term physiologic and behavioral impacts of ER and PUFA restriction in the juvenile brain.