Matthew J Picklo1, LuAnn Johnson2, Joseph Idso2. 1. USDA Agricultural Research Service Grand Forks Human Nutrition Research Center, Grand Forks, ND matthew.picklo@ars.usda.gov. 2. USDA Agricultural Research Service Grand Forks Human Nutrition Research Center, Grand Forks, ND.
Abstract
BACKGROUND: 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. OBJECTIVE: We tested the hypothesis that ER reduces n-3 LCPUFA concentrations in tissues of growing rats fed diets replete with and deficient in ALA. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. OBJECTIVE: We tested the hypothesis that ER reduces n-3 LCPUFA concentrations in tissues of growing rats fed diets replete with and deficient in ALA. METHODS: 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. RESULTS:ALrats 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. CONCLUSIONS: 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.