TY - JOUR

T1 - Acute and perinatal programming effects of a fat-rich diet on rat muscle mitochondrial function and hepatic lipid accumulation

AU - Hellgren, Lars I

AU - Jensen, Runa I

AU - Waterstradt, Michelle S Gundel

AU - Quistorff, Bjørn

AU - Lauritzen, Lotte

N1 - CURIS 2014 NEXS 213

PY - 2014

Y1 - 2014

N2 - OBJECTIVE: Maternal high-fat intake during pregnancy may have long-term consequences in the offspring. Since this might relate to the capacity of mitochondrial metabolic adaptation and hepatic lipid metabolism, we investigated how maternal high-fat intake affected mitochondrial function and hepatic steatosis in the offspring.DESIGN: Sprague-Dawley rats were fed a high-fat (20% w/w) (HF) or a control diet from ten days before pregnancy and throughout lactation. At weaning the litters were split into two groups; one continued on the maternal diet and the other was fed the opposite.SAMPLE: Skeletal muscle mitochondria and liver lipids.METHODS: Mitochondrial respiration and hepatic lipid content were determined during and after weaning, day 20 and 70 postpartum.MAIN OUTCOME MEASURES: Mitochondrial function and hepatic lipids.RESULTS: At 20 days, maternal high-fat diet caused increased VO2max with pyruvate as substrate (p=0.047), at 70 days, pups born by C-dams, but not those born by HF-dams, showed increased oxidation of palmitoylcarnitine in the absence of ADP (p=0.018). Rates of ADP-stimulated oxygen consumption, maximal respiratory capacity and mitochondrial respiratory control ratio (RCR) with pyruvate, increased post weaning (p<0.001), whereas RCR with PC decreased (p=0.013). The increase in RCR was most pronounced in pups from C-dams (p=0.05). The HF-diet caused pronounced hepatic steatosis in pups at weaning (p<0.001), without concomitant ceramide accumulation, while HF-feeding after weaning induced TAG and ceramide accumulation (p<0.01), regardless of maternal diet.CONCLUSION: Intake of a fat-rich diet during pregnancy and lactation reduced the age-induced increases in un-coupled fat oxidation. This article is protected by copyright. All rights reserved.

AB - OBJECTIVE: Maternal high-fat intake during pregnancy may have long-term consequences in the offspring. Since this might relate to the capacity of mitochondrial metabolic adaptation and hepatic lipid metabolism, we investigated how maternal high-fat intake affected mitochondrial function and hepatic steatosis in the offspring.DESIGN: Sprague-Dawley rats were fed a high-fat (20% w/w) (HF) or a control diet from ten days before pregnancy and throughout lactation. At weaning the litters were split into two groups; one continued on the maternal diet and the other was fed the opposite.SAMPLE: Skeletal muscle mitochondria and liver lipids.METHODS: Mitochondrial respiration and hepatic lipid content were determined during and after weaning, day 20 and 70 postpartum.MAIN OUTCOME MEASURES: Mitochondrial function and hepatic lipids.RESULTS: At 20 days, maternal high-fat diet caused increased VO2max with pyruvate as substrate (p=0.047), at 70 days, pups born by C-dams, but not those born by HF-dams, showed increased oxidation of palmitoylcarnitine in the absence of ADP (p=0.018). Rates of ADP-stimulated oxygen consumption, maximal respiratory capacity and mitochondrial respiratory control ratio (RCR) with pyruvate, increased post weaning (p<0.001), whereas RCR with PC decreased (p=0.013). The increase in RCR was most pronounced in pups from C-dams (p=0.05). The HF-diet caused pronounced hepatic steatosis in pups at weaning (p<0.001), without concomitant ceramide accumulation, while HF-feeding after weaning induced TAG and ceramide accumulation (p<0.01), regardless of maternal diet.CONCLUSION: Intake of a fat-rich diet during pregnancy and lactation reduced the age-induced increases in un-coupled fat oxidation. This article is protected by copyright. All rights reserved.

U2 - 10.1111/aogs.12458

DO - 10.1111/aogs.12458

M3 - Journal article

C2 - 25052904

VL - 93

SP - 1170

EP - 1180

JO - Acta Obstetricia et Gynecologica Scandinavica

JF - Acta Obstetricia et Gynecologica Scandinavica

SN - 0001-6349

IS - 11

ER -