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Acute and perinatal programming effects of a fat-rich diet on rat muscle mitochondrial function and hepatic lipid
Lars I Hellgren1, Runa I Jensen, Michelle S G Waterstradt
1Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Kongens Lyngby, Denmark.
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) or a control diet (chow, C) from 10 days before pregnancy and throughout lactation. At weaning the litters were split into two groups; one was continued on the maternal diet and the other was fed low-fat chow.
Sample:
Skeletal muscle mitochondria and liver lipids.
Methods:
Mitochondrial respiration and hepatic lipid content were determined during and after weaning, on days 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 high-fat-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 with pyruvate, increased post weaning (p<0.001), whereas respiratory control ratio with palmitoylcarnitine decreased (p=0.013). The increase in respiratory control ratio was most pronounced in pups from C-dams (p=0.05). The high-fat-diet caused pronounced hepatic steatosis in pups at weaning (p<0.001), without concomitant ceramide accumulation, while high-fat-feeding after weaning induced triacylglycerol 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.
