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.

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.

Skeletal muscle mitochondria and liver lipids.

Mitochondrial respiration and hepatic lipid content were determined during and after weaning, on days 20 and 70 postpartum.

Mitochondrial function and hepatic lipids.

At 20 days, maternal high‐fat diet caused increased Vo_2max 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.

Intake of a fat‐rich diet during pregnancy and lactation reduced the age‐induced increases in un‐coupled fat oxidation.