The available evidence suggests that metabolic control mechanisms are programmed early in life. Previous studies of pregnant rats fed low-protein diets have suggested that the vegetable oils used in the experimental diets influence the outcome. The present study investigated the offspring of female rats fed semi-synthetic diets containing either 180 or 90 g casein/kg with 70 g/kg (w/w) of either corn oil or soya oil during gestation. During lactation, the dams received stock diet, and the offspring were subsequently weaned onto the stock diet. The offspring of dams fed the low-protein diets were smaller at birth. At 25 weeks of age, the offspring were subjected to an oral glucose tolerance test. In the offspring of dams fed the diet containing soya oil, the area under the insulin curve was affected by the protein content of the maternal diet. There was no effect of protein on the area under the insulin curve in the offspring of dams fed the diet prepared with corn oil. There were no differences in plasma glucose concentrations. The levels of mRNA for acetyl-CoA carboxylase-1 in the livers of female offspring were affected by the protein and oil content of the maternal diet. The level of carnitine palmitoyl transferase mRNA was affected by the protein content of the maternal diet. The present study suggests that PUFA in the maternal diet can interact with protein metabolism to influence the development of the offspring. This may involve the higher content of α-linolenic acid in soya oil compared with corn oil.

Mice fed diets containing trans 10, cis 12 (t10, c12)-conjugated linoleic acid (CLA) develop fatty livers and the role of hepatic fatty acid oxidation enzymes in this development is not well defined. We examined the effects of dietary cis 9, trans 11-CLA (c9, t11-CLA) and t10, c12-CLA on the expression of hepatic genes for fatty acid metabolism. Female mice, 8 weeks old, (six animals per group) were fed either a control diet or diets supplemented with 0·5 % c9, t11- or t10, c12-CLA for 8 weeks. DNA microarray analysis showed that t10, c12-CLA increased the expression of 278 hepatic genes and decreased those of 121 genes (>2-fold); c9, t11-CLA increased expression of twenty-two genes and decreased those of nine. Real-time PCR confirmed that t10, c12-CLA reduced by the expression of fatty acid oxidation genes including flavin monooxygenase (FMO)-3 95 %, cytochrome P450 (cyt P450) 69 %, carnitine palmitoyl transferase 1a 77 %, acetyl CoA oxidase (ACOX) 50 % and PPARα 65 %; it increased the expression of fatty acid synthase by 3·5-fold (P < 0·05 for all genes, except ACOX P = 0·08). It also reduced the enzymatic activity of hepatic microsomal FMO by 40 % and the FMO3 specific protein by 67 %. c9, t11-CLA reduced FMO3 and cyt P450 expression by 61 % (P = 0·001) and 38 % (P = 0·06) and increased steoryl CoA desaturase transcription by 5·9-fold (P = 0·07). Both decreased fatty acid oxidation and increased fatty acid synthesis seem to contribute to the CLA-induced fatty liver. Since FMO and cyt P450 are also involved in drug detoxification, suppression of the transcription of these genes by CLA may have other health consequences besides development of fatty liver.