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Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. A maternal high LA (HLA) diet alters cardiovascular development in adolescent rats and hepatic function in adult rats in a sex-specific manner. We investigated the effects of an HLA diet on adolescent offspring hepatic lipids and hepatic lipid metabolism gene expression, and the ability of the postnatal diet to alter these effects. Female Wistar Kyoto rats were fed low LA (LLA; 1.44% energy from LA) or high LA (HLA; 6.21% energy from LA) diets during pregnancy and gestation/lactation. Offspring, weaned at postnatal day (PN) 25, were fed LLA or HLA and euthanised at PN40 (<i>n</i> = 6–8). Maternal HLA increased circulating uric acid, decreased hepatic cholesterol and increased hepatic <i>Pparg</i> in males, whereas only hepatic <i>Srebf1</i> and <i>Hmgcr</i> increased in females. Postnatal (post-weaning) HLA decreased liver weight (% body weight) and increased hepatic <i>Hmgcr</i> in males, and decreased hepatic triglycerides in females. Maternal and postnatal HLA had an interaction effect on <i>Lpl</i>, <i>Cpt1a</i> and <i>Pparg</i> in females. These findings suggest that an HLA diet both during and after pregnancy should be avoided to improve offspring disease risk.