An increasing number of women are obese during pregnancy, which has an adverse effect on the cardiovascular health of their offspring. In mice, we have previously shown that a maternal high fat diet (mHFD) increased the offspring’s risk to cardiovascular disease (1, 2). Nevertheless, the molecular mechanisms involved are unclear. Endogenous clock networks regulate near 24-hour or circadian rhythms in physiological processes, and the molecular components of this clock network are found in nearly all mammalian cells, including cardiovascular-related cells, and are also expressed in early life. Disrupting circadian clock function has been shown to increase cardiometabolic pathologies, including cardiovascular disease and the metabolic syndrome (3, 4). We therefore investigated whether mHFD could disrupt clock and metabolism-associated genes in the offspring heart, precipitating its abnormal development in adulthood. Female C57/BL6J mice were maintained under controlled conditions and fed either a HF diet (HF; 45% kcal fat) or standard chow diet (C; 21% kcal fat) 4 weeks prior to and during gestation and lactation. Weaned offspring were fed the HF or C diet, generating the dam-offspring groups: C/C, C/HF, HF/C, HF/HF. Hearts were taken from 15-week old male offspring killed at 6 time points over a 24h light-dark period (n=5-6 per time point per treatment group). The left ventricle (LV) was dissected, weighed and processed for real-time-PCR quantification for the clock genes Cry1 and Cry2, the metabolic markers Sirtuin3 (Sirt3) and insulin receptor (Insr), and the apoptosis-associated gene Foxo3a. The LV mass were 1.4-fold heavier (p<0.01, ANOVA) in offspring from HF-fed dams (HF/C and HF/HF groups) vs C/C group. Circadian rhythms in mRNA expression for all genes examined phase-shifted, except for Sirt3, in the HF/HF offspring heart vs C/C. The amplitude of peak expression in the HF/HF group was 1.5-fold and 1.2-fold lower for Cry1 and Cry2, respectively, and 2.1-fold lower for both Foxo3a and Insr (p<0.05), vs C/C. Although there was no shift in rhythms of Sirt3 expression, amplitude of peak expression in the HF/HF group was 2.9-fold lower group vs C/C (p<0.05). Mean mRNA levels over the 24h period was found to be 1.2-fold lower for both Cry1 and Cry2, 1.7-fold lower for both Foxo3a and Insr, and 3.7-fold lower for Sirt3 in HF/HF vs C/C offspring hearts. The results suggest that mHFD leads to LV hypertrophy. Alterations in circadian expression patterns and levels of clock and metabolism-associated genes due to mHFD may contribute to the abnormal development of the offspring heart, leading to increase risk to cardiometabolic pathologies in later life.