Epidemiological studies in man have suggested that obesity may have origins early in life. We have previously reported an increase in fat depots in adult offspring of rats fed a lard rich diet during weaning [1]. In this study we have determined whether prenatal and suckling exposure to a maternal lard rich diet leads to altered adipose tissue metabolism which could contribute to development of obesity in the adult offspring. Sprague-Dawley dams were fed either control (RM1, 5% corn oil) or fat-rich (24% lard; a combination of predominantly monounsaturated and saturated fatty acids) diet for 10 days prior to mating, through pregnancy and weaning. Offspring were fed standard chow from weaning onwards. When animals (n=5 per group) were 12 months of age they were terminally exposed to a rising CO₂ concentration. Visceral adipose tissue was removed, weighed and processed for histological and molecular analyses. Adipose expression of β–3 adrenergic receptor 3 (β3-AR), and peroxisome proliferator-activated receptor (PPAR α and γ) were determined by real time PCR using the standard curve method (User Bulletin 2, PE Applied Biosystems) and adjusted for 18 sRNA (endogenous control). Adipocyte histology (n=5 per group) was assessed by hematoxylin eosin staining and visualized by light microscopy. Plasma cholesterol, HDL, and LDL were measured by enzymatic colorimetric assays (Roche/BCl). Results were expressed as means ± SEM and analysed by an unpaired t test. One year old offspring of dams fed a lard-rich diet during pregnancy and suckling developed a significant increased fat pad weight, compared to control (34.4 ± 2.4 g vs 25.5 ± 2.7 g, p<0.05, n=5 per group). This was characterized by adipocyte hypertrophy. Adipose tissue mRNA expression of PPAR-γ, which may indicate enhanced adipogenesis was increased in offspring of lard-fed dams compared to controls (1.48 ± 0.12 vs 0.85 ± 0.05, p<0.05, n=5 per group), whereas β3-AR (1.69 ± 0.09 vs 2.66 ± 0.13, p<0.05, n=5 per group) and PPAR-α (2.10 ± 0.15 vs 1.09 ± 0.09, p<0.01, n=5 per group) were reduced compared to control, and indicative of increased lipogenesis. Obesity is increasingly prevalent in western society. Diet-induced programming of adipocyte function early in life could contribute to adulthood obesity. This study indicates that a maternal diet rich in animal fat may influence adipose metabolism of the offspring. Increasing the understanding of the regulatory pathways behind maternal origins of offspring obesity may provide alternative strategies to reduce the incidence of obesity.