H19 gene produces the most abundant mRNA in the murine embryo. It has been mapped on the same chromosome as IGF-II. Like IGF-II, the murine H19 gene is highly expressed during fetal life and is repressed postnatally. H19 and IGF-II are both parentally imprinted and follow the same regulatory mechanisms. The role of H19 is unknown, evidence exists that it is important during embryogenesis. Lacking an encoded protein, it is believed to function as an RNA. H19 gene and its imprinting mechanisms have been extensively studied in mice. We studied the ontogeny of H19 in sheep and the effect of maternal fasting (MF) on the expression of fetal H19 mRNA, this latter was compared to that of IGF-II. The ontogeny of H19 was studied in liver, muscle and heart of ovine fetuses at 62, 100, 130 and 140 d and lambs at 5 d and 1 month. We detected, amplified, isolated and sequenced the ovine H19 cDNA for quantitation by RNase protection analysis (RPA). RPA results were consistent with a gradual increase of H19 mRNA with advancing gestational age and decrease after birth. Six fetal sheep following 48 hours of MF and six controls at 130 d gestation were used to study the effect of MF. Quantitation of H19 mRNA by RPA demonstrated a significant decrease in expression following MF in liver, muscle and kidney. IGF-II mRNA, on the other hand, did not change significantly in these tissues. In summary, this study demonstrates that H19 mRNA is highly expressed in ovine fetal tissues indicating an important role during fetal life. Moreover, 48 hours of MF decreases expression of H19 mRNA in late gestation. Knowing that MF results in intrauterine growth retardation, we suggest that H19 may play a role in regulation of fetal growth. The absent effect of MF on IGF-II could be secondary to various posttranslational regulatory mechanisms of IGF-II following short term fasting.