Maternal undernutrition can induce intrauterine growth restriction and contribute to the development of adult metabolic diseases. Ghrelin, a peptide hormone purified from the gastric mucosa, activates food intake and energy homeostasis. Ghrelin exists in 2 forms, the non-acylated ghrelin and acylated ghrelin (active form). The acylation of ghrelin is mediated by membrane bound O-acyltransferase 4 (Mboat4). We hypothesized that maternal undernutrition would increase the acylated ghrelin in the blood of the fetus during gestation. Twin bearing western whiteface ewes were either fed 100% (C, n = 12), or 50% of their global nutrient requirements from 28 to 78 d of gestational age (dGA) and readjusted to 100% beginning at 79 dGA (LC, n = 12), or continuously restricted until 135 dGA (LL, n = 12). At 135 dGA, umbilical artery and vein plasma, and fetal abomasum samples were collected. Umbilical arterial and venous ghrelin concentrations were measured by radioimmunoassay. Mboat4 gene expression in fetal abomasum was measured using quantitative real-time PCR. Mboat4 protein concentration in the fetal abomasum was analyzed by Western blot analysis. Each ewe was treated as one experimental unit and twin fetuses were nested within the ewe. All data are presented as least squares means ± SEM using the PROC MIXED model of SAS. The umbilical arterial active ghrelin concentration tended to be greater in LL fetuses (41.63 ± 5.49 pg/mL) compared with control (27.17 ± 5.76 pg/mL; P = 0.0523) and LC fetuses (22.81 ± 5.28 pg/mL; P = 0.0197). The active to total ghrelin ratio was higher in LL than LC fetuses (P < 0.05). Umbilical vein active ghrelin concentration tended to be greater in LL, when compared with LC fetuses (P = 0.0812). No significant difference was observed in Mboat4 mRNA expression in fetal abomasum. Mboat4 protein concentration tended to be greater in fetal abomasum of LC and LL fetuses compared with control fetuses (P = 0.0584). These results are interpreted to mean that elevated active ghrelin but not total ghrelin in fetal circulation may be an adaptation of the fetus to prolonged undernutrition during gestation. USDA-AFRI Grant no. 2009–65203–05670.