Periparturient metabolic disease in small ruminants: interactions among maternal adaptation, nutrient partitioning, and placental-mammary function.

Periparturient metabolic diseases remain a major challenge to the productivity, health, and welfare of small ruminants. Traditionally, disorders including pregnancy toxemia, early lactation ketotic disorders, hypocalcemia, and hypomagnesemia have been considered distinct disease entities arising primarily from nutritional deficiencies during late gestation and early lactation. However, increasing evidence suggests these conditions represent interconnected manifestations of disrupted physiological adaptation during the transition from pregnancy to lactation. During this period, maternal tissues must coordinate nutrient partitioning among maternal maintenance, fetal growth, placental function, colostrum production, and milk synthesis. Rapid fetal growth during late gestation, declining dry matter intake, and increasing mammary demand impose substantial energetic and mineral requirements that challenge metabolic homeostasis, particularly in prolific females carrying multiple fetuses. Failure of adaptive mechanisms regulating glucose metabolism, lipid mobilization, mineral homeostasis, oxidative balance, and endocrine signaling reduce capacity to adapt to increasing nutritional demands during gestation and lactation. This review integrates current understanding of metabolic adaptation during the periparturient period in small ruminants, with emphasis on interactions among nutrient partitioning, placental demand, fetal growth, and mammary function. Relationships among energy metabolism, mineral regulation, oxidative stress, inflammatory signaling, and endocrine adaptation in the context of maternal health, neonatal viability, and lactational performance are discussed highlighting the importance of coordinated maternal, placental, fetal, and mammary adaptation in regulating susceptibility to periparturient metabolic disease in small ruminants.