Stearoyl-CoA desaturase-1 is vital for milk lipid synthesis: Deletion impairs mammary gland and neonatal development.

The mammary gland synthesizes and secretes nutrient-rich milk containing lactose, protein, and lipids, with the complex assortment of lipids providing more than half of the energy and bioactive factors that impact the growth and development of neonates. The birth of neonates initiates the lipogenic capacity of the mammary gland with upregulation in expression of lipogenic genes, including Stearoyl-CoA desaturase (Scd1). SCD1 plays a critical role in lipogenesis, catalyzing the conversion of saturated fatty acids to monounsaturated fatty acids. Previous studies of Scd1 knockout mice revealed that SCD1 impacts several metabolic processes in the liver and adipose tissue, including fat synthesis. However, the role of SCD1 in lactation is not fully understood. Our study aimed to determine the role of SCD1 in lactation and the effects of maternal knockout of Scd1 on the growth of the lactating neonates. We employed second-parity Scd1-deficient female mice (n = 7) that we compared with wild-type mice (n = 6). To determine lipid and metabolic alterations, mammary gland and milk samples were harvested on lactation day 10. Relative to wild-type mice, mammary gland weight, alveolar area, and milk glycerolipid content were reduced in lactating Scd1-deficient mice. Scd1 deficiency also diminished mammary gland biosynthetic metabolic pathways, such as glycerolipid and phospholipid synthesis, while enhancing catabolic pathways, such as fatty acid oxidation. Neonates nursed by Scd1-deficient mice exhibited lower body weights. These findings highlight the critical role of SCD1 in orchestrating metabolic adaptations during lactation to ensure adequate milk synthesis to support the rapidly growing neonates.