Maternal nicotinamide supplementation during late gestation and early lactation alters hepatic glucose and lipid metabolism in kids

Abstract

The objective of this study was to determine whether maternal nicotinamide (NAM) supplementation in does during the late pregnancy and early lactation results in differences in intestinal glucose transporters and hepatic genes and enzymes regulating glucose and fatty acid metabolism of kids. Fifteen multiparous does were paired into 5 blocks based on similarities in BW, previous milking yield, and the number of fetuses then randomly assigned within block to 1 of 3 treatments: control (C, no supplementation), postpartum (P, supplemented post-kidding), and entire-perinatal (EP, supplemented from d -21 to 28 around kidding). The NAM at 5 g/d were drenched to does in P and EP daily at 0700 h. After kidding, the kids were separated from their dams, named LC, LP, and LEP, respectively, and fed equal amounts of milk from their mothers until 28 days of age. The DMI and milk of the does were measured weekly, and the blood and tissue samples of the kids were taken at d 28. Data were analyzed using the MIXED procedure of SAS. For the does, the DMI and lactation performance of does were not affected (P > 0.10). For the kids, the plasma triglyceride (TG) concentration was greater in LEP than in LC and LP (P < 0.01). The enzyme activity of alanine transaminase was decreased and lipase was increased in both LP and LEP (P < 0.01). The Glucose transporter 2 (GLUT2) relative mRNA expression in the jejunum was increased in LP (P < 0.01), and the sodium-dependent glucose transporters 1 relative mRNA expression was greater in both LP and LEP than in LC (P < 0.01). The hepatic free fatty acid was increased in LP and LEP, and glycogen tended to decrease (P = 0.05 and 0.06, respectively). Liver TG and cholesterol were not affected (P> 0.10). The hepatic enzyme activity of 1- acylglycerol-3-phosphate acyltransferases 6 was decreased in LEP (P = 0.04), and hormone-sensitive lipase activity was increased in LP compared that in LC (P = 0.04). Furthermore, the hepatic relative mRNA expression of phosphoenolpyruvate carboxykinase, glycogen synthase and GLUT2 were reduced in LP and LEP, (P < 0.05). The fatty acid synthase relative mRNA expression was downregulated in LEP (P = 0.05) and microsomal triglyceride transfer protein was upregulated in LEP (P < 0.01). The relative mRNA expression of peroxisome proliferator- activated receptor-γ coactivator α and forkhead box protein O1 were also reduced by maternal NAM supplementation in both LP and LEP (P ⩽ 0.05). These findings suggested that NAM supplementation during late gestation and early lactation inhibited hepatic fat synthesis and promoted lipolysis of kids. Further research on glucose metabolism is needed.