Buffering agent-induced lactose content increases via growth hormone-mediated activation of gluconeogenesis in lactating goats.

摘要

Dairy goats are often fed a high-concentrate (HC) diet to meettheir lactation demands; however, long-term concentrate feedingis unhealthy and leads to milk yield and lactose contentdecreases. Therefore, we tested whether a buffering agent isable to increase the output of glucose in the liver and influencelactose synthesis. Eight lactating goats were randomlyassigned to two groups: one group received a HC diet(Concentrate : Forage = 6:4, HG) and the other group receivedthe same diet with a buffering agent added (0.2 % NaHCO3,0.1 % MgO, BG) over a 19-week experimental period. The totalvolatile fatty acids and lipopolysaccharide (LPS) declined in therumen, which led the rumen pH to become stabile in the BGgoats. The milk yield and lactose content increased. The alanineaminotransferase, aspartate transaminase, alkaline phosphatase,pro-inflammatory cytokines, LPS and lactate contents in theplasma significantly decreased, whereas the prolactin and growthhormone levels increased. The hepatic vein glucose contentincreased. In addition, pyruvate carboxylase (PC),phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6PC) expression in the liver was significantlyup-regulated. In the mammary glands, the levels of glucosetransporter type 1, 8, 12 as well as of sodium-glucosecotransporter 1 increased. Cumulative buffering agent treatmentincreased the blood concentrations of glucose via gluconeogenesisand promoted its synthesis in the liver. This treatment maycontribute to the increase of the milk yield and lactose synthesisof lactating goats.