Changes in milk performance and hepatic metabolism in mid-lactating dairy goats after being fed a high concentrate diet for 10 weeks

Abstract

Feeding a high concentrate (HC) diet is a widely used strategy for supporting high milk yields, yet it may cause certain metabolic disorders. This study aimed to investigate the changes in milk production and hepatic metabolism in goats fed different proportions of concentrate in the diet for 10 weeks. In total, 12 mid-lactating goats were randomly assigned to an HC diet (65% concentrate of dry matter, n = 6) or a low concentrate (LC) diet (35% concentrate of dry matter, n = 6). Compared with LC, HC goats produced greater amounts of volatile fatty acids and produced more milk and milk lactose, fat and protein ( P < 0.01). HC goats showed a greater concentration of ATP, NAD, plasma non-esterified fatty acids and hepatic triglycerides than LC goats ( P < 0.05). Real-time PCR results showed that messenger RNA (mRNA) expression of gluconeogenic genes, namely, glucose-6-phosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase were significantly up-regulated and accompanied greater gluconeogenic enzyme activities in the liver of HC goats. Moreover, the expression of hepatic lipogenic genes including sterol regulatory elementbinding protein 1c, fatty acid synthase and diacylglycerol acyltransferase mRNA was also up-regulated by the HC diet ( P < 0.05). HC goats had greater hepatic phosphorylation of AMP-activated protein kinase than LC ( P < 0.05). Furthermore, histone-3-lysine-27-acetylation contributed to this elevation of gluconeogenic gene expression. These results indicate that lactating goats fed an HC diet for 10 weeks produced more milk, which was associated with up-regulated gene expression and enzyme activities involved in hepatic gluconeogenesis and lipogenesis.Keywords: milk performance, gluconeogenesis, lipogenesis, high concentrate diet, lactating dairy goats ImplicationsFeeding a high concentrate diet to ruminants is a common strategy for maintaining high milk yields. Unfortunately, there is a strong correlation between the amount of concentrate feeding and the occurrence of acidosis and fatty liver in practice, which will decrease animal welfare and result in significant economic losses. As the vital metabolic organ, the liver is responsible for nutrient partitioning and contributes to the input of substrate precursors to the mammary gland for milk production. Therefore, it is important to investigate changes of hepatic metabolism in lactating ruminants fed a high concentrate diet, which will help elucidate the internal mechanism behind these metabolic changes.

Sodium Butyrate More Effectively Mitigates the Negative Effects of High-Concentrate Diet in Dairy Cows than Sodium β-Hydroxybutyrate via Reducing Free Bacterial Cell Wall Components in Rumen Fluid and Plasma

“…In dairy production, dairy cows are commonly fed HC diet to meet the needs of energy and nutrients during lactation to increase milk yield. In this study, the milk yield in the HC group was higher than that in the LC group, which was consistent with the results of previous studies [ 31 , 32 ]. Although HC diet increased milk yield of dairy cows, it resulted in adverse effects on milk components.…”

Elevated thyroid hormone caused by high concentrate diet participates in hepatic metabolic disorders in dairy cows

“…Therefore, we further investigated hepatic morphology and metabolism. Previous studies reported that high concentrate diet can induce TG accumulation, in ammation, and tissue damages in ruminants (Dong et al, 2017, Guo et al, 2017. Although no obvious in ammation, steatosis, and damages were shown in HE staining sections, we observed remarkable glycogen deposition in HC group via PAS staining.…”

“…Unlike non-ruminant mammals, ruminants primarily depend on hepatic gluconeogenesis as their source of glucose to meet their energy demand (Overton et al, 1999). Dong et al found that high concentrate diet signi cantly increased the enzyme activities involved in glucogenesis, including G6PC and PCK1, whereas no obvious changes in the enzyme activities involved in glycolysis (Dong et al, 2017). It is highly consistent with our data, high concentrate diet signi cantly up-regulated the expression of G6PC and PCK1 at gene and protein levels, however, the other genes involved in glycolysis and glucose transport did not show statistical signi cance.…”

“…In ruminants, liver is an important metabolic organ responsible for gluconeogenesis and lipogenesis (Dong et al, 2017). Hepatic gluconeogenesis is responsible for maintaining an adequate glucose supply to the mammary glands (Zhao and Keating, 2007).…”

“…Glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxykinase 1 (PCK1) are the rate-limiting enzymes involved in hepatic gluconeogenesis (Al-Trad et al, 2010). In the liver, sterol regulatory element-protein 1 (SREBP1), fatty acid synthase (FAS), and long-chain acyl CoA synthet binding ase 1 (ACSL1) are important for de novo fatty acid synthesis (Phillips et al, 2010, Dong et al, 2017. In addition, CPT1α and PPARα are responsible for dairy cows to regulate the entry of fatty acids into the mitochondria for oxidation (Dann and Drackley, 2005).…”