Abstract
In this study, we explored mechanisms related to glucose and fatty acid metabolism in Holstein–Friesian multiparous dairy cows during lactation under two feeding strategies. From 0 to 180 days postpartum, cows were fed total mixed ration (TMR) ad libitum (non-grazing group, G0) or grazed Festuca arundinacea or Medicago sativa and were supplemented with 5.4 kg DM/d of an energy-protein concentrate (grazing group, G1). From 180 to 250 days postpartum, all cows grazed F. arundinacea and were supplemented with TMR. Plasma samples and liver biopsies were collected at −14, 35, 60, 110, 180, and 250 days in milk (DIM) for metabolite, hormone, gene expression, and western blot analysis. Our results showed increased levels of negative energy balance markers: plasma non-esterified fatty acids (NEFA), liver triglyceride and plasma β-hydroxybutyrate (BHB) (P < 0.01), triglyceride and β-hydroxybutyrate concentration were especially elevated for G1 cows. Also, hepatic mRNA expression of gluconeogenic enzymes was upregulated during early lactation (P < 0.05). In particular, methymalonyl-CoA mutase expression was increased for G0 cows (P < 0.05) while pyruvate carboxylase (PC) expression was increased for G1 cows (P < 0.05), suggesting differential gluconeogenic precursors for different feeding strategies. Phosphorylation of AMP-activated protein kinase was increased in early lactation vs. late lactation (P < 0.01) and negatively correlated with PC mRNA levels. The positive association of gluconeogenic genes with proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A) hepatic expression supported the importance of this transcription factor in glucose metabolism. The peroxisome proliferator-activated receptor alpha (PPARA) mRNA was increased during early lactation (P < 0.05), and was positively associated to PPARGC1A, carnitine palmitoyl-transferase 1, and hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) mRNA expression. Alongside, hepatic mRNA expression of FABP was decreased for G1 vs. G0 cows (P < 0.05), possibly linked to impaired fatty acid transport and related to accumulation of liver triglycerides, evidencing G1 cows fail to adapt to the demands of early lactation. In sum, our results showed that metabolic adaptations related to early lactation negative energy balance can be affected by feeding strategy and might be regulated by the metabolic sensors AMPK, SIRT1, and coordinated by transcription factors PPARGC1A and PPARA.
Highlights
High producing dairy cows undergo extreme metabolic adaptations during lactation
RQUICKI was not affected by the interaction between stage of lactation and treatment, it was affected by stage of lactation (P < 0.001) and treatment (P < 0.0001) as it increased only for grazing cows (G1 cows) from 35 days in milk (DIM) onwards
PCK1 mRNA was similar for both groups, indicative of similar enzyme activity (Greenfield et al, 2000), we found G0 and G1 cows were likely using different precursors for gluconeogenesis which was evidenced by methylmalonyl-CoA mutase (MMUT) and pyruvate carboxylase (PC) differential mRNA expression (Figure 4A)
Summary
The transition period from late gestation to early lactation is the time where most diseases and metabolic disorders occur (Drackley, 1999). It represents a moment of almost 4-fold increases in energy, protein, and mineral requirements and when multiple organs orchestrate metabolic adaptations which will be critical in defining the success of the oncoming lactation (Bauman, 2000; Roche et al, 2013). The challenges faced in grazing systems include assuring sufficient energy intake through quantity and quality of the forage and taking strategic decisions to account for a stable stocking rate during the different seasons of the year (Chilibroste et al, 2005; Mattiauda et al, 2013; Gregorini et al, 2017). Previous research has shown that in order to achieve high milk yields or to maintain body reserves (i.e., body condition score) in Holstein cows on intensive grazing systems, supplemental energy is needed (Kolver and Muller, 1998)
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