Liver phosphorus content and liver function in states of phosphorus deficiency in transition dairy cows

PLoS One. 2019 Jul 22;14(7):e0219546. doi: 10.1371/journal.pone.0219546. eCollection 2019.

Abstract

Phosphorus (P) deficiency in early lactating dairy cows is receiving increased attention because of incentives aiming at curtailing environmental pollution with P by reducing dietary P in ruminant diets. An in-vitro study using bovine hepatocytes incubated for 7 days with phosphate (Pi) concentrations of 0.9, 1.8 or 2.7 mmol/L, and an in-vivo study feeding late pregnant dairy cows diets with either adequate (0.28% and 0.44% in DM ante-partum and post-partum respectively) or low P content (0.15% and 0.20% in DM ante-partum and post-partum respectively) from 4 weeks before to 4 weeks after calving were conducted to explore effects of P deprivation on liver function. In vitro the relative abundance of mRNA of key enzymes of the carbohydrate metabolism in incubated hepatocytes and liver metabolites in culture medium were determined. In vivo health and productivity of experimental cows on low and adequate dietary P supply were monitored, and liver tissue and blood samples were obtained repeatedly. Liver tissue was assayed for its triacylglycerol-, mineral and water content as well as for the relative abundance of mRNA of enzymes of the carbohydrate-, fat- and protein metabolism. Reduced Pi-availability was not associated with altered enzyme transcription rates or metabolic activity in-vitro. The most prominent clinical finding associated with P deprivation in-vivo was feed intake depression developing after the first week of lactation. Accordingly cows on low P diets had lower milk yield and showed more pronounced increases in liver triacylglycerol after calving. Although the liver P content decreased in P deficient cows, neither negative effects on enzyme transcription rates nor on blood parameters indicative of impaired liver metabolic activity or liver injury were identified. These results indicate the P deprivation only indirectly affects the liver through exacerbation of the negative energy balance occurring as P deficient cows become anorectic.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Cattle
  • Cells, Cultured
  • Dairying*
  • Feeding Behavior
  • Glucose / metabolism
  • Hepatocytes / metabolism
  • L-Lactate Dehydrogenase / metabolism
  • Liver / metabolism*
  • Liver / physiology*
  • Milk
  • Phosphates / blood
  • Phosphorus / deficiency*
  • Phosphorus / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Urea / metabolism

Substances

  • Phosphates
  • RNA, Messenger
  • Phosphorus
  • Urea
  • L-Lactate Dehydrogenase
  • Glucose

Grants and funding

We received funding for this study from Boehringer Ingelheim Vetnedica. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. IDEXX Laboratories also provided support in the form of a salary for author A.E.M., but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of this author are articulated in the ‘author contributions’ section.