Review: State of the knowledge on the importance of folates and cobalamin for dairy cow metabolism

Abstract

Synthesis of B vitamins by the rumen microbiota is usually sufficient to avoid the appearance of clinical deficiency symptoms in dairy cows under normal feeding conditions. Nevertheless, it is now generally accepted that vitamin deficiency is much more than the appearance of major functional and morphological symptoms. Subclinical deficiency, which is present as soon as the supply is lower than the need, causes cellular metabolic changes leading to a loss of metabolic efficiency. Folates and cobalamin, two B vitamins, share close metabolic relationships. Folates act as co-substrates in one-carbon metabolism, providing one-carbon unit for DNA synthesis and de novo synthesis of methyl groups for the methylation cycle. Cobalamin acts as a coenzyme for reactions in the metabolism of amino acids, odd-numbered chain fatty acids including propionate and de novo synthesis of methyl groups. Both vitamins are involved in reactions to support lipid and protein metabolism, nucleotide synthesis, methylation reactions and possibly, maintenance of redox status. Over the last decades, several studies have reported the beneficial effects of folic acid and vitamin B₁₂ supplements on lactation performance of dairy cows. These observations indicate that, even when cows are fed diets adequately balanced for energy and major nutrients, B-vitamin subclinical deficiency could be present. This condition reduces casein synthesis in the mammary gland and milk and milk component yields. Folic acid and vitamin B₁₂ supplements, especially when given together, may alter energy partitioning in dairy cows during early and mid-lactation as indicated by increased milk, energy-corrected milk, or milk component yields without affecting DM intake and BW or even with reductions in BW or body condition loss. Folate and cobalamin subclinical deficiency interferes with efficiency of gluconeogenesis and fatty acid oxidation and possibly alters responses to oxidative conditions. The present review aims to describe the metabolic pathways affected by folate and cobalamin supply and the consequences of a suboptimal supply on metabolic efficiency. The state of knowledge on the estimation of folate and cobalamin supply is also briefly mentioned.

Keywords: Methylmalonyl-CoA mutase; Methylneogenesis; Propionate; Subclinical deficiency; β-hydroxybutyrate.