There are different names for nicotinic acid: niacin, vitamin PP (Pellagra preventis), and vitamin B3. Vitamin B3, and its inclusion in the vitamin B group, is not quite accurate. In organisms, niacin is presented as nicotinamide and is necessary for the synthesis of nicotinamide adenine dinucleotide (NAD) and nicotinamide dinucleotide phosphate (NADP (H)). These two molecules are important coenzymes involved in reducing oxide reactions and are present in over 100 enzymes. Niacin derives from tryptophan, both from the diet and from endogenous and ruminal synthesis. It is not clear if animal requirements are fully met by the synthesis of niacin molecules, or if a dietary supplementation is needed. These molecules can be used by rumen microflora but, if delivered in the free form, dietary supplementation is not completely available for animal absorption.
Niacin may reduce lipid tissue mobilization, especially during negative energy balance (NEBAL), typical of the transition period in ruminants. This lipolysis control leads to a lower non-esterified fatty acid (NEFA) and β- hydroxybutyrate circulating concentration, with consequent reduced risk of ketosis, and improved production and animal general health. Niacin dietary supplementation in a non-protected form may increase rumen protozoa and bacteria and, consequently, milk protein.
Niacin supplementation effects on dairy cows were investigated in past years. Nielsen et al. in their paper “A review of the effects of feeding niacin to early lactating dairy cows” (Acta Vet. Scand., 2003) concluded as follows: “Supplementary niacin does not reduce the mobilization of adipose tissue or the content of lipid in the liver. It is therefore unlikely that niacin can prevent fatty liver and ketosis. Furthermore, niacin does not affect feed intake, milk yield or milk composition in early lactating dairy cows”.
On the other hand, in 2005, Schwab et al. published “Review: a meta-analysis of lactation responses to supplemental dietary niacin in dairy cows”. They analyzed 27 studies published between 1980 and 1998 about the productive performance of dairy cows receiving niacin dietary supplementation. Their conclusion was that 6 g/head/day of niacin did not affect feed intake, feed efficiency, milk production and composition, BHBA, NEFA, or glycemia. On the contrary, 12 g/head/day improved milk production (FCM 4%) and feed efficiency. They individuated a positive correlation between niacin and metabolism, especially during the transition period, even if more studies were needed to completely understand the mechanisms.
These two papers indicated that the supplementation of niacin (lower than 12 g/cow/day) has only mild effects. But all these and previous studies were conducted with niacin in the free form. Nowadays it is well known that this type of niacin gives very few benefits in lactating dairy cows, while the synthesis of NAD and NADP(H) has been related to rumen microflora modulation.
In 2008, Niehoff et al. (Br. J. Nutr. 101:5-19) published their “Niacin for dairy cattle: a review” with interesting thoughts about niacin. They suggested that the rumen microflora of a 650 kg dairy cow, producing 35 kg/day of milk (FCM 4%), synthesizes 1800 mg/day of niacin. The niacin requirement for an animal of this size is 256 mg for tissues and 33 mg for milk production, so dietary supplementation is not needed. It should be noted that there are many factors influencing rumen niacin production and degradation, and the Niehoff study investigated only a few animals; even the authors had some doubt about the reliability of the data.
Many of the following studies, however, were conducted using rumen-protected niacin: results indicated positive effects on animal metabolism. Niacin reduces lipolysis and NEFA mobilization from lipid tissue during NEBAL. The weight loss due to the transition period and the NEBAL is physiological in dairy cows but if NEFA concentration increases more than 0.29 mmol/l in the peripartum and 0.6 mmol/l during lactation there is an ongoing pathology. When more than 15% of a herd has these NEFA concentrations, this can be due to incorrect diet, the environment, or poor management.
Lipolysis is determined by hormonal status, typical of the transition period (low insulinemia, tissue insulin-resistance, higher concentrations of glucagon and somatotropic hormone). The increase in plasma NEFA negatively influences the hypothalamic-pituitary-ovarian axis. It causes a delayed resumption of ovarian activity after calving, a higher risk of cystic degeneration of follicles, poor quality oocytes and corpus luteum, and an unfavorable uterine environment for the embryo in the pre-engraftment phase. It is clear there is a connection between dietary rumen-protected saturated fatty acids and NEFA from the endogenous lipid tissue, although it is possible to know plasma NEFA concentration, without distinguishing NEFA origin.
High NEFA also interferes with the immune system: Table 1 highlights some of their negative effects.
Table 1: Effects of the increase in plasma NEFA on the immune response of transition dairy cows. (Contreras et al. JDS 101:2737-2752)
|Cell type||Effect on the function||Variation||Reference|
|Polymorphonuclear leukocytes||Cell number||–||Sander et al. 2011|
|Chemotactic ability||–||Hammon et al. 2006;
Hoeben et al. 2000
|Phagocytic activity||–||Nonnek et al. 2003|
|Oxidative activity||Inhibition||Ster et al. 2012|
|ROS||+||Scalia et al. 2006|
|Mononuclear leukocytes||Apoptosis||+||Buhler et al. 2016|
|Proliferation and stimulation||–||Petzold et al. 2015;
Ster et al. 2012
|IgM and IFN-τ secretion||–||Lacetera et al. 2005 e 2004|
|Neutrophils||Apoptotic genes expression||+||Buhler et al. 2016|
|Lymphocytes||Mitogenic agents response||–||Lacetera et al. 2004;
Nonnecke et al. 2003
|IgM secretion||Inhibition||Lacetera et al. 2004|
|B cells||Immunoglobulin production||–||Lacetera et al. 2004|
Ruminants that mobilize a huge amount of NEFA (huge weight loss after calving) have a high risk of liver steatosis, ketosis, and related metabolic pathologies (abomasal dislocation, placenta retention, and puerperal metritis). Numbers of studies indicate that niacin is a good helper in lipolysis management. Diets that stimulate insulin production and the tissue sensitivity to this hormone are frequently insufficient to prevent NEBAL negative effects. Rumen-protected niacin reaches lipid tissue and adipocytes, inhibiting adenyl cyclase activity and consequently reducing the intracellular cyclic AMP activity.
There are three methods to quantify bovine weight loss and lipolysis management, both subjective and objective. The most frequent subjective method is the BCS evaluation through visual instrumental (BCS-camera, DeLaval) analysis. The objective methods are plasma NEFA determination, evaluation of milk fat production (less than 4.8% during the first 8 weeks of lactation), and milk analysis (FT-MIR).
Niacin has positive effects not only on lipid tissue mobilization but is useful also during heat stress periods. Rumen-protected niacin (8-16 g of active principle) induces peripheral vasodilation and increases sweat gland activity: the positive consequence is body heat dispersion through the skin. The experimental on-farm method to determine the efficacy of niacin supplementation is rectal temperature monitoring. An organism under heat stress (high environmental humidity and temperature) is unable to keep its body temperature stable. In dairy cows, even a 0.5°C increase in rectal temperature indicates heat stress so that niacin effectiveness is easily controlled in the herd.
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