Specially designed to meet the needs for a healthy...
The horse is able to synthesize vitamin A (retinol) from ß-carotene and as such strictly speaking has a dietary requirement for the latter only.
The horse is able to synthesize vitamin A (retinol) from ß-carotene and as such strictly speaking has a dietary requirement for the latter only. In the small intestine, ß-carotene from the diet is converted to retinol by enzymes. ß-carotene is a natural pigment found in plants. Vitamin A is fat soluble, so it is stored in fatty tissues and, above all, in the liver.
Vision: A metabolite of vitamin A is a major compound of the retina rod and cone cells, allowing the photoreception of the light by the eye. Its function in night vision is very important.
Vitamin A functions in cell differentiation and as a result, plays crucial roles in reproduction and development of the foal in utero. Immunity: Vitamin A is important for maintaining immune response to infection. Skin and mucosa: Preservation of skin epithelial tissues and mucous membranes. Growth: Vitamin A is a cofactor stimulating chondrocyte differentiation (cartilage growth).
ß-carotene from plants (pasture>forage>grain) is the primary naturally occurring pro-vitamin A source in feedstuffs used for horses. Lucerne meal, red carrots or grass silage can help to counteract a vitamin A deficiency. Cod-liver oil is also a vitamin A source.
Daily Requirements (NRC, 2007):
30 to 60 IU/kg body weight (9 to 18 μg/kg body weight).
Anorexia, salivary gland abscesses, higher incidence of respiratory and intestinal disease, low rate of growth, weight loss, dull hair, anaemia, tearing and night blindness, keratinisation of skin and cornea. In reproduction: sub fertility, lower birth weights and contracted tendon in foal following vitamin A depletion of the dam.
Bone fragility, hyperostosis (excess bone formation), developmental orthopaedic disease in growing horses, exfoliation (flaking) of the epidermis, teratogenesis (strange tissues appearing in other tissues e.g. tooth growing in a testicle) and increased blood clotting time.
When problems may occur?:
Clinical signs of deficiency occur under fairly extreme conditions of deprivation. Deficiencies may arise from failure to supplement feed or from the provision of badly stored old feed: *horses stabled for most of their time, consuming little or no fresh herbage *Horses fed with old forage stored for a long time, with no other intake *Breeding mares deprived of pasture during winter. Toxicity is very rare, it only occurs when an owner over-supplements the diet.