Vitamin A

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.

Description:

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.

Function:

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.

Reproduction:

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).

Sources:

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).

Deficiency:

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.

Excess:

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.

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