Pantothenic acid deficiency in black and brown rats leads to a loss of fur color - at one time, pantothenic acid was known as the antigray hair factor. There is no evidence that the normal graying of hair with age is related to pantothenic acid nutrition, nor that pantothenic acid supplements have any effect on hair color.
In pantothenic acid-deficient rats, tissue CoA is depleted, affecting mainly the peroxisomal oxidation of fatty acids, which is mainly concerned with detoxication; mitochondrial f -oxidation, which is an essential energy-yielding pathway, is spared to a great extent (Youssef et al., 1997). However, relatively moderate deficiency in animals results in increased plasma triacylglycerol and nonesterified fatty acids, suggesting some impairment of lipid metabolism (Wittwer et al., 1990).
Rats on a pantothenic acid-free diet show rapid depletion of adrenal corti-costeroids, and reduced production of the steroids in isolated adrenal glands in response to stimulation with adrenocorticotrophic hormone (ACTH). This presumably reflects the role of acetyl CoA in the synthesis of steroids; deficiency also results in atrophy of the seminiferous tubules of male rats and delayed sexual maturation in females. As deficiency progresses, there is enlargement, then congestion, and finally hemorrhage, of the adrenal cortex. In young animals, but not in adults, pantothenic acid deprivation eventually leads to necrosis of the adrenal cortex.
Deficient animals have an impaired ability to respond to metabolic and physical stress as a result of this decreased adrenocortical hormone synthesis, although this may be accompanied by enhanced sensitivity of target tissues to hormone action. Some strains of rat are susceptible to the development of duodenal ulcers in pantothenic acid deficiency. Ulceration can be prevented by adrenalectomy and is exacerbated by administration of glucocorticoid hormones.
Dogs develop severe and potentially fatal hypoglycemia in pantothenic acid deficiency - this responds to the administration of glucocorticoid hormones, suggesting that it is secondary to impairment of adrenal cortical function.
Deficient animals are also more susceptible to infection than are adequately nourished control animals, with impaired antibody responses. This seems to be due to a defect in the transport of proteins destined for export from the cell as a result of the impairment of acylation of Golgi proteins.
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