Adrenal cortex pantothenic acid

Folic acid and pantothenic acids maintain secretions of steroids by adrenal cortex Niacin nicotinamide adenine dinucleotide (phosphate)... 

Rats on a pantothenic acid-free diet show rapid depletion of adrenal corticosteroids, 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 mbules 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. 

Relation of Pantothenic Acid to Salt and to the Adrenal Cortex. 150... 

With the development of knowledge concerning the role of pantothenic acid in intermediary metabolism, the critical importance of this vitamin to adrenocortical function becomes more understandable. When the adrenal cortex is stimulated by stressful situations, its function is to respond rapidly by secreting steroid hormones which initiate and maintain a variety of physiological reactions. Its ability to synthesize these hormones may depend on its capacity to mobilize energy rapidly. Pantothenic acid, as part of coenzyme A, plays a critical role in the oxidative metabolism of both carbohydrate and fatty acids and may also be involved directly in lipid synthesis. Therefore, a deficiency in pantothenic acid can create a situation in which the ability of the adrenocortical cells to secrete steroid hormones is seriously impaired. 

Pantothenic acid appears to be of critical importance in maintaining the integrity of the cells of the adrenal cortex. Morgan and Simms (1939) were the first to point out that the adrenals of rats on diets deficient... 

In pantothenate-deficient intact rats subjected to forced swimming or injected with ACTH, the typical lymphocytic response was abolished (Dumm et al., 1949). If the deficient animals received a high pantothenic acid diet for 4 days, a more nearly normal response followed either swimming or the injection of ACTH. These findings were attributed to the effects of pantothenic acid deficiency on the structure and function of the adrenal cortex. Winters el al. (1952a) observed that the lymphopenic and eosinopenic responses to ACTH and epinephrine were abolished following a 5- to 6-week period of pantothenate deficiency. However, fol-... 

In similar stress experiments following therapy with orally administered vitamin B12, no significant differences were observed in the determinations before and after therapy. Consequently, adaptation to the stress was not the cause of the changes which occurred following pantothenate therapy. The decrease in the eosinopenia and in uric acid/ creatinine ratio after pantothenate treatment suggests that the same environmental stress constituted a less severe stimulus to the adrenal cortex under these conditions. It may be that the increased level of pantothenate in the tissue cells contributed to their capacity to carry out the oxidative reactions which are part of the total physiological response to cold stress. It is possible that under these conditions the demand for adrenocortical hormones might be somewhat reduced. 

Pantothenic acid will affect both the structure and the function of the adrenal cortex. Changes in adrenocortical function are suggested by the decrease in adrenal cholesterol concentration in pantothenate deficiency. Additiomd evidence of impaired adrenocortical function in pantothenate deficiency is provided by the abnormal response of animals to various types of stress stimuli. The effects of pantothenate deficiency on the... 

Cowgill et stated that their own and previous work had established that a characteristic lesion developed in the adrenal cortex in response to pantothenic acid deficiency and that this lesion was more severe following treatment with ACTH but that cortisone prevented development microscopically. They concluded that the above work together with functional studies on carbohydrate metabolism supported the view that in pantothenic acid deficiency there was inadequate cortical function. They believe that pantothenic acid acting as coenzyme A is necessary for the synthesis of adrenal steroids. 

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