Pantothenic Acid Deficiency Induced in Human Subjects.

Bean, William B.; Hodges, Robert E.

doi:10.3181/00379727-86-21204

Cited by 59 publications

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“…These were the theoretical considerations which led to the special study of gastric function during pantothenic acid deficiency in the hope of obtaining information of physiological and possibly therapeutic interest. This paper reports the results of these studies which were undertaken concurrently with those reported by Bean, Hodges, and Daum (2).…”

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confidence: 60%

“…Such was the case (2). Insofar as it was possible to predict the metabolic changes in this experiment it seemed likely that one feature would be a suppression of adrenal cortical function and that this might lead to a secondary reduction of gastric secretion.…”

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confidence: 99%

“…Reports of animal experiments and results of preliminary studies by Bean and Hodges (1) in man indicated that the metabolic effects of pantothenic acid deficiency in human subjects would be widespread and profound. Such was the case (2).…”

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The Effect of Pantothenic Acid Deficiency on Gastric Secretion and Motility

Thornton¹,

Bean²,

Hodges³

1955

J. Clin. Invest.

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Reports of animal experiments and results of preliminary studies by Bean and Hodges (1) in man indicated that the metabolic effects of pantothenic acid deficiency in human subjects would be widespread and profound. Such was the case (2). Insofar as it was possible to predict the metabolic changes in this experiment it seemed likely that one feature would be a suppression of adrenal cortical function and that this might lead to a secondary reduction of gastric secretion. On the other hand, following Lipmann's (3) demonstration that pantothenic acid is the active principle of coenzyme A, it has been shown that many metabolic processes involve acetylation reactions in which coenzyme A is essential (4). This led to the hypothesis that coenzyme A might play a fundamental part in the metabolism of parietal cells and that pantothenic acid deficiency would, therefore, have a direct inhibitory effect on their production of hydrochloric acid. These were the theoretical considerations which led to the special study of gastric function during pantothenic acid deficiency in the hope of obtaining information of physiological and possibly therapeutic interest. This paper reports the results of these studies which were undertaken concurrently with those reported by Bean, Hodges, and Daum (2). MATERIALS AND METHODSThe subjects of the experiment were three normal young adult men who had no previous history of gastrointestinal disease. During the experiment there were five different dietary periods. Since a palatable diet deficient in pantothenic acid cannot be prepared from natural foods, a synthetic liquid formula was prepared and this was administered directly into the stomach through a plastic tube 5 mm. in diameter. This formula, which contained an adequate supply of all essential food factors, including pantothenic acid, was given for an initial control period of 12 days. For a second period of 25 days the same formula was used but pantothenic acid was omitted and omega-methylpantothenic acid, a metabolic antagonist to pantothenic acid, was substituted.In the third phase of the experiment both pantothenic acid and the antagonist were administered with the object of correcting the deficiency. After six days of this regimen the expected improvement in the manifestations of deficiency had not occurred and it became necessary to allow a general diet by mouth supplemented by pantothenic acid and other vitamins. At this stage there were manifestations of insufficiency of the adrenal cortex and cortisone was administered in small daily doses for four days (2). Three days after terminating cortisone therapy tube feeding was resumed and continued for nine days as a final control period. The original formula containing pantothenic acid, but not the antagonist, was administered during this final period.Three tests were selected to compare gastric secretory and motor function during the development of deficiency with the normal function during the initial control period and during the final recovery period. These tests were a modificati...

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The Effect of Pantothenic Acid Deficiency on Gastric Secretion and Motility

Thornton¹,

Bean²,

Hodges³

1955

J. Clin. Invest.

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“…Because of the widespread occurrence of pantothenic acid (PA) in foods , deficiency symptoms in humans have not been observed except in cases of severe malnutrition [ 1 ] and in volunteers fed either the antagonist f2-methylpanthothenic acid or a semisynthetic diet virtually free of pantothenate [2,3]. Thus many of the known symptoms of a manifest PA deficiency have been seen only in experimental animals, which can be more rigorously controlled.…”

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Effects of Pantothenate Deficiency on Steroid Hormone Secretion in Rats

Pietrzik

1989

J. Clin. Biochem. Nutr.

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SummaryThe effect of pantothenic acid (PA) deficiency on the adrenocortical function was investigated in young male rats fed a PAdeficient (PAD) diet over a period of about three months. Pair-weight (PW) and ad libitum (AL) fed rats served as controls. Basal 08.00 h (lights on) plasma levels of corticosterone were regularly found to be reduced in PAD and AL rats compared with those in PW animals. Investigation of the circadian rhythm of plasma corticosterone revealed that the elevated 08.00 h hormone concentrations of PW rats are due to a biphasic 24-h pattern of plasma corticosterone with a distinct glucocorticoid peak at lights on and another one at lights off (20.00 h), whereas PAD and AL rats only show one clear increase in plasma corticosterone levels at the beginning of the dark period. However, the evening glucocorticoid peak of the PAD rats was markedly higher than that of the PW and AL groups. Thus an adrenocortical overactivity is ascertained in PA deficiency which is presumably responsible for the adrenal hypertrophy generally observed in earlier studies on PA depletion in rats. Multiple examinations of the secretory capacity for corticosterone, each carried out half an hour after i.m. administration of 2.5 IU ACTH1-24, revealed comparable plasma responses to supraphysiological ACTH stimulation in PAD, PW, and AL rats. Therefore we concluded that corticosterone secretion is not impaired in PA deficiency, at least not that elicited for short periods by adrenocortical overstimulation. Additional measurem ents of the adrenal cholesterol content and the circadian plasma levels of dehydroepiandrosterone-sulphate were carried out in all three diet groups. The respective results are discussed with regard to the stress situation produced by the experimental PA deficiency.

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“…Position Gastrointestinal changes are the subject of a The three subjects showed less evidence of cardioseparate report (38). vascular changes (Figure 3), but during the deIn our first patient (J. S.) we noted lability of ficiency period they had pulse rates of up to 120 pulse rate and a very wide pulse pressure (1) panied by dyspnea or distress. The basal systolic and diastolic blood pressures decreased.…”

Section: Clinicalmentioning

confidence: 99%