Journal of Clinical Biochemistry and Nutrition
Online ISSN : 1880-5086
Print ISSN : 0912-0009
ISSN-L : 0912-0009
Effects of Pantothenate Deficiency on Steroid Hormone Secretion in Rats
I. Assessment of the State of Function of the Adrenal Cortex
Thomas REMERKlaus PIETRZIK
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1989 年 6 巻 1 号 p. 1-14

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The effect of pantothenic acid (PA) deficiency on the adrenocortical function was investigated in young male rats fed a PA-deficient (PAD) diet over a period of about three months. Pair-weight (PW) and ad libitum (AL) fed rats served as controls. Basal 08.00h (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 08.00h 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 (20.00h), 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 measurements 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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