Interrelationships between vitamin B12 and patothenic acid in the rat in experimental thyrotoxicosis.

A general increase in metabolic rate in the hyperthyroid animal, leading to an
enhanced requirement of several growth essentials, including vitamin B12, has been
reported in literature (Emerson, 1949 ; Betheil and Lardy, 1949 ; Sure and Easterling,
1950 ; Kasbekar et ah, 1959). The retardation of growth in animals and
derangements in various phases of metabolism followed subsequently by a high
mortality rate are partially counteracted by supplementation with vitamin B12
(Kasbekar et al., loc. cit.).
On the basis of their observations on their reversal, by vitamin B12, of many
of the changes resulting from hyperthyroidism, Fatterpaker et al. (1955) indicate
that the primary manifestation of thyrotoxicosis is a deficiency of vitamin B12 and
that vitamin B12 probably acts by restoration, in part at least, of oxidative phosphorylation.
Kasbekar et al. (loc. cit.) in a detailed study of the effect of thyrotoxicosis
on mitochondrial morphology, composition and function, observe that the
depletion of liver stores of vitamin B12 is followed by a major derangement in the
metabolism of soluble sulfhydryl compounds and that these are corrected by
vitamin B12. Protective effects of dietary magnesium (Baltcheffsky, 1956 ; Vitale
et al, 1957; Gershoff et al., 1958) and of methionine (Boldt et al, 1958) against
several metabolic disturbances occurring in thyrotoxicosis are also known.
In view of the metabolic relationship between vitamin B12 and pantothenic acid
(Aiyar and Sreenivasan, 1961), it was thought of interest to study the changes in the
metabolism of coenzyme A and related sulfhydryl compounds in hyperthyroidism,
as also the protection afforded by vitamin B12, magnesium and l-methίonine against
these changes.