The effect of dietary protein deficiency on transport of vitamin A in the blood and its storage in the liver

Friend, Colin; Heard, C. R. C.; Platt, B. S.; Stewart, R. J. C.; Turner, M.

doi:10.1079/bjn19610028

Cited by 66 publications

(7 citation statements)

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“…Heard (1966) reported that the carbohydrate metabolism of protein-calorie deficient pigs was modified in a manner in keeping with a widespread diminution of endocrine secretions with a relatively excessive secretion of glucocorticoids. In such pigs the blood composition (Heard, Platt & Stewart, 1958), transport of vitamin A (Friend, Heard, Platt, Stewart & Turner, 1961) and growth of bone (Platt & Stewart, 1962a), as well as the electro¬ encephalograms and morphology of the nerve cells (Platt, Pampiglione & Stewart, experiments in Table 3. Towards the end of the experiments the food consumption of some of the animals, especially those receiving carbohydrate supplements, fell below the amounts shown and the supplements were then usually withdrawn.…”

Section: Introductionmentioning

confidence: 97%

Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Platt¹,

Stewart²

1967

Journal of Endocrinology

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The endocrine glands of the protein-calorie deficient animals were smaller than those of pigs of the same age normally fed. However, relative to body weight, the adrenals were large, the hypophysis within the normal range, the thymus small and the pancreas and thyroid showed wide variations attributable to different degrees of oedema.In the tissues of the endocrine glands of the protein-calorie deficient animals the cells exhibited a loss of cytoplasm and, when normally present, of secretory granules, the severity of the change varying widely between the different organs of the same animal. Thus the exocrine portion of the pancreas was more severely affected than the islet tissue; within the latter \ g=b\ cells showed greater changes than did \g=a\cells. The cells of the thyroid gland were flattened and epithelioid in shape and those of the hypophysis were small, with many partially or wholly degranulated chromophiles. The zona fasciculata of the adrenal cortex was usually less severely affected, with, at some stages, a relatively excessive activity which contributed to the precarious endocrine balance. Since most of the animals were killed before sexual maturity less attention was given to the gonads. Testes, however, appeared to be affected by the deficiency to a greater extent than did ovaries.The relationships between protein-calorie deficiency, hypophysectomy and an excess of corticosteroids are discussed. It is suggested that in protei n\x=req-\ calorie deficiency, an adequate supply of protein for anabolic purposes is the primary factor with a subsequent alteration in hormonal secretions playing an important, but secondary, role.

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Section: Introductionmentioning

confidence: 97%

Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Platt¹,

Stewart²

1967

Journal of Endocrinology

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“…Clinical vitamin A deficiency with low serum levels of vitamin A has been observed in children suffering from protein-calorie deficiency (Trowell, Moore & Sharman, 1954 Gopalan, Venkatachalam & Bhavani, 1960); administration of protein without added vitamin A results in an increase in the serum level of vitamin A (Gopalan et al 1960;Arroyave, Wilson, Mendez, Behar & Scrimshaw, 1961). An impaired utilization of vitamin A by protein-deficient pigs has been observed by Friend, Heard, Platt, Stewart & Turner (1961). They also reported that the level of serum vitamin A correlated well with the level of serum albumin.…”

Section: Discussionmentioning

confidence: 85%

Effect of protein depletion on the electric response of the retina in albino rats

Auerbach¹,

Guggenheim²,

Kaplansky³

et al. 1964

The Journal of Physiology

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The limiting factor for seeing in dim light is the concentration ofrhodopsin in the retina. The formation of rhodopsin from opsin and the carotenoid retinene (vitamin A aldehyde) is the pre-requisite for the absorption of energy quanta. This in turn triggers electrical impulses which are propagated along the nervous pathways which connect the receptors with the brain. Deficiency of vitamin A leads, therefore, to hemeralopia. Wald (1955) has pointed out that the role played by opsin has been neglected in favour of its prosthetic group, vitamin A. Opsin may indeed be of equal importance, and a 'failure of opsin rather than vitamin A may be the predominant cause of night blindness'. It is therefore most probable that the lack of opsin would result in effects which are similar to those resulting from vitamin A deficiency.Since the impact of light quanta on the molecules of rhodopsin results in the elicitation of a nervous impulse, the measurement of the electrical response of the retina has proved to be an indicator of the rhodopsin concentration in the retina and, therefore, of the effects of deprivation of vitamin A. Moreover, the existence of a linear relation between the log threshold and the rhodopsin concentration could be demonstrated electroretinographically in albino rats (Dowling, 1960a, b;Dowling & Wald, 1960), and densitometrically in a colour-normal human observer and in a monochromat (Rushton, 1961a, b).In this paper the effect of protein depletion on the electrical response is investigated. It deals indirectly, therefore, with two further questions: whether the lack of protein interferes with the formation of opsin in the retina; and whether dietary deficiency of protein leads to changes in the electrical response of the retina similar to those found in vitamin A deficiency. Physiol. 172 27

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“…The diet contained all known vitamin and mineral requirements, but proteincalorie deficiency can modify the transport of some of these; for instance, a low serum albumin reduces the concentration in serum of vitamin A (Friend et al 1961) and calcium (Linneweh 1939). It is therefore possible that a similar impaired transport or utilisation of other nutrients could be involved.…”

Section: Plate V Photomicrographs Of the Gyms Suprasylvius Of The Cementioning

confidence: 99%

Effects of Protein‐Calorie Deficiency on Dogs 2. Morphological Changes in the Nervous System

1969

Develop Med Child Neuro

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SUMMARY An increased concentration of neuroglial cells was found in the spinal cords of dogs maintained from weaning on diets of low protein value. Most of the additional cells were perineuronal oligodendrocytes, but some activated astrocytes were present and there was an increase in the size and number of their fibres. The walls of the myelin sheaths were thinner than in age‐controls. During the more severe stages of the protein‐calorie deficiency syndrome (8–11 weeks of age), there was a loss of Nissl substance from the motor cells of the anterior horns and small changes occurred in the histochemical activity of the glutamic and succinic dehydrogenases. Changes in the basal ganglia and thalamus, although definite, were less marked, and in the cerebral cortex the changes were minimal. Only in the cerebellum was there any evidence of cell loss. Changes of similar type but greater severity were found in the congenitally malnourished pups and, in addition, there was a reduced number and concentration of nerve cells in the cerebral cortex. The morphological changes observed in the dogs are discussed in relation to clinical signs described in malnourished children. It is suggested that malnutrition during intrauterine and early postnatal life may lead to irreversible changes within the central nervous system. Resume Effets de l' insuffisance alimentaire en proteines et en calories chez le chien II. Changements morphologiques dans le système nerveux Une concentration accrue de cellules neurogliales a été trouvee dans la moelle épinière de chiens, maintenus à un régime appauvri en protéine et calories depuis le sevrage. La plupart des cellules supplémentaires étaient du type oligodendrocytes péri‐neuronales, mais quelques astrocytes actifs étaient présents; et il y avait une augmentation en taille et en nombre de leurs fibres. L'épaisseur des gaines de myéline était plus fine que chez les sujets contrôles du même âge. Au cours des périodes les plus sévères du syndrome de deaficience protéinique et calorique (8 à 11 semaines d'âge chronologique), on notait une perte des corps de Nissl au niveau des cellules motrices de la come antérieure et de légeres modifications dans les activités histo‐chimiques des déhydrogénases glutamiques et succiniques. Les modifications dans les noyaux gris centraux et dans le thalamus, quoique certaines, étaient moins marquées et au niveau du cortex cérébral les perturbations étaient minimes. C'est seulement au niveau du cervelet que l'on pouvait noter quelques pertes cellulaires. Des troubles identiques mais beaucoup plus sévères ont été trouves chez les chiots mal nourris depuis le moment de la naissance et de plus, on a trouve un nombré et une concentration de cellules nerveuses diminuées dans le cortex cérébral. Les changements morphologiques observés chez le chien sont discutés par comparaison avec les signes cliniques décrits chez les enfants insuffisamment alimentés. II est suggéié que le malnutrition durant la vie intra‐utérine et immédiatement post‐natale peut conduire à des modifica...

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The effect of dietary protein deficiency on transport of vitamin A in the blood and its storage in the liver

Cited by 66 publications

References 16 publications

Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Experimental Protein-Calorie Deficiency: Histopathological Changes in the Endocrine Glands of Pigs

Effect of protein depletion on the electric response of the retina in albino rats

Effects of Protein‐Calorie Deficiency on Dogs 2. Morphological Changes in the Nervous System

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