Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of vitamin A deficiency on the pituitary-gonadal function were examined by measurements of serum and pituitary level of pituitary hormones and serum testosterone concentration, and by investigations of histological changes in the testis and the pituitary gland in vitamin A-deficient (VAD) and supplemented (VAS) rats. The growth of VAD rats was retarded and their body weights were decreased after 9 weeks of experiments and attained about one half of the weight of control animals at 12 weeks. In the VAD rats, serum testosterone concentrations were decreased significantly compared with those in the VAS controls. Serum and pituitary concentrations of GH were significantly lower but those of LH were slightly lower in the VAD rats than those in the controls, while the serum FSH concentration was significantly higher than that in the control rats. The seminiferous tubules in the testes of VAD rats were comprised largely of Sertoli cells and a reduced number of spermatogonia and contained fibrous formation in their lumen. In the pituitary gland, GH cells were significantly reduced in number in the VAD rats, but gonadotropic (GTH) cells were increased remarkably in size and number, showing hypertrophy and vacuolation similar to those in castration cells. The cytological changes in the pituitary gland and the increased discharge of FSH represent a secondary and compensatory change similar to that seen following castration and vitamin E deficiency.
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PMID:Effects of vitamin A deficiency on the function of pituitary-gonadal system in male rats. 251 46

Chronological changes of gonadotropin (FSH and LH) and testosterone concentrations in the serum were measured in vitamin E deficient rats to investigate the effects of vitamin E deficiency on the pituitary-gonadal function in rats. The receptor sites and association constant (Ka) for LH and the formation of cyclic AMP in the Leydig cells were also investigated. The results obtained in the present study are as follows: 1) The vitamin E deficient rats showed almost complete hemolysis and extremely increased TBA reacting substances (TBARS) in the serum and liver. 2) The serum LH concentration in the vitamin E deficient group was slightly higher than in the vitamin E supplemented group during the later periods of experiment. 3) The serum FSH concentration in the vitamin E deficient group did not differ significantly from that in vitamin E supplemented group, but became significantly higher than that in the latter at 186 days of experiment. 4) The serum testosterone concentration was always lower in the vitamin E deficient group than in the control. 5) The vitamin E deficient group showed slightly large number of LH/hCG receptor and significantly small Ka (low affinity), as compared with vitamin E supplemented group. The formation of cyclic AMP by Leydig cells decreased significantly in vitamin E deficient group. These results suggest that the vitamin E deficiency exerted a suppressive effect directly on the gonadal function to decrease the hormone synthesis in the Leydig cells and caused the increased secretion of pituitary LH owing to the feedback mechanism.
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PMID:Effects of vitamin E deficiency on the hormone secretion of the pituitary-gonadal axis of the rat. 282 55

Although vitamin E has been recognized as a requirement for normal testicular function for more than 50 yr, the functional role of this fat soluble vitamin in the maintenance of spermatogenesis has not been clarified. Vitamin E deficiency has a deleterious effect on germ cell proliferation and differentiation in the rat and a variety of other animal species. The potential effect of vitamin E on the sensitivity of the hypothalmo-hypophyseal-gonadal feedback system has not been previously evaluated. Therefore, serum testosterone concentrations, androgen function in maintaining seminal vesicle weight, and citrate synthesis, as well as the circulating amounts of FSH, were determined in rats fed semipurified diets with vitamin E, control, and without vitamin E, vitamin E-deficient. To assess dietary effects before, during, and after testicular degeneration, analyses were carried out on animals fed the diets starting at 3 weeks of age and continuing for 1 yr. The defect produced by vitamin E deficiency does not reflect impaired gonadotropin function. There are no effects of vitamin E deprivation on either serum levels of testosterone or on seminal vesicle weight and citrate content suggesting that the LH-testosterone feedback loop is not impaired. The feedback loop of FSH and inhibin also appears to be normal. Serum FSH concentrations are not elevated, although the testis is germ cell depleted. Comparison of the vitamin E-deficient model to other models of testicular degeneration suggests that the effect of vitamin E occurs directly or indirectly on the regulation of intratesticular factors which regulate specific steps of germ cell development.
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PMID:Effect of vitamin E deficiency on serum concentrations of follicle-stimulating hormone and testosterone during testicular maturation and degeneration. 309 3

Vitamin E is one of the most important lipid-soluble antioxidant nutrient. Severe vitamin E deficiency (VED) can have a profound effect on the central nervous system. VED causes ataxia and peripheral neuropathy that resembles Friedreich's ataxia. We report here a patient presenting this syndrome, but also a prolactin and FSH adenoma. Both the neurological syndromes and the adenoma regressed after treatment with alpha-tocopherol. Although, the presence of the prolactinoma in this patient may not be related to his vitamin E deficiency, alpha-tocopherol treatment seems to be beneficial and might usefully be tested in patients with hypophyseal secreting other forms of adenoma.
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PMID:Vitamin E deficiency ataxia associated with adenoma. 1006 78