BLOOD TRANSAMINASE ACTIVITIES IN VITAMIN B6 DEFICIENCY: EFFECT OF DEPLETION AND REPLETION ON THE ERYTHROCYTE ENZYMES

1967 ◽  
Vol 45 (2) ◽  
pp. 343-351 ◽  
Author(s):  
M. C. Cheney ◽  
Z. I. Sabry ◽  
G. H. Beaton

To assess the usefulness of the erythrocyte transaminases, glutamic–oxaloacetic and glutamic–pyruvic, in the evaluation of vitamin B6 nutritional status, the response of these enzymes to repletion following 1, 4, and 10 weeks of vitamin B6 depletion was compared with that of the plasma and liver transaminases in the rat. The responses of the erythrocyte enzymes reflected the state of vitamin B6 nutrition most accurately and, unlike the plasma and liver transaminases, were not affected by other factors. Repletion produced a rapid response in the erythrocyte enzymes; however, restoration of control levels appeared to depend on red cell turnover, particularly after prolonged depletion periods. This finding suggests that the apoenzyme, as well as the coenzyme, is depleted during vitamin B6 deficiency.

1965 ◽  
Vol 43 (4) ◽  
pp. 591-599 ◽  
Author(s):  
M. C. Cheney ◽  
G. H. Beaton

Factorial design experiments in rats revealed that blood transaminase activity was sensitive to vitamin B6 dosage and was not affected by concurrent variation in riboflavin or thiamine administration.The blood transaminase activity was a better index of vitamin B6 nutritional status than was body weight response or liver transaminase activity. Similarly, erythrocyte transketolase activity was found to reflect thiamine dosage, and plasma riboflavin level to reflect riboflavin dosage, regardless of manipulation of pyridoxine dosage.


2021 ◽  
pp. 247412642110287
Author(s):  
Diana Driscoll ◽  
David Callanan

Purpose: This work reports retinal findings in an adult patient with vitamin B6 deficiency. Methods: A case review of a single patient is presented. Results: A patient with a Roth-type retinal lesion and a history of nonepileptic seizures was found to have lymphocytic colitis. She was treated with pyridoxine, which resolved her seizures and the white-centered hemorrhage. Conclusions: Vitamin B6 deficiency should be considered in the differential diagnosis of patients presenting with white-centered hemorrhages and a history of nonepileptic seizures.


1959 ◽  
Vol 5 (2) ◽  
pp. 45-50 ◽  
Author(s):  
A. S. ABBASSY ◽  
M. M. ZEITOUN ◽  
M. H. ABOUIWFA

1987 ◽  
Vol 44 (1) ◽  
pp. 219-222 ◽  
Author(s):  
Ronald W. Hardy ◽  
Edmundo Casillas ◽  
Toshiro Masumoto

Rainbow trout (Salmo gairdneri), initially averaging 125 g, were fed a complete or a pyridoxine-deficient diet for 14 wk. Vitamin B6 status was evaluated biweekly by direct measurement of liver pyridoxine and pyridoxal levels by HPLC and by determining pyridoxal-5′-phosphate-enhanced liver aspartate aminotransferase (ASAT) activity. By 14 wk, mortality had severely reduced the number of fish remaining in the pyridoxine-deficient group. At 14 wk, no significant differences in liver pyridoxine and pyridoxal levels were detected between the trout fed the complete or pyridoxine-deficient diet. Significant differences between dietary groups are found in ASAT activity in liver and percent stimulation of liver ASAT by the addition of pyridoxal-5′-phosphate after 8 wk. Clinical signs of vitamin B6 deficiency including anorexia, listlessness, frantic and erratic swimming, and ataxia were observed after 11 wk of feeding a pyridoxine-deficient diet. This study shows that vitamin B6 deficiency in rainbow trout can be readily determined weeks before signs of clinical deficiency are apparent by measuring pyridoxine-enhanced liver ASAT activity. However, liver levels of pyridoxine and pyridoxal are not sensitive indicators of vitamin B6 status.


1965 ◽  
Vol 43 (4) ◽  
pp. 579-589 ◽  
Author(s):  
M. C. Cheney ◽  
D. M. Curry ◽  
G. H. Beaton

The lowering of blood glutamic–oxaloacetic (GOT) and glutamic–pyruvic (GPT) transaminase activities was found to be specific for vitamin B6 deprivation among several B vitamins tested and in the presence of a simultaneous restriction of eight B vitamins, cortisone administration, or variation of dietary protein level. It was found that changes in blood transaminase activity did not always parallel those seen in liver transaminase activity. In the determination of vitamin B6 nutritional status, blood GPT activity appeared to be more sensitive than GOT activity and would seem to be as sensitive an indicator as xanthurenic acid excretion after a tryptophan load.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ashley M. Fields ◽  
Kevin Welle ◽  
Elaine S. Ho ◽  
Clementina Mesaros ◽  
Martha Susiarjo

AbstractIn pancreatic islets, catabolism of tryptophan into serotonin and serotonin receptor 2B (HTR2B) activation is crucial for β-cell proliferation and maternal glucose regulation during pregnancy. Factors that reduce serotonin synthesis and perturb HTR2B signaling are associated with decreased β-cell number, impaired insulin secretion, and gestational glucose intolerance in mice. Albeit the tryptophan-serotonin pathway is dependent on vitamin B6 bioavailability, how vitamin B6 deficiency impacts β-cell proliferation during pregnancy has not been investigated. In this study, we created a vitamin B6 deficient mouse model and investigated how gestational deficiency influences maternal glucose tolerance. Our studies show that gestational vitamin B6 deficiency decreases serotonin levels in maternal pancreatic islets and reduces β-cell proliferation in an HTR2B-dependent manner. These changes were associated with glucose intolerance and insulin resistance, however insulin secretion remained intact. Our findings suggest that vitamin B6 deficiency-induced gestational glucose intolerance involves additional mechanisms that are complex and insulin independent.


1980 ◽  
Vol 170 (4) ◽  
pp. 376-387 ◽  
Author(s):  
U.N. Riede ◽  
W. Sandritter ◽  
A. Pietzsch ◽  
R. Rohrbach

1998 ◽  
Vol 217 (1) ◽  
pp. 97-103 ◽  
Author(s):  
P. G. Masse ◽  
I. Ziv ◽  
D. E. C. Cole ◽  
J. D. Mahuren ◽  
S. M. Donovan ◽  
...  

1994 ◽  
Vol 50 (2) ◽  
pp. 127-129 ◽  
Author(s):  
T. Oka ◽  
N. Komori ◽  
M. Kuwahata ◽  
I. Suzuki ◽  
M. Okada ◽  
...  

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