Vitamin B-6 deficiency vs folate deficiency: Comparison of responses to methionine loading in rats

Joshua W. Miller, Marie R. Nadeau, Donald Smith, Jacob Selhub

Research output: Contribution to journalArticle

164 Citations (Scopus)

Abstract

The plasma homocysteine response to methionine loading was assessed in vitamin B-6- and folate-deficient rats. Rats fed vitamin B-6-or folate- deficient diets for 4 wk were administered a gastric gavage of methionine (100 mg/kg body wt). Subsequent plasma analyses revealed a peak post- methionine load increase in plasma homocysteine concentration of > 300 μmol/L in the vitamin B-6-deficient rats. Folate-deficient rats exhibited no significant changes in plasma homocysteine after the load. These disparate responses can be explained by the observed increase in hepatic S- adenosylmethionine (SAM) concentration because of the load. In vitamin B-6 deficiency, increased SAM inhibits homocysteine remethylation, which, in conjunction with the impaired homocysteine catabolism due to the deficiency and the increased synthesis of homocysteine due to the methionine load, leads to a large elevation of homocysteine in the blood. In folate deficiency, increased SAM activates homocysteine catabolism, which compensates for the increased synthesis of homocysteine due to the load and thus no change in blood homocysteine is observed. These results have significant bearing on the interpretation of both positive and negative responses to methionine loading in humans.

Original languageEnglish (US)
Pages (from-to)1033-1039
Number of pages7
JournalAmerican Journal of Clinical Nutrition
Volume59
Issue number5
StatePublished - May 1994
Externally publishedYes

Fingerprint

Vitamin B 6 Deficiency
homocysteine
Homocysteine
pyridoxine
Folic Acid
folic acid
Methionine
methionine
rats
S-Adenosylmethionine
Vitamin B 6
S-adenosylmethionine
metabolism
synthesis
blood
Stomach
stomach

ASJC Scopus subject areas

  • Food Science
  • Medicine (miscellaneous)

Cite this

Vitamin B-6 deficiency vs folate deficiency : Comparison of responses to methionine loading in rats. / Miller, Joshua W.; Nadeau, Marie R.; Smith, Donald; Selhub, Jacob.

In: American Journal of Clinical Nutrition, Vol. 59, No. 5, 05.1994, p. 1033-1039.

Research output: Contribution to journalArticle

Miller, Joshua W. ; Nadeau, Marie R. ; Smith, Donald ; Selhub, Jacob. / Vitamin B-6 deficiency vs folate deficiency : Comparison of responses to methionine loading in rats. In: American Journal of Clinical Nutrition. 1994 ; Vol. 59, No. 5. pp. 1033-1039.
@article{615cfe2dc6f74b40b087c203b05509a7,
title = "Vitamin B-6 deficiency vs folate deficiency: Comparison of responses to methionine loading in rats",
abstract = "The plasma homocysteine response to methionine loading was assessed in vitamin B-6- and folate-deficient rats. Rats fed vitamin B-6-or folate- deficient diets for 4 wk were administered a gastric gavage of methionine (100 mg/kg body wt). Subsequent plasma analyses revealed a peak post- methionine load increase in plasma homocysteine concentration of > 300 μmol/L in the vitamin B-6-deficient rats. Folate-deficient rats exhibited no significant changes in plasma homocysteine after the load. These disparate responses can be explained by the observed increase in hepatic S- adenosylmethionine (SAM) concentration because of the load. In vitamin B-6 deficiency, increased SAM inhibits homocysteine remethylation, which, in conjunction with the impaired homocysteine catabolism due to the deficiency and the increased synthesis of homocysteine due to the methionine load, leads to a large elevation of homocysteine in the blood. In folate deficiency, increased SAM activates homocysteine catabolism, which compensates for the increased synthesis of homocysteine due to the load and thus no change in blood homocysteine is observed. These results have significant bearing on the interpretation of both positive and negative responses to methionine loading in humans.",
author = "Miller, {Joshua W.} and Nadeau, {Marie R.} and Donald Smith and Jacob Selhub",
year = "1994",
month = "5",
language = "English (US)",
volume = "59",
pages = "1033--1039",
journal = "American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "5",

}

TY - JOUR

T1 - Vitamin B-6 deficiency vs folate deficiency

T2 - Comparison of responses to methionine loading in rats

AU - Miller, Joshua W.

AU - Nadeau, Marie R.

AU - Smith, Donald

AU - Selhub, Jacob

PY - 1994/5

Y1 - 1994/5

N2 - The plasma homocysteine response to methionine loading was assessed in vitamin B-6- and folate-deficient rats. Rats fed vitamin B-6-or folate- deficient diets for 4 wk were administered a gastric gavage of methionine (100 mg/kg body wt). Subsequent plasma analyses revealed a peak post- methionine load increase in plasma homocysteine concentration of > 300 μmol/L in the vitamin B-6-deficient rats. Folate-deficient rats exhibited no significant changes in plasma homocysteine after the load. These disparate responses can be explained by the observed increase in hepatic S- adenosylmethionine (SAM) concentration because of the load. In vitamin B-6 deficiency, increased SAM inhibits homocysteine remethylation, which, in conjunction with the impaired homocysteine catabolism due to the deficiency and the increased synthesis of homocysteine due to the methionine load, leads to a large elevation of homocysteine in the blood. In folate deficiency, increased SAM activates homocysteine catabolism, which compensates for the increased synthesis of homocysteine due to the load and thus no change in blood homocysteine is observed. These results have significant bearing on the interpretation of both positive and negative responses to methionine loading in humans.

AB - The plasma homocysteine response to methionine loading was assessed in vitamin B-6- and folate-deficient rats. Rats fed vitamin B-6-or folate- deficient diets for 4 wk were administered a gastric gavage of methionine (100 mg/kg body wt). Subsequent plasma analyses revealed a peak post- methionine load increase in plasma homocysteine concentration of > 300 μmol/L in the vitamin B-6-deficient rats. Folate-deficient rats exhibited no significant changes in plasma homocysteine after the load. These disparate responses can be explained by the observed increase in hepatic S- adenosylmethionine (SAM) concentration because of the load. In vitamin B-6 deficiency, increased SAM inhibits homocysteine remethylation, which, in conjunction with the impaired homocysteine catabolism due to the deficiency and the increased synthesis of homocysteine due to the methionine load, leads to a large elevation of homocysteine in the blood. In folate deficiency, increased SAM activates homocysteine catabolism, which compensates for the increased synthesis of homocysteine due to the load and thus no change in blood homocysteine is observed. These results have significant bearing on the interpretation of both positive and negative responses to methionine loading in humans.

UR - http://www.scopus.com/inward/record.url?scp=0028220787&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028220787&partnerID=8YFLogxK

M3 - Article

C2 - 8172087

AN - SCOPUS:0028220787

VL - 59

SP - 1033

EP - 1039

JO - American Journal of Clinical Nutrition

JF - American Journal of Clinical Nutrition

SN - 0002-9165

IS - 5

ER -