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Thiamin, riboflavin and vitamin B6: impact of restricted intake on
physical performance in man.J
Am Coll Nutr. 1994 (6):629-40.
OBJECTIVE: A
combined marginally deficient status of thiamin, riboflavin, vitamin
B6 and vitamin C may affect physical performance, but the relative
contribution of each vitamin can only be speculated. In a previous
study we did not find any effect of restricted intake of vitamin C
individually. Therefore, the functional effect of restriction of
thiamin, riboflavin or vitamin B6, individually or in conjunction, was
investigated. METHODS: A double-blind, 2 x 2 x 2 complete factorial
experiment on the effects of thiamin, riboflavin and vitamin B6
restriction on physical performance was executed with 24 healthy men.
During 11 weeks of low vitamin intake, the subjects were given a daily
diet of regular food products providing no more than 55% of the Dutch
Recommended Dietary Allowances (RDA) for thiamin, riboflavin and
vitamin B6. Other vitamins were supplemented at twice the RDA level.
RESULTS: In vitamin-restricted subjects, blood vitamin levels,
erythrocytic enzyme activities and urinary vitamin excretion decreased
and in vitro erythrocytic enzyme stimulation increased. Short-time
vitamin restriction had no harmful effects on health. A significant
overall decrease was observed in aerobic power (VO2-max; 11.6%), onset
of blood lactate accumulation (OBLA; 7.0%) and oxygen consumption at
this power output (VO2-OBLA; 12.0%), peak power (9.3%), mean power
(6.9%) and related variables (p < 0.01). However, the observed
performance decrements could not be attributed to marginal deficiency
for any of the vitamins studied. CONCLUSION: The absence of
vitamin-specific effects on performance decrements due to thiamin,
riboflavin and vitamin B6 restriction suggests quantitatively similar
but non-additive effects of these B-vitamins on mitochondrial
metabolism.
Riboflavin
deficiency is associated with selective preservation of critical
flavoenzyme-dependent metabolic pathways.Biofactors.
1992 Jan;3(3):185-90.
Riboflavin is
a water soluble vitamin that serves as a precursor of flavin
mononucleotide and flavin adenine dinucleotide. These two compounds
are coenzymes in a variety of electron transfer reactions that occur
in energy producing, biosynthetic, detoxifying and electron scavenging
pathways. When an organism is confronted with inadequate dietary
riboflavin, characteristic changes occur in the cellular distribution
of the various flavin fractions as well as in the activities of flavin-dependent
enzymes. These changes suggest a specific hierarchic response to
riboflavin deficiency, e.g. the core electron transfer chain required
for ATP synthesis is preserved while the enzymes required for the
first step of fatty acid beta-oxidation are diminished. The mechanisms
by which the specific changes in enzyme activity are mediated have not
been completely identified, but appear to result from a combination of
diminished access of normal or near normal levels of apoenzyme to
coenzyme and diminished abundance of apoenzyme. The changes in
apoenzyme content potentially result from alterations in either
protein stability or gene expression. The response to riboflavin
deficiency of several key enzyme systems and the pathways affected
will be discussed and a hierarchic order by which specific enzyme
activities are preserved while others are decreased will be proposed.
The current understanding of the molecular mechanisms by which these
changes are mediated will be discussed.
Riboflavin
requirement of Filipino women.Eur
J Clin Nutr. 1992 Apr;46(4):257-64.
The level of
riboflavin intake that will correct riboflavin deficiency in seven
non-pregnant and in twelve pregnant Filipino women was determined in
order to reassess the adequacy of the current Recommended Dietary
Allowance (RDA) for riboflavin in Filipinos. Increasing levels of
riboflavin were given to the subjects who were rated as
riboflavin-deficient based on an initial erythrocyte glutathione
reductase activation coefficient (EGR-AC) of greater than or equal to
1.3 in screening. The minimum riboflavin requirement, defined as the
intake of riboflavin required to achieve an EGR-AC of less than 1.3,
was estimated from the regression of EGR-AC on riboflavin intake
(mg/1000 kcal). The estimates of minimum riboflavin requirement from
the non-pregnant women ranged from 0.16 to 0.42 with a mean of 0.35
+/- 0.09 (SD) mg/1000 kcal. For the pregnant subjects, the estimates
of minimum riboflavin requirement ranged from 0.36 to 0.81 with a mean
of 0.58 +/- 0.18 (SD) mg/1000 kcal. Adding 30% to the mean, to cover
the upper limits of 97.5% of the population, the estimated RDA for
non-pregnant women is 0.46/1000 kcal. This value is approximately
equal to the 1976 Philippine RDA of 0.5 mg riboflavin/1000 kcal. For
pregnant women, adding 30% to the mean minimum requirement of 0.58
mg/1000 kcal, the estimated RDA is 0.75 mg/1000 kcal or 1.75 mg/day
computed at the energy allowance of 2350 kcal during pregnancy. This
value is 25% higher than the current Philippine RDA of 1.4 mg/day for
pregnant women.
Riboflavin
deficiency and iron absorption in adult Gambian men.Ann
Nutr Metab. 1992;36(1):34-40.
Iron
absorption from 3.38 mg 58Fe was measured in riboflavin-deficient
Gambian men with haemoglobin (Hb) less than 11.5 g/dl before and after
oral riboflavin therapy, and the results compared with a group not
receiving riboflavin. Riboflavin status (as determined by erythrocyte
glutathione reductase activation coefficient) and Hb increased in teh
riboflavin-supplemented but not placebo group. Plasma ferritin levels
were low and did not change in either group. There was very wide
variation in percentage iron absorption between individuals and also
within single individuals on two separate occasions but no measurable
change with riboflavin supplementation. The results of the study
indicate that the efficiency of iron utilization is impaired in
riboflavin deficiency, but that iron absorption is unaffected.
Significance
of phototherapy-induced riboflavin deficiency in the full-term
neonate.Biol
Neonate. 1992;61(2):76-81.
As a result of
impaired fatty acid oxidation, a characteristic urinary dicarboxylic
aciduria occurs in the riboflavin deficient animal. We compared the
occurrence of riboflavin deficiency induced by phototherapy with
changes in urinary organic acid profiles in 8 full-term, breast-fed
neonates who received phototherapy for hyperbilirubinemia, and in 10
full-term, breastfed controls. Riboflavin status was assessed by
measuring flavin adenine dinucleotide saturation of erythrocyte
glutathione reductase. All 8 neonates exposed to phototherapy
developed riboflavin deficiency (p less than 0.001). Riboflavin
deficiency was progressive with the duration of phototherapy. None of
the controls was riboflavin deficient. Urine organic acid profiles
indicative of mitochondrial acyl-CoA dehydrogenase activity (fatty
acid beta-oxidation, quantitated by gas chromatography mass
spectrometry) showed no changes between the study and control groups
in mono-, di-, or tricarboxylic acids or other organic acids. The
riboflavin deficiency induced by phototherapy in full-term neonates
was not of sufficient severity to limit riboflavin-dependent fatty
acid oxidation.
Intramitochondrial fatty acid metabolism: riboflavin deficiency and
energy production.
Biochem Cell Biol. 1991 Jul;69(7):490-7.
Inborn errors
of fatty acid beta-oxidation have contributed significantly to our
understanding of intracellular fatty acid metabolism. The first
intramitochondrial step in beta-oxidation of fatty acyl-CoA of
different chain lengths is catalyzed by the three chain length
specific acyl-CoA dehydrogenases. Inherited deficiency of these
enzymes has been reported. Some are riboflavin responsive. The first
step of fatty acid oxidation is reviewed with specific emphasis on
beta-oxidation in newborn infants, rendered riboflavin deficient by
phototherapy. Given that medium chain fatty acids are not stored as
triacylglycerols and undergo rapid beta-oxidation, they have been
proposed as superior substrates compared with long chain triglycerides
in times of metabolic stress. This review also examines medium chain
triglycerides as an alternate energy source. When medium chain
triglycerides were fed as 50% of total energy, glucose sparing was
present with little loss of energy as dicarboxylic acids.
Recurrent
aphthous ulceration: vitamin B1, B2 and B6 status and response to
replacement therapy.
J Oral Pathol Med. 1991
Sep;20(8):389-91.
An evaluation
of the thiamine, riboflavin and pyridoxine (vitamin B1, B2 and B6)
status of 60 patients with recurrent mouth ulcers was performed.
Seventeen patients (28.2%) were found to be deficient in one or more
of these vitamins. Replacement therapy of these vitamins was given to
a study group of deficient patients and a non-deficient group for one
month. At the end of therapy and after a follow-up period of 3 months,
only those patients who had a B complex deficiency had a significant
sustained clinical improvement in their mouth ulcers. Vitamin B1, B2
and B6 deficiencies should, therefore, be considered as another
possible precipitating factor in recurrent aphthous ulceration.
Vitamin
B1, B2 and B6 status of vegetarians.:
J Med Assoc Thai. 1991 Oct;74(10):465-70.
The vitamin
B1, B2 and B6 status was determined in 132 healthy vegetarians, age
range 25-57 years who have been practising vegetarianism for 1-22
years. Sixty-eight healthy non-vegetarians were chosen as controls.
The conventional methods to measure the activation coefficient alpha
ETK, alpha EGR and alpha EAST were applied to assess the vitamin
status of B1, B2 and B6 respectively. The value of 1.25 alpha ETK, 1.5
alpha EGR and 2.0 alpha EAST and above indicate a deficiency in the
vitamin status. The results showed significantly poorer vitamin B1 and
B6 status in vegetarians than in non-vegetarians, whereas, no
significant difference in vitamin B2 status was found. None of the
non-vegetarians were deficient in vitamin B1 but 3 of them (4.4%) were
deficient in vitamin B6. On the other hand, 10 of vegetarians (7.6%)
were deficient in vitamin B1; 38 (28.8%) in vitamin B6. A high
prevalence of riboflavin deficiency was found in 32 (24.2%) of the
vegetarians; as well as in 15 (22.2%) of the non-vegetarians. Only
riboflavin status was significantly related with the duration of
vegetarianism practiced. Vegetarians should be considered as the
vulnerable group for vitamin B2 and vitamin B6 deficiencies.
B-vitamins status should be checked and efforts should be made to
improve through dietary counselling and nutritional education should
be included and stress in the health education program in order to
improve nutritional deficiencies.
Riboflavin
deficiency caused by treatment with adriamycin.:
J Nutr
Sci Vitaminol (Tokyo). 1991 Oct;37(5):473-7.
The present
study was undertaken to determine whether administration of adriamycin
causes the depletion of riboflavin content. Rats received
intraperitoneal injections of adriamycin (4 mg per kg body weight) for
6 consecutive days. Urinary riboflavin excretion began to increase
after 2 days of treatment with adriamycin. Erythrocyte FAD levels
decreased gradually and plasma lipid peroxide contents increased
markedly at the 6th day. The activity coefficient of erythrocyte
glutathione reductase showed a significant increase before the
decrease of flavin content and the elevation of lipid peroxide level.
Therefore, the value of this coefficient obtained from erythrocyte
appears to be a reliable index of riboflavin deficiency, particularly
during the early stage.
Effect of
riboflavin or pyridoxine deficiency on inflammatory response.Indian
J Biochem Biophys. 1991
Oct-Dec;28(5-6):481-4.
Inflammatory
response has been assessed in riboflavin or pyridoxine deficient rats.
Edema was increased by 54% in pyridoxine deficiency as compared to
weight-matched control rats. Food restriction per se reduced the
volume of edema by 63%. In pyridoxine deficiency, concentrations of
thiobarbituric acid reactive substances (which indicate the extent of
lipid peroxidation) increase by 30 and 43% respectively in the
edematous tissues of the paw as well as in the wounded skin. Both
these parameters were not affected by riboflavin deficiency.
Activities of NADPH oxidase and superoxide dismutase in elicited
leukocytes from peritoneal cavity were reduced by 54 and 52%,
respectively, in riboflavin deficiency but were unaltered in
pyridoxine deficiency. Superoxide level and acid phosphatase activity
were not influenced by either of the deficiencies, whereas hydrogen
peroxide level was increased by 48% in riboflavin deficiency. Food
restriction did not affect leukocyte enzymes or the levels of reduced
oxygen species. The data suggest that inflammation is enhanced in
pyridoxine deficiency but not in riboflavin deficiency.
Riboflavin
deficiency: mucocutaneous signs of acute and chronic deficiency.
Semin
Dermatol. 1991 Dec;10(4):293-5.
Mucocutaneous lesions are present in both acute and chronic riboflavin
deficiency. The distribution of the lesions varies with the age and
gender of the patient. Lesions of acute riboflavin deficiency are
similar to those observed in protein-energy malnutrition of the
kwashiorkor type. In chronic riboflavin deficiency the cutaneous
lesions resemble monilial intertrigo and the mucous membrane lesions
include a characteristic glossitis. Prompt resolution of lesions after
therapeutic doses of the vitamin are given confirms the diagnosis.
Biochemical changes caused by riboflavin deficiency, which explain the
dermatoses and mucous membrane lesions, have not as yet been
determined. Lack of information in this area is explained by the
difficulty of separating cutaneous changes caused by the deficiency
from those caused by trauma or other proximate etiologic agents. |
Riboflavin, a vitamin derived from many plant and
animal sources, is important for the synthesis of flavin nucleotides,
which play an important role in electron transport and other reactions in
which the transfer of energy is crucial.