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Effect of controlled vitamin B-6 intake and pyridoxine supplementation on B-6 status of smokersSindihebura-Ruhumba, Pascaline 05 May 1999 (has links)
Previous studies have found that smoking may have a negative effect on
vitamin B-6 indices and have demonstrated a possible association between smoking
and depressed plasma pyridoxal-5'-phosphate (PLP) concentration. Individuals with
plasma PLP values below the adequate level of 30 nmoles/L might benefit from
consumption of vitamin B-6 supplements, but no data are available on vitamin B-6
status in smokers consuming a controlled vitamin B-6 intake and receiving a vitamin
B-6 supplement. The objectives of this research were to assess vitamin B-6 status in
smokers as compared to non-smokers receiving a controlled diet and to evaluate the
effect of an oral vitamin B-6 supplementation in these subjects.
The vitamin B-6 (B-6) status of 5 (four males / one female) smokers (S) and 4
(three males / one female) non-smokers (NS) was assessed. A constant diet was fed
for 20 days and provided 1.95 mg of B-6 or 1.65 mg of B-6 for males and females,
respectively. For the last 10 days, an additional 2-mg of pyridoxine (PN) was given
daily. Blood samples were collected on days 1.7, 11.14 and 21; and 24 hour urine samples were collected daily. Urinary 4-pyridoxic acid (4-PA) and total B-6 (UB6)
excretion, plasma B-6 vitamers (PLP, PN, pyridoxal and 4-PA) and red blood cell
PLP (RBC PLP) concentrations, as well as plasma alkaline phosphatase activity
(APA) were determined. Mean plasma PLP, 4-PA, and RBC PLP concentrations
were significantly lower (P [less than or equal to] 0.05) at all time points in S compared to NS. With a
daily supplement of 2-mg vitamin B-6, the mean plasma PLP concentration of S
increased 85.8% but was 48.5% lower than that of NS consuming 1.65-1.95 mg/d of
B-6. Mean plasma pyridoxal concentrations were not different between S and NS
before and after supplementation. Excretion of 4-PA was not significantly different
between S and NS, but the mean values of 4-PA excretion were consistently greater
in NS compared to that of S throughout the 20-day study. The percent of ingested B-6 excreted as 4-PA for the S and NS was 38 and 49 in the non-supplemented period,
and 47 and 53 in the supplemented period, respectively, indicating that non-smokers
excreted more 4-PA than smokers. However, the difference in 4-PA excretion
between S and NS was not significantly different both before and after
supplementation (P>0.05). In addition, there was no significant difference between S
and NS for plasma PN concentration, AP, and UB6 excretion for both periods.
Results suggested an adverse effect of smoking on B-6 metabolism, thus an increased
requirement of vitamin B-6 in smokers. A 2-mg PN supplement was sufficient to
bring the concentration of plasma PLP in smokers to the level suggested as adequate,
but it didn't bring it to the level of non-smokers. / Graduation date: 1999
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Rolle der Pyridoxal 5´-Phosphat Phosphatase PDXP im Vitamin B6-Metabolismus muriner Erythrozyten und Hippocampi / Role of the pyridoxal 5´-phosphate phosphatase PDXP in the vitamin B6 metabolism of murine red blood cells and hippocampiWitzinger, Linda January 2020 (has links) (PDF)
Die Phosphatase PDXP (auch bekannt als Chronophin) gehört zur Familie der HAD Phosphatasen, einer ubiquitär exprimierten Enzymklasse mit wichtigen physiologischen Funktionen. PDXP zeigt Phosphatase-Aktivität gegenüber seinem Substrat Pyridoxal 5´-Phosphat (PLP), der aktivierten Form von Vitamin B6. PDXP-defiziente Mäuse (Knockout-Mäuse) weisen im Vergleich zu Wildtypen verdoppelte PLP-Konzentrationen in Erythrozyten sowie im Gesamthirn auf. Vermutlich kommt PDXP daher eine wichtige Funktion in Erythrozyten und im Hirn zu. Ziel dieser Arbeit war es, erste Einblicke in diese Funktion(en) von PDXP zu erlangen.
Hierzu wurden HPLC-basierte Analysen der erythrozytären PLP-Konzentrationen in Wildtyp- sowie PDXP-defizienten Mäusen durchgeführt. Dabei ließen sich die rund doppelt so hohen erythrozytären PLP-Level in den KO-Mäusen bestätigen. Zudem ist es gelungen, eine Methode zur Messung der endogenen Phosphatase-Aktivität von PDXP in Erythrozytenlysaten zu etablieren. So konnte im Wildtyp anhand der Verringerung der PLP-Konzentrationen pro Zeiteinheit eine erythrozytäre PDXP-Aktivität nachgewiesen werden. Dazu waren die Inkubation mit Pyridoxin, sowie die Anwendung eines Inhibitors der PDXK notwendig. Eine bis dato vermutete Funktion der PDXP, zur Mobilisation von erythrozytärem PLP während Fastenzeiten, konnte ausgeschlossen werden. So zeigte der Vergleich der erythrozytären PLP-Konzentrationen aus gefasteten mit normal gefütterten Tieren in beiden Genotypen exakt dieselbe prozentuale PLP-Verringerung. Während Nahrungszufuhr ließ sich jedoch eine Funktion der Phosphatase PDXP als „Converter“ von Pyridoxin zu Pyridoxal erkennen. Ausgehend von PN konnte im Wildtyp (über die Zwischenprodukte PNP und PLP) eine PDXP-abhängige Dephosphorylierung von PLP zu PL erfolgen. So wies der Wildtyp eine rund vierfach höhere PL-Produktion auf, verglichen mit der PDXP-defizienten Maus. Die Phosphatase PDXP erwies sich als essenziell für die erythrozytäre Konversion von Pyridoxin zu Pyridoxal. Dadurch erreicht der Organismus eine metabolische Flexibilität, die ihn bis zu einem gewissen Grad unabhängig von der Nahrungsauswahl macht. Zudem können Zellen oder Organe, denen durch das Fehlen der PNPO, die Konversion zu PLP nicht möglich ist, mit PL versorgt werden.
Aus der hohen Reaktivität von PLP mit umliegenden Nucleophilen ergibt sich eine gewisse Problematik für die Zelle im Umgang mit freiem PLP. So liegt der Großteil des erythrozytären PLPs gebunden an Proteine (vor allem Hämoglobin) vor. Anhand von Filtern (MWCO, 3000) ließ sich zwischen der hier definiert als „freien“ und der „gebundenen“ Form von PLP differenzieren. So konnten erste Erkenntnisse zur Rolle von PDXP als Determinator freier PLP-Konzentrationen in Erythrozyten und insbesondere im Hippocampus erlangt werden. Im Hippocampus ergaben sich insgesamt deutlich höhere Konzentrationen an freiem PLP als in den Erythrozyten und es bestand zudem ein Unterschied zwischen den Genotypen. So wiesen die KO-Mäuse ~1/3 höhere freie PLP-Konzentrationen im Vergleich zu den Wildtypen auf. Schließlich konnte ein Effekt des Tieralters auf den PLP-Metabolismus festgestellt werden. Sowohl in den Erythrozyten als auch im Hippocampus ergaben sich alterskorrelierte Änderungen ihrer PLP-Konzentrationen. Zudem zeigten Western Blot Analysen altersbedingte Unterschiede ihrer Vitamin B6-Enzymexpressionen. So wiesen ältere Wildtypen im Hippocampus eine fünffach erhöhte PDXP-Expression verglichen mit jüngeren Tieren auf. In den Erythrozytenlysaten hingegen zeigten ältere Tiere beider Genotypen eine rund vierfach geringere PNPO-Expression gegenüber jüngeren Tieren. Die mit dem Alter eintretende physiologische Verringerung der erythrozytären PNPO-Expression würde somit für den Organismus einen Verlust seiner metabolischen Flexibilität bedeuten, die mit der Konversion von PN zu PL einhergeht. / The phosphatase PDXP, also called Chronophin, is a member of the ubiquitously expressed HAD-phosphatases, which have some important physiological functions in the organism. Its substrate pyridoxal 5´-phosphate (PLP) is the active form of vita-min B6, an important cofactor of several reactions. PDXP-deficient mice (KO-mice) have PLP-concentrations in erythrocytes and in the whole brain twice as high as wildtype mice. It is assumed that PDXP therefore has an important function in erythrocytes and in the brain. The aim of the study was to gain initial insights into these functions of PDXP.
For this purpose, HPLC-based analyses of the PLP-concentrations in erythrocytes from WT- and KO-mice were carried out. The doubled PLP-levels in the RBCs of KO-mice could be confirmed. In addition, a method for measuring the endogenous phosphatase activity of PDXP in red cell lysates was established. The activity of PDXP could be measured by the reduction of its substrate PLP over time. This required the incubation with pyridoxine and the inhibition of PDXK by ginkgotoxine. An assumed function of PDXP in mobilization of PL(P) from the erythrocytes in fasting conditions could be ruled out. Therefore, a comparison between the PLP-concentrations in RBCs of fasted mice with normal fed ones was done. Surprisingly the fasted KO-mice showed the same percentaged decrease of cellular PLP-level as the fasted WT-mice. During vitamin B6 intake however, a function of PDXP as being a “converter” of pyridoxine to pyridoxal was found. Starting with PN, a PDXP-mediated dephosphorylation from PLP to PL could take place in the wildtype mice (via the intermediate steps PNP and PLP). Consequently, the WT´s production of PL quadrupled compared to the KO´s. PDXP turned out to be essential for the conversion of pyridoxine to pyridoxal in erythrocytes. This conversion confers some metabolic flexibility to the organism and to a certain extent makes it independent of the choice of food. Moreover, cells and organs, that due to the absence of PNPO cannot produce PL(P) themselves, can be provided via erythrocytes.
The high reactivity of PLP with surrounding nucleophiles poses a certain problem for the cell in dealing with free PLP. The majority of the PLP in RBCs is bound to proteins (primarily hemoglobin). It was distinguished between the here termed “free” PLP and the bound PLP by using filter devices with a MWCO at 3 kDa. First insights could be gained about PDXP as a determinant of free PLP-levels in erythrocytes and hippocampus. The amount of free PLP in the hippocampus was significantly higher than in the RBCs. Additionally, the hippocampus showed some differences in the con¬centration of free PLP between WT- and KO-mice. The level of free PLP in PDXP deficient mice was one third higher than in wildtype mice. Finally, some correlation between the age of the mice and their PLP-metabolism was found. The results revealed changes of the PLP-concentrations with age in the RBCs and the hippocampus. Moreover, western blot analyses showed some age-related differences in the expression of vitamin B6 enzymes. In the hippocampus older wildtype mice showed a quintupled expression of PDXP compared to younger ones. However, western blot analyses of red blood cell lysates from older animals revealed a lower expression of PNPO by a factor of four. For the organism this physiological reduction of its PNPO expression with age would mean a loss of metabolic flexibility, that is accompanied by the conversion from PN to PL.
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The effect of two levels of glucose ingestion on plasma pyridoxal 5'-phosphate concentrationHuang, Ying-Hui 11 January 2000 (has links)
This study was designed to evaluate the effect of glucose on plasma pyridoxal 5'-
phosphate (PLP) concentration. The objective was to determine whether there was a
negative relationship between glucose ingestion and plasma PLP concentration and to
evaluate the possible mechanism of decreased PLP after acute glucose ingestion.
Seven healthy subjects (three males and four females) completed the oral glucose
tolerance test (OGTT) on three separate occasions over a period of three weeks. Each
week, subjects ingested the assigned solutions (a water solution with artificial sweetener
equivalent to 25g glucose, a 25g glucose or a 75g glucose load) in a randomized order.
Plasma PLP, pyridoxal (PL), 4-pyridoxic acid (4-PA), pyridoxine (PN), glucose, insulin,
alkaline phosphatase (AP) activity and red blood cell PLP concentrations were measured
at 0 (fasting) (TO), 1 (T1), 2 (T2) and 3 (T3) hours.
The mean vitamin B-6 intake based on two 3-day dietary records was 1.57 ± 0.34
mg/day. All subjects had normal glucose tolerance. There were gender differences
among the three solutions. Both the water solution and the 75g glucose load showed a significant decrease in the mean plasma PLP concentration was observed at T3 for males
and at T2 for females (p<0.05). An overall mean decrease of 20% (9nmol/L) and 15% (7
nmol/L) was observed for males and females, respectively, after the 75g glucose load.
The 25g glucose load resulted in a lower decrease in the mean plasma PLP concentration
at each time point compared with the 75g glucose load, but no significant difference was
found in the level of decrease between the two glucose loads.
Both genders had a non-significant increase in the mean plasma PL and PN
concentrations for the three solutions. Mean plasma 4-PA concentration was decreased at
T1 with the three solutions. There was no significant change in the plasma AP activity at
any time points after the three solutions. In addition, no significant increase in mean red
blood cell PLP concentration was observed at all time points after the three solutions.
This study found a negative relationship between glucose ingestion and plasma PLP
concentration. However, it did not provide clear evidence for the hypothesized
mechanism of the decreased plasma PLP concentration after acute glucose load. Further
studies are required to determine the mechanism by which glucose decreases plasma PLP
concentration. / Graduation date: 2000
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Changes in plasma pyridoxal 5'-phosphate and red blood cell pyridoxal 5'-phosphate concentration during an oral glucose tolerance test in persons with diabetes mellitusMartinson, Kerry Elizabeth 11 March 1994 (has links)
The purpose of this study was to determine the relationship between the overall
changes in concentration of plasma pyridoxal 5'-phosphate (PLP), red blood cell PLP (rbc
PLP) and plasma glucose during an oral glucose tolerance test (OGTT) in persons with
diabetes mellitus (DM), and to test the hypothesis that the decrease in plasma PLP concentration
that occurs with increasing plasma glucose would be explained by a subsequent
increase in rbc PLP concentration. A second objective was to compare the distribution
of PLP between the red blood cell and the plasma (as measured by the rbc PLP/
plasma PLP ratio) in persons with diabetes to the distribution in non-diabetic controls.
The third objective was to measure fasting plasma alkaline phosphatase (AP) activity,
and to compare it to fasting plasma PLP concentrations, fasting rbc PLP concentrations,
and the rbc PLP/plasma PLP ratio. The purpose of this third objective was to test the
hypothesis that an increased plasma AP activity in persons with DM would be associated
with decreased plasma PLP and increased rbc PLP concentrations.
The study included 8 persons (3F; 5M) with insulin dependent diabetes mellitus
(IDDM), 9 persons (5F; 4M) with non-insulin dependent diabetes mellitus (NIDDM) and
18 healthy control individuals (9F; 9M). All subjects were given a 75 gm oral D-glucose
dose, and blood was drawn at 0 (fasting), 30, 60 and 120 minutes after the glucose load. Plasma glucose, PLP, insulin, and rbc PLP concentrations were measured at all time
points during the OGTT. Fasting plasma alkaline phosphatase (AP) activity, percent
glycosylated hemoglobin (%GlyHb), and the ratio between fasting rbc PLP and fasting
plasma PLP were also determined.
In general, females with DM were in poorer diabetic control as compared to males
with DM. Mean fasting glucose levels, %GlyHb and body mass index (BMI) were
highest in females with DM as compared to all other groups, and fasting insulin was
nearly 2x higher in females with NIDDM as compared to males with NIDDM.
There was an overall decrease in plasma PLP during the OGTT with increasing
plasma glucose, which agrees with results from other studies. The overall decrease in
plasma PLP (as measured by the negative, cumulative area under the curve: -AUC plp)
was significantly correlated with the overall increase in plasma glucose (as measured by
the positive, cumulative area under the curve: +AUC glu) for all study groups. The
relationship was stronger in all males, and control females as compared to females with
diabetes (p< 0.001 vs. p< 0.01, respectively). This difference was in part explained by
lower mean fasting PLP levels in females with DM (19.3 nmol/L), as compared to males
with DM (47.2nmol/L) and male and female controls (35.4 nmol/L and 34.0 nmol/L,
respectively).
The changes in rbc PLP during the OGTT were minimal, and did not significantly
correlate with the increase in plasma glucose or the decrease in plasma PLP. Thus, the
acute drop in plasma PLP concentration that occurred during the OGTT was not explained
by a subsequent increase in rbc PLP concentration, as had been hypothesized.
However, the higher than normal % glycosylated hemoglobin levels along with elevated
rbc PLP concentrations in persons with diabetes as compared to controls suggests that
chronically elevated blood glucose can contribute to increased rbc PLP concentrations.
This was the first study to date that has measured rbc PLP in persons with diabetes
mellitus. Rbc PLP values for persons with DM were 20-40% greater than respective control values at all time points during the OGTT. These differences between mean rbc
PLP in persons with DM as compared to control groups were all statistically significant
(p< 0.05) with the exception of the difference in the mean fasting rbc PLP value for
females with NIDDM as compared to controls. The mean values ± standard deviations
(SD) for fasting rbc PLP (nmol/L) were as follows: Females-IDDM, 49.5 ± 6.5;
NIDDM, 39.3 ± 4.9; controls, 31.4 ± 9.0; Males-IDDM, 37.8 ± 10.9; NIDDM, 45.6 ±
12.3; controls, 28.3 ± 4.4. The ratio of fasting rbc PLP concentration to fasting plasma
PLP concentration was 2-3x higher in females with DM as compared to control females
and all male groups. Females with IDDM had a ratio of 3.2, and the ratio for females
with NIDDM was 2.2. The ratios for all male groups, and control females were approximately
1:1, with a range of 0.8-1.2.
The mean fasting plasma AP activity was within the normal range for all study
groups. However, females with DM had higher AP activity (0.543 μkat/L) as compared
to female controls and males with DM (0.408 μkat/L, .425 μkat/L, respectively p<0.05).
There were no significant differences in mean fasting plasma AP activity between any
male group (range 0.390-0.465 μkat/L).
These results suggest that increased plasma glucose levels, increased AP activity,
and overall poor glycemic control contribute to decreased plasma PLP concentrations,
increased rbc PLP concentrations, and possibly to changes in the PLP distribution within
the body. / Graduation date: 1994
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The effect of vitamin B-6 supplementation on fuel utilization and plasma amino acids during exhaustive endurance exercise in menVirk, Ricky S. 16 August 1994 (has links)
Previous studies suggest that vitamin B-6 supplementation can alter fuel metabolism during
exercise and plasma amino acid levels at rest. To examine the effect of vitamin B-6
supplementation on plasma fuel substrates and amino acid levels during exercise, five trained
males (age: 29±7; V0₂ max: 54.7±6.2 ml/kg/min) performed two separate submaximal,
endurance, exercise tests on a cycle ergometer. Subjects were exercised to exhaustion at
74.5±7.8% V0₂ max in a fasted condition on the seventh morning of two separate nine day
controlled diet periods. The first exercise test (T1) occurred following a control or non-supplemented
(NS) diet (i.e. 1.9 mg B-6/day), and the second exercise test (T2) occurred
following a vitamin B-6 supplemented (S) diet (i.e. 1.9 mg B-6/day + 20 mg PN/day). Blood
was drawn pre, during (i.e. 60 minutes into exercise), post, and post-60 minutes of exercise,
and plasma was analyzed for glucose, lactic acid, glycerol, free fatty acids (FFA), and amino
acids. Expired air was collected for three minutes at 10 minute intervals during both tests.
Although not statistically different, there were observed trends for higher mean lactate levels
and lower mean glycerol and FFA levels in T2 (S) compared to T1 (NS). Mean lactate, glycerol,
and FFA concentrations all changed statistically significantly over time in both exercise tests.
Mean plasma tyrosine levels were significantly lower (p = 0.007) at post-60 minutes of exercise
and mean plasma methionine levels were significantly lower (p = 0.03) at post-exercise in T2
relative to T1. Of the 13 amino acids quantitated, only alanine and histidine concentrations changed significantly over time. Although not statistically significant, mean respiratory
exchange (R) values tended to be higher in T2 compared to T1. Mean oxygen consumption
values were significantly higher (p = 0.02) during the first 10 minutes of exercise and at
multiple later time points showed a trend for being higher in T2 compared to T1. No
statistically significant differences were observed in subjects' performance times to exhaustion
between T1 (1:35:49; hr:min:sec) and T2 (1:31:56). These results indicate that vitamin B-6
supplementation can potentially alter fuel metabolism and plasma amino acid levels during
exhaustive endurance exercise; however, not to such a degree that one's endurance capacity
is affected. / Graduation date: 1995
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Carbohydrate loading, vitamin B-6 supplementation, and fuel metabolism during exercise of differing intensity in post-absorptive manDeVos, Ann 21 May 1982 (has links)
Four young trained men were studied during 50 min of continuous
bicycle ergometer exercise [30 min at 60%, 15 min at 80%,
and 5 min at 90% maximal heart rate (MHR)] to elucidate changes
in fuel metabolism resulting from a glycogen depletion-repletion
regimen, and to determine the effect of supplemental vitamin B-6
(B6). The diets were: Week 1, 40% CHO normal diet (NC); Week 2,
days 1-3 CHO 11% (LC), days 4-7 CHO 71% (HC); Week 3, same as week
2 but with an 8 mg B6 supplement each day (LC+B6, HC+B6). The men
exercised after an overnight fast on days 4 and 7, upon completing
the depletion or repletion phase. Blood was collected before
exercise (PRE), during the 80% MHR work (DURING), immediately
after completion of the 90% MHR work (POST), and 30 min and 60
min after exercise (30 MIN POST, 60 MIN POST).
Plasma FFA concentrations were from 30% to 75% higher (p<0.05)
after the LC and LC+B6 diets than after the NC-1, NC-2, HC, or
HC+B6 diets, and B6 did not appear to affect plasma FFA levels.
Plasma glucose values were from 3% to 4% lower (p<0.01) for DURING
HC and HC+B6 than DURING NC-1. Since plasma HC and HC+B6 lactate
values were 57% higher (p<0.05) than DURING control values, the
simultaneously low glucose and high lactate levels indicate that
glucose was primarily derived from muscle glycogen in the HC and
HC+B6 conditions. Addition of B6 to the HC diet resulted in
elevated POST lactate levels, but this difference was not significant.
LC glucose and lactate values did not differ significantly
from control values. However, PRE LC+B6 glucose values
were 12% lower than PRE control values (p<0.02) and continued to
be lower during exercise. POST and 30 MIN POST LC+B6 values were
47% lower than the LC values (p<0.005 and p<0.01, respectively).
The glucose and lactate data indicate that B6 supplementation does
alter CHO metabolism when added to a glycogen depletion-repletion
regimen. Due to the possible role of glycogen phosphorylase as
an expanding depot for B6 storage, supplementation with B6 may
cause a more rapid emptying of muscle glycogen stores and a
reduction of athletic endurance. / Graduation date: 1983
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Determination of vitamin B-6 and pyridoxine-glucoside in selected Malawi foods and the effect of preparation techniques on vitamin B-6 and pyridoxine-glucoside contentKaunda, Jean R. 30 January 2002 (has links)
There were two main purposes to this study. The first was to determine the
vitamin B-6 and pyridoxine β-glucoside content of selected foods commonly
consumed in Malawi. The second was to examine the effect of preparation
procedures of foods in Malawi on the content of vitamin B-6 and pyridoxine β-
glucoside in foods. Seventeen plant foods commonly eaten in Malawi were
determined for vitamin B-6 and pyridoxine β-glucoside using a microbiological
assay. In addition, two commercial weaning foods, roasted maize-soy bean blend
and extruded maize-soy bean blend, were also determined for vitamin B-6 and
pyridoxine β-glucoside contents. Among all the foods analyzed, whole maize flour
contained the highest amount of vitamin B-6 (0.66 mg/100 g), therefore, an
excellent source of vitamin B-6 content in foods. Cooking decreased vitamin B-6
in pinto beans, kidney beans, sugar beans and cow peas by 34%, 45%, 14% and
48%, respectively. Roasting decreased vitamin B-6 in chick peas and soy beans by
59% and 38%, respectively. Soaking and fermentation reduced vitamin B-6 in
soaked maize flour and cassava flour by 86% and 89 %, respectively. Therefore,
these data suggest that some of the preparation procedures practiced in Malawi
have a negative impact on the vitamin B-6 content of the processed foods. Cooked
and roasted foods contained lower total amount of pyridoxine-glucoside than that
of the raw food. The high pyridoxine β-glucoside content have adverse impact on the bioavailability of vitamin B-6 content. Based on typical diets for the urban and
rural populations in Malawi, the rural diet contained less vitamin B-6 compared to
that of urban diet. Therefore, the rural population may be at risk of inadequate
vitamin B-6 intake compared to the urban population. / Graduation date: 2002
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Vitamin B-6 status of persons with diabetes mellitusSmith, Daniel E. 18 February 1991 (has links)
The status of vitamin B-6 (B6) nutriture of nine
persons (4F;5M) with insulin dependent diabetes mellitus
(IDDM), nine persons (5F;4M) with non-insulin dependent
diabetes mellitus (NIDDM), and 18 control individuals
(9F;9M) was evaluated, using biochemical and dietary
indicators of B6 status. The biochemical indices employed
were plasma concentration of pyridoxal 5'-phosphate (PLP),
urinary 4-pyridoxic acid (4PA) excretion, and urinary
kynurenic acid (KA) and xanthurenic, acid (XA) excretion
following a tryptophan load test (2 g L-tryptophan oral
load). Dietary B6 intake and the ratio of B6 (mg) to
dietary protein (g) (B6:protein) were determined.
Fasting blood, two consecutive 24 h urine collections
and three consecutive daily weighed diet records were
obtained on each of two occasions, separated by 30-70 d.
Diet records were analyzed for vitamin B-6 and protein
intake using nutrient data bases. Samples of 70 foods, for
which the data bases lacked B6 values, were obtained and
analyzed for total B6 content by a microbiological method.
The plasma concentration of PLP was determined by an
enzymatic method, and plasma alkaline phosphatase activity
by a colorimetric method. Urinary 4PA was separated by
HPLC, urinary KA and XA by ion exchange, and each
metabolite was determined fluorometrically.
The mean daily vitamin B-6 intake of each group
exceeded the recommended dietary allowance (RDA). The mean
B6:protein ratios ± standard deviations (SD) for the groups
of females were 0.0200±0.0027, 0.0304±0.0101, and
0.0254±0.0099 for IDDM, NIDDM and control (C),
respectively. The respective B6:protein ratios for the
males were 0.0280±0.0040, 0.0242±0.0038 and 0.0241±0.0078.
The mean±SD plasma PLP concentrations for females were
22.4±6.8, 21.8±9.6 and 37.4126.8 nmol/L for IDDM, NIDDM and
C, respectively. The mean plasma PLP concentrations of the
two groups of females with diabetes were at the low end of
a range (22.4-25.3 nmol/L) suggested to indicate marginal
status, and 56% of the females with diabetes had PLP
concentrations below the lower boundary of the marginal
range. For the three groups of males the PLP
concentrations were in the same rank order as dietary B6
intake; 53.9±18.2, 43.6±7.2 and 37.5±17.7 nmol/L for IDDM,
NIDDM and C, respectively. Plasma PLP concentration was
strongly and significantly correlated with B6 intake in
both diabetes (n=18, r=.744, p<.001) and C (n=18, r=.695,
p<.001) groups, but was also negatively associated with
plasma AP activity only for the diabetes group (n=18, r=-
.454, a=.058). The mean plasma AP activity of females with
NIDDM was significantly higher than that of the female C
group (p<.01). Greater than normal AP hydrolysis of PLP is
thought to have contributed to the low plasma PLP
concentrations observed in the females with NIDDM.
Levels of urinary 4PA excretion by females were
8.76±2.10, 7.61±12.57 and 8.15±14.43 μmol/d for IDDM, NIDDM
and C, respectively, or 87, 63 and 72% of B6 intake. For
males the urinary 4PA levels were 12.76±14.53, 10.32±11.77
and 9.81+3.34 μmol/d, respectively, or 76, 68 and 78% of B6
intake. All subjects excreted 4-PA in amounts indicative
of adequate B6 status.
All means for tryptophan metabolites were within
ranges seen for normal subjects, both pre and post-tryptophan load. None of the subjects with diabetes and
only one female C subject excreted more than 65 μmol XA in
24 h after the tryptophan load (upper boundary of normal
response to 2 g tryptophan load). Mean post-load excretion
of XA and KA of diabetes groups was numerically lower than
that of same sex controls in all comparisons, although in
only one instance was the difference significant (NIDDM
females post-load KA, p<.05). The results of the
tryptophan load test suggest adequate B6 function in the
kynurenine pathway those with diabetes and controls.
Individuals with diabetes were found to consume
adequate or above amounts of B6 by the standard of the RDA.
Low plasma PLP levels were observed in females with IDDM
who had the lowest B6 intake, and in females with NIDDM who
had the highest plasma AP activity. The present research
indicates that low PLP may be present in diabetes, as
observed by other investigators, despite seemingly adequate
B6 nutriture. However, normal to above normal amounts of
urinary 4-PA excretion indicated adequate body stores of
B6, and normal response to the tryptophan load test
suggested adequate function of B6 in the liver of persons
with diabetes. Plasma PLP concentration alone may not be
an adequate B6 status indicator in persons with diabetes.
Based upon the levels of multiple indicators, the vitamin
B-6 status of those persons with diabetes studied was
judged to be adequate. / Graduation date: 1991
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The effect of two carbohydrate diets and vitamin B-6 on vitamin B-6 and fuel metabolism and cardiac function during exercise in trained and untrained womenManore, Melinda, 1951- 30 July 1984 (has links)
Graduation date: 1985
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Synthesis and antioxidant properties of vitamin B₆ derivates; and [omega]-alkynylated fatty acids as substrates for preparation of modified phospholipids, novel probes for evaluating lipid-protein interactionsSerwa, Remigiusz. January 2008 (has links)
Thesis (Ph. D. in Chemistry)--Vanderbilt University, May 2008. / Title from title screen. Includes bibliographical references.
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