scholarly journals The influence of riboflavin deficiency on absorption and liver storage of iron in the growing rat

1986 ◽  
Vol 56 (1) ◽  
pp. 171-179 ◽  
Author(s):  
Delana A. Adelekan ◽  
David I. Thurnham
Keyword(s):  
Small Intestine ◽  
Iron Absorption ◽  
Separate Experiment ◽  
Intragastric Administration ◽  
Riboflavin Deficiency ◽  
Growing Rat ◽  
Liver Ferritin ◽  
Riboflavin Deficient ◽  
Liver Storage

1. Iron absorption was measured in weanling riboflavin-deficient (RD) rats or weight-matched (WM) controls fed on appropriate diets for 7 weeks. Concentrations of radio-Fe (68Fe) in plasma were monitored every 30 min for 4 h following intragastric administration.2. Total Fe absorption in RD rats was significantly lower than that in WM controls, and the tissues of the stomach and small intestine of RD rats retained significantly (P < 0.001) more 68Fe by comparison with WM groups.3. In a separate experiment, ferritin-Fe concentrations were measured in the livers of four groups of rats (adlib. (C), pair-fed (PF) and WM controls and RD) at day 0, and subsequently at days 14, 21, 28, 35 and 49.4. Liver ferritin-Fe concentration was significantly lower (P < 0.05) in RD rats than in all other controls after 3 weeks on the respective diets and remained lower for the remainder of the experiment.

scholarly journals Riboflavin deficiency in the rat: effects on iron utilization and loss

1991 ◽  
Vol 65 (3) ◽  
pp. 487-496 ◽  
Author(s):  
Hilary J. Powers ◽  
L. T. Weaver ◽  
S. Austin ◽  
A. J. A. Wright ◽  
Susan J. Fairweather-Tait
Keyword(s):  
Small Intestine ◽  
Test Meal ◽  
Proliferative Response ◽  
Iron Absorption ◽  
Whole Body ◽  
Separate Experiment ◽  
Riboflavin Deficiency ◽  
Riboflavin Deficient ◽  
Iron Utilization

Iron absorption and daily loss of Fe were measured in riboflavin-deficient (B2-) Norwegian hooded rats and controls (B2+). Animals were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d. Riboflavin deficiency led to a reduction in the percentage of the 59Fe dose absorbed and an increased rate of 59Fe loss. All post-absorption 59Fe loss could be accounted for by faecal 59Fe, confirming that the loss was gastrointestinal. Fe concentrations and 59Fe as a percentage of retained whole-body 59Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. These observations may explain the enhanced Fe loss in riboflavin deficiency.

scholarly journals A proposed intestinal mechanism for the effect of riboflavin deficiency on iron loss in the rat

1993 ◽  
Vol 69 (2) ◽  
pp. 553-561 ◽  
Author(s):  
Hilary J. Powers ◽  
Lawrence T. Weaver ◽  
Steven Austin ◽  
John K. Beresford
Keyword(s):  
Small Intestine ◽  
Iron Loss ◽  
Intestinal Epithelial ◽  
Riboflavin Deficiency ◽  
Cell Production ◽  
Twofold Increase ◽  
Fe Content ◽  
Weanling Rats ◽  
Small Intestinal ◽  
Riboflavin Deficient

The effect of riboflavin deficiency on gastrointestinal Fe distribution and loss was studied in weanling rats. Riboflavin deficiency was associated with a significant increase in crypt depth in the upper and mid small intestine and a twofold increase in the rate of crypt cell production compared with weight-matched and ad lih.-fed control rats. The rate of loss of endogenous Fe, measured as faecal 59Fe after intraperitoneally administered 59Fe, was twice that from riboflavin-deficient rats compared with weightmatched controls. We suggest that while there may be a contribution from turnover of enterocytes with an enhanced Fe content, enhanced Fe loss associated with riboflavin deficiency is due predominantly to an accelerated rate of small-intestinal epithelial turnover.

scholarly journals Cytokinetic and structural responses of the rat small intestine to riboflavin depletion

1996 ◽  
Vol 75 (2) ◽  
pp. 315-324 ◽  
Author(s):  
E. A. Williams ◽  
R. D. E. Rumsey ◽  
H. J. Powers
Keyword(s):  
Small Intestine ◽  
Wistar Rats ◽  
Rat Small Intestine ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Structural Responses ◽  
Normal Increase ◽  
Riboflavin Deficient

Abstract:The impaired absorption and metabolism of Fe seen in riboflavin defiaency is attributed, at least in part, to a hyperproliferative response in the small intestine, associated with an altered morphology. Studies were conducted in female weanling Wistar rats to explore further the effect of riboflavin deficiency on the cytokinetics and structure of the small intestine. Feeding a riboflavin-deficient diet for 8 weeks from weaning resulted in a significantly lower villus number, a significant increase in villus length and an increased rate of transit of enterocytes along the villi, compared with weight-matched controls. A second experiment focused on the 3 weeks after weaning and showed that riboflavin deficiency inhibits the increase in villus number observed in control animals over this period. We suggest that riboflavin deficiency induced at weaning impairs the normal increase in villus number and that prolonged deficiency leads to an adaptive increase in length of villi and depth of crypts.

Effect of Ethanol on Iron Absorption the Small Intestine of Rats

1972 ◽  
Vol 33 (4) ◽  
pp. 958-961 ◽  
Author(s):  
J. Wójcicki, ◽  
L. Samochowiec ◽  
M. Kadyków
Keyword(s):  
Small Intestine ◽  
Iron Absorption

Effect of Riboflavin Deficiency on the Metabolism of Oxypurines in Chicks

1971 ◽  
Vol 49 (12) ◽  
pp. 1059-1062 ◽  
Author(s):  
S. T. Chou
Keyword(s):  
Uric Acid ◽  
Acid Synthesis ◽  
Xanthine Dehydrogenase ◽  
Broiler Chicks ◽  
Uric Acid Concentration ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
High Incidence ◽  
Liver And Kidney ◽  
Riboflavin Deficient

Day-old broiler chicks of both sexes were used in three experiments to determine the effect of riboflavin deficiency on oxypurine metabolism catalyzed by xanthine dehydrogenase, a riboflavin-containing enzyme. Chicks fed a riboflavin-deficient diet (1.38 mg/kg) for 3 weeks exhibited depressed growth and a high incidence of curled-toe paralysis (higher than 80%) as compared to control chicks (15.1 mg riboflavin per kilogram diet; no incidence of curled-toe paralysis). In addition, the precursors of uric acid, hypoxanthine and/or xanthine, accumulated in the liver and kidney of deficient chicks showing curled-toe paralysis. These observations show that dietary riboflavin being incorporated into xanthine dehydrogenase is essential for oxypurine metabolism. Moreover in the chick, the liver and the kidney may be important sites of uric acid synthesis. The low uric acid concentration in the plasma of the deficient chicks appeared to be indicative of a disturbance in uric acid synthesis in the liver and kidney.

scholarly journals Glutathione peroxidase (EC 1.11.1.9) and superoxide dismutase (EC 1.15.1.1) activities in riboflavin-deficient rats infected with Plasmodium berghei malaria

1998 ◽  
Vol 79 (3) ◽  
pp. 305-309 ◽  
Author(s):  
D. A. Adelekan ◽  
D. I. Thurnham
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Plasmodium Berghei ◽  
Control Group ◽  
Riboflavin Deficiency ◽  
Sod Activity ◽  
Parasite Protein ◽  
Riboflavin Deficient ◽  
Gpx Activity ◽  
Deficient Group

Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC1.11.1.9; GPx) and superoxide dismutase (EC1.15.1.1; SOD) in rats infected withPlasmodium bergheimalaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 × 106P. bergheiparasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P= 0.004). GPx activity was higher in erythrocytes of rats parasitized withP. bergheithan comparable non-infected rats regardless of riboflavin status (P< 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.

Regulators of Iron Absorption in the Small Intestine

1990 ◽  
pp. 117-121 ◽  
Author(s):  
Marcel E. Conrad ◽  
Jay N. Umbreit ◽  
Raymond D. A. Peterson ◽  
Elizabeth G. Moore
Keyword(s):  
Small Intestine ◽  
Iron Absorption

Enhanced riboflavin incorporation into flavins in newborn riboflavin-deficient rats.

1977 ◽  
Vol 233 (5) ◽  
pp. E397
Author(s):  
C Muttart ◽  
R Chaudhuri ◽  
J Pinto ◽  
R S Rivlin
Keyword(s):  
Subcutaneous Injection ◽  
Flavin Adenine Dinucleotide ◽  
The Other ◽  
Flavin Mononucleotide ◽  
Newborn Rats ◽  
Riboflavin Deficiency ◽  
Riboflavin Deficient ◽  
Covalently Bound

The incorporation of a subcutaneous injection of [14C]riboflavin (2.5 muCi/100 g body wt) into flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and flavins bound covalently to proteins was determined at 1, 6, and 18 h in liver, cerebrum, and cerebellum from progeny of normal and maternally riboflavin-deficient Holtzman rats. Radioactivity remaining as riboflavin was also determined under these circumstances. Experiments were initiated within 24 h of birth. In both groups of newborn rats, the incorporation of radioactive riboflavin into covalently bound flavins in liver and brain proceeded more slowly than into the other flavin fractions. In addition, radioactivity incorporated into covalently bound flavins comprised a relatively smaller proportion of the total amount incorporated in brain than in liver. In progeny of riboflavin-deficient dams, an increased rate of incorporation of riboflavin into all three flavin derivatives, particularly FAD, was observed in liver and brain, compared to results in normal progeny. These data provide evidence that maternal riboflavin deficiency enhances the incorporation of riboflavin into tissue flavins in liver, cerebrum, and cerebellum from newborn rats.

Regional localization of iron absorption in the guinea-pig small intestine during development

1990 ◽  
Vol 18 (4) ◽  
pp. 612-613 ◽  
Author(s):  
GEORGE CHOWRIMOOTOO ◽  
EDWARD DEBNAM ◽  
OWEN EPSTEIN ◽  
SURJIT SRAI
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Iron Absorption ◽  
Regional Localization
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