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

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.

1986 ◽  
Vol 56 (1) ◽  
pp. 171-179 ◽  
Author(s):  
Delana A. Adelekan ◽  
David I. Thurnham

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.


1988 ◽  
Vol 59 (3) ◽  
pp. 381-387 ◽  
Author(s):  
Hilary J. Powers ◽  
A. J. A. Wright ◽  
Susan J. Fairweather-tait

1. Riboflavin may play a part in the transport of iron across the gastrointestinal mucosa. Fe absorption was measured in the rat by monitoring whole-body retention of a dose of 59Fe using a small-animal γ-counter.2. Female Norwegian Hooded rats were fed on a diet deficient in riboflavin (B2−) from 5 weeks of age. Control animals, fed on a complete diet (B2+), were weight-matched to rats fed on the B2− diet. After 7 weeks all rats were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d.3. Riboflavin deficiency was associated with a reduction in the percentage of the dose absorbed and an increase in the rate of loss of Fe post absorption.4. A smaller percentage of the absorbed dose was present in the livers of the riboflavin-deficient animals.


Gut ◽  
1998 ◽  
Vol 43 (5) ◽  
pp. 699-704 ◽  
Author(s):  
J P Kaltwasser ◽  
E Werner ◽  
K Schalk ◽  
C Hansen ◽  
R Gottschalk ◽  
...  

Background—Black tea is known to be a potent inhibitor of intestinal absorption of non-haem iron at least in healthy subjects.Aims—To investigate this effect in patients with genetic haemochromatosis, and, more importantly, the effect of regular tea drinking on the accumulation of storage iron in these patients over one year.Patients—Investigations were carried out on 18 patients with clinically proven genetic haemochromatosis. For the study of storage iron accumulation, they were separated into a group instructed to drink a particularly tannin rich tea regularly with meals and a control group.Methods—Intestinal iron absorption from a test meal was measured using whole body counting. Body iron stores were evaluated quantitatively by exhaustive phlebotomy, using haemoglobin, saturation of serum iron binding capacity, and serum ferritin for the assessment of body iron status.Results—A significant reduction in iron absorption was observed when the test meal was accompanied by drinks of tea instead of water. In the tea drinking group, the increase in storage iron was reduced by about one third compared with that of the control group.Conclusions—Regular tea drinking with meals reduces the frequency of phlebotomies required in the management of patients with haemochromatosis.


1989 ◽  
Vol 61 (3) ◽  
pp. 475-483 ◽  
Author(s):  
B. E. Patterson ◽  
C. J. Bates

1. The effects of riboflavin deficiency on growth, whole-body oxygen consumption, cytochrome c oxidase (EC 1.9.3.1) activity and GDP-binding capacity of brown adipose tissue were measured in three groups of rats: sucking pups, weanling rats, and dams. Control groups were weight-matched, pair-fed or fed ad lib.2. Riboflavin deficiency reduced growth rate and increased the activation coefficient of erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2), as predicted. In sucking pups it also reduced whole-body O2 consumption per unit body-weight, especially after noradrenaline stimulation. In weanling rats, however, it increased O2 consumption both before and after noradrenaline stimulation.3. Cytochrome c oxidase (EC 1.9.9.1) activity of brown adipose tissue was not consistently affected by riboflavin deficiency. Binding of [3H]GDP to the mitochondria was increased in the deficient weanling rats.4. Weanling rats therefore, seemed better able to withstand the effects of severe depletion. Their reduced growth and increased non-shivering thermogenesis helped to counteract the unfavourable ratio of riboflavin: other tissuebuilding materials. The relevance for thermoregulation in riboflavin-deficient children is discussed.


1993 ◽  
Vol 69 (2) ◽  
pp. 553-561 ◽  
Author(s):  
Hilary J. Powers ◽  
Lawrence T. Weaver ◽  
Steven Austin ◽  
John K. Beresford

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.


1996 ◽  
Vol 75 (2) ◽  
pp. 315-324 ◽  
Author(s):  
E. A. Williams ◽  
R. D. E. Rumsey ◽  
H. J. Powers

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.


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

1997 ◽  
Vol 128 (2) ◽  
pp. 233-246 ◽  
Author(s):  
S. A. NEUTZE ◽  
J. M. GOODEN ◽  
V. H. ODDY

This study used an experimental model, described in a companion paper, to examine the effects of feed intake on protein turnover in the small intestine of lambs. Ten male castrate lambs (∼ 10 months old) were offered, via continuous feeders, either 400 (n = 5) or 1200 (n = 5) g/day lucerne chaff, and mean experimental liveweights were 28 and 33 kg respectively. All lambs were prepared with catheters in the cranial mesenteric vein (CMV), femoral artery (FA), jugular vein and abomasum, and a blood flow probe around the CMV. Cr-EDTA (0·139 mg Cr/ml, ∼ 0·2 ml/min) was infused abomasally for 24 h and L-[2,6-3H]phenylalanine (Phe) (420±9·35 μCi into the abomasum) and L-[U-14C]phenylalanine (49·6±3·59 μCi into the jugular vein) were also infused during the last 8 h. Blood from the CMV and FA was sampled during the isotope infusions. At the end of infusions, lambs were killed and tissue (n = 4) and digesta (n = 2) samples removed from the small intestine (SI) of each animal. Transfers of labelled and unlabelled Phe were measured between SI tissue, its lumen and blood, enabling both fractional and absolute rates of protein synthesis and gain to be estimated.Total SI mass increased significantly with feed intake (P < 0·05), although not on a liveweight basis. Fractional rates of protein gain in the SI tended to increase (P = 0·12) with feed intake; these rates were −16·2 (±13·7) and 23·3 (±15·2) % per day in lambs offered 400 and 1200 g/day respectively. Mean protein synthesis and fractional synthesis rates (FSR), calculated from the mean retention of 14C and 3H in SI tissue, were both positively affected by feed intake (0·01 < P < 0·05). The choice of free Phe pool for estimating precursor specific radioactivity (SRA) for protein synthesis had a major effect on FSR. Assuming that tissue free Phe SRA represented precursor SRA, mean FSR were 81 (±15) and 145 (±24) % per day in lambs offered 400 and 1200 g/day respectively. Corresponding estimates for free Phe SRA in the FA and CMV were 28 (±2·9) and 42 (±3·5) % per day on 400 g/day, and 61 (±2·9) and 94 (±6·0) on 1200 g/day. The correct value for protein synthesis was therefore in doubt, although indirect evidence suggested that blood SRA (either FA or CMV) may be closest to true precursor SRA. This evidence included (i) comparison with flooding dose estimates of FSR, (ii) comparison of 3H[ratio ]14C Phe SRA in free Phe pools with this ratio in SI protein, and (iii) the proportion of SI energy use associated with protein synthesis.Using the experimental model, the proportion of small intestinal protein synthesis exported was estimated as 0·13–0·27 (depending on the choice of precursor) and was unaffected by feed intake. The contribution of the small intestine to whole body protein synthesis tended to be higher in lambs offered 1200 g/day (0·21) than in those offered 400 g/day (0·13). The data obtained in this study suggested a role for the small intestine in modulating amino acid supply with changes in feed intake. At high intake (1200 g/day), the small intestine increases in mass and CMV uptake of amino acids is less than absorption from the lumen, while at low intake (400 g/day), this organ loses mass and CMV uptake of amino acids exceeds that absorbed. The implications of these findings are discussed.


1989 ◽  
Vol 76 (6) ◽  
pp. 595-598 ◽  
Author(s):  
R. A. Goodlad ◽  
H. Gregory ◽  
N. A. Wright

1. Intestinal epithelial cell proliferation was measured in rats maintained on total parenteral nutriton (TPN), in TPN rats given 300 μg of recombinant human epidermal growth factor (urogastrone-epidermal growth factor, URO-EGF) day−1 kg−1, and in further groups given URO-EGF and difluoromethylornithine (DFMO), an inhibitor of the enzyme ornithine decarboxylase (ODC). 2. URO-EGF significantly increased intestinal cell proliferation throughout the gastrointestinal tract. The proliferative response of the colon was particularly pronounced. 3. DFMO reduced the proliferative effect of urogastrone in the stomach and small intestine. DFMO also reduced URO-EGF-stimulated intestinal cell proliferation in the colon, but to a lesser extent. 4. It is concluded that ODC is essential for effecting the proliferative response of the stomach and small intestine to URO-EGF, but this role may be less important in the colon.


1971 ◽  
Vol 49 (12) ◽  
pp. 1059-1062 ◽  
Author(s):  
S. T. Chou

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.


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