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 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.

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 ◽  
Rat Small Intestine ◽  
Structural Responses

scholarly journals Refection in rats fed on a sucrose-based, riboflavin-deficient diet

1980 ◽  
Vol 43 (1) ◽  
pp. 171-177 ◽  
Author(s):  
A. M. Prentice ◽  
C. J. Bates
Keyword(s):  
Biochemical Tests ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Biochemical Effects ◽  
Severe Deficiency ◽  
Riboflavin Deficient ◽  
Riboflavin Status

1. Refection, resulting in an increased supply of riboflavin to riboflavin-deficient rats through coprophagy, was demonstrated on a sucrose-based diet when sensitive biochemical tests of riboflavin status were employed: these included measurements of NAD(P)H2:glutathione oxidoreductase (EC 1.6.4.2); succinate:(acceptor) oxidoreductase (EC 1.3.99.1) and NADH:(acceptor) oxidoreductase (EC 1.6.99.3).2. The use of tail-cups to eliminate coprophagy, and hence refection, resulted in a more rapid and reproducible progress into severe deficiency.3. The occurrence of refection on a sucrose-based diet may account for hitherto unexplained differences between previous publications on the biochemical effects of riboflavin deficiency.

scholarly journals Effects of riboflavin deficiency and clofibrate treatment on the five acyl-CoA dehydrogenases in rat liver mitochondria

1988 ◽  
Vol 254 (2) ◽  
pp. 477-481 ◽  
Author(s):  
K Veitch ◽  
J P Draye ◽  
F Van Hoof ◽  
H S A Sherratt
Keyword(s):  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Straight Chain ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Mitochondrial Fractions ◽  
Chain Acyl ◽  
Branched Chain ◽  
Acyl Coa Dehydrogenases ◽  
Riboflavin Deficient

Rats were maintained on a riboflavin-deficient diet or on a diet containing clofibrate (0.5%, w/w). The activities of the mitochondrial FAD-dependent straight-chain acyl-CoA dehydrogenases (butyryl-CoA, octanoyl-CoA and palmitoyl-CoA) and the branched-chain acyl-CoA dehydrogenases (isovaleryl-CoA and isobutyryl-CoA) involved in the degradation of branched-chain acyl-CoA esters derived from branched-chain amino acids were assayed in liver mitochondrial extracts prepared in the absence and presence of exogenous FAD. These activities were low in livers from riboflavin-deficient rats (11, 28, 16, 6 and less than 2% of controls respectively) when prepared in the absence of exogenous FAD, and were not restored to control values when prepared in 25 microM-FAD (29, 47, 28, 7 and 17%). Clofibrate feeding increased the activities of butyryl-CoA, octanoyl-CoA and palmitoyl-CoA dehydrogenases (by 48, 116 and 98% of controls respectively), but not, by contrast, the activities of isovaleryl-CoA and isobutyryl-CoA dehydrogenases (62 and 102% of controls respectively). The mitochondrial fractions from riboflavin-deficient and from clofibrate-fed rats oxidized palmitoylcarnitine in State 3 at rates of 32 and 163% respectively of those from control rats.

Peripheral Neuropathy Associated with Dietary Riboflavin Deficiency in the Chicken I. Light Microscopic Study

1988 ◽  
Vol 25 (1) ◽  
pp. 9-16 ◽  
Author(s):  
W. D. Johnson ◽  
R. W. Storts
Keyword(s):  
Peripheral Neuropathy ◽  
Schwann Cell ◽  
Cell Swelling ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Tissue Separation ◽  
Leukocytic Infiltration ◽  
Leg Weakness ◽  
Demyelinating Peripheral Neuropathy ◽  
Riboflavin Deficient

Chickens fed a riboflavin-deficient diet from hatching had leg weakness and paralysis as early as 12 days of age. Signs worsened through day 16; after 35 days, recovery was evident. Sciatic nerves from affected chickens were enlarged. Significant microscopic lesions were confined to peripheral nerves and included tissue separation (suggesting interstitial edema), Schwann cell swelling, perivascular leukocytic infiltration, and segmental demyelination accompanied by accumulation of osmiophilic debris in Schwann cell cytoplasm. Axon degeneration was present, but was not a primary lesion. Acid phosphatase enzyme activity of Schwann cells was increased in affected nerves. These results demonstrate that dietary riboflavin deficiency causes a demyelinating peripheral neuropathy in young, rapidly growing chickens.

scholarly journals Riboflavin deficiency: early effects on post-weaning development of the duodenum in rats

2001 ◽  
Vol 86 (5) ◽  
pp. 593-599 ◽  
Author(s):  
Catherine A Yates ◽  
Gareth S. Evans ◽  
Hilary J. Powers
Keyword(s):  
Wistar Rats ◽  
Developmental Changes ◽  
Riboflavin Deficiency ◽  
Show Evidence ◽  
Activation Coefficient ◽  
Early Effects ◽  
Riboflavin Deficient ◽  
Rates Of Growth ◽  
Riboflavin Status

The aim of this present study was to identify the earliest point at which riboflavin deficiency affects post-weaning bowel development in rats. After weaning, eighty Wistar rats were weight-matched as pairs, one animal being fed a normal synthetic diet and the other being fed the same diet but deficient in riboflavin. Body weight, feeding and rates of growth were monitored and eight pairs of animals were taken for analysis at 45, 69, 93, 117 and 141 h. Riboflavin status was monitored by determining the erythrocyte glutathione reductase activation coefficient (EGRAC), and hepatic flavins were measured by a fluorescence assay. Changes to the number and dimensions of villi and crypts in the duodenum were determined, as well as crypt division (bifurcation) and the DNA synthesis index of the crypt epithelium by bromodeoxyuridine (BrdU) labelling. Riboflavin deficiency was established in the experimental rats, as demonstrated by a significant increase in EGRAC after 45 h (P<0·001) and decreased liver flavins after 96 h (P<0·001). After 96 h a significant increase in the size and cellularity of the crypts (P<0·001 in both cases) was seen in these riboflavin-deficient animals, with a decreased incidence of bifurcating crypts and of BrdU-labelled cells. No changes to villus number or size were observed. The present study has demonstrated that developmental changes to the duodenal crypt arise shortly after circulating riboflavin measurements show evidence of deficiency. These changes primarily affect cell proliferation and crypt bifurcation, and precede long-term changes such as the reduction of villus number.

STUDIES OF THE MOLECULAR BASIS OF CONGENITAL MALFORMATIONS

PEDIATRICS ◽  
1969 ◽  
Vol 43 (6) ◽  
pp. 915-926
Author(s):  
Bruce Mackler
Keyword(s):  
Congenital Malformations ◽  
Transport Systems ◽  
Congenital Defects ◽  
Synthetic Analog ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Adult Rats ◽  
Prenatal Environment ◽  
Better Regulation ◽  
Riboflavin Deficient

With recent advances in treatment of many acute and chronic diseases, the problems associated with congenital malformations in children have assumed a greater importance in pediatrics. Previous to the work of Warkany and Nelson in 19401, it was recognized that many congenital defects were genetically determined and hereditary. The finding by Warkany and co-workers1-3 that modification of the prenatal environment by severe states of riboflavin deficiency produced congenital malformations in mammals demonstrated clearly the importance of the prenatal environment in the development of the fetus and gave impetus to searches for other environmental factors of importance to the developing organism. The syndrome resulting from severe maternal riboflavin deficiency in rats is characterized mainly by micrognathia and reduction type of defects in the distal extremities of the fetuses, and by a wide number of other anomalies such as cleft palate and hydronephrosis. More recently, Nelson and co-workers4 demonstrated that galactoflavin, a synthetic analog of riboflavin, produced a rapid riboflavin deficiency syndrome in pregnant rats. The addition of galactoflavin to a riboflavin-deficient diet materially shortened the time required to produce riboflavin deficiency, and permitted much better regulation of the experimental model. In other studies of riboflavin deficiency, Miller and co-workers5 showed a lower flavin content in fetuses from riboflavindeficient rats than in control fetuses, suggesting the possibility that there may be corresponding deficiencies in the activities of flavin-dependent enzymes such as the terminal electron transport systems (ETP). Other investigators6 have reported studies of enzymatic activities in liver mitochondria of adult rats fed a riboflavin-deficient diet with added galactoflavin, but with varying results.

scholarly journals The Anemia of Human Riboflavin Deficiency

Blood ◽  
1965 ◽  
Vol 25 (4) ◽  
pp. 432-442 ◽  
Author(s):  
MONTAGUE LANE ◽  
CLARENCE P. ALFREY
Keyword(s):  
Bone Marrow ◽  
Normocytic Anemia ◽  
Adult Males ◽  
Normal Range ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
Platelet Counts ◽  
Leukocyte Counts ◽  
Riboflavin Deficient

Abstract 1. Riboflavin deficiency was induced in 8 adult males with a riboflavin deficient diet and a riboflavin antagonist, galactoflavin. 2. Each patient developed a normochromic normocytic anemia and reticulocytopenia. 3. The leukocyte counts and platelet counts remained within the normal range throughout the period of deficiency. 4. The bone marrow changes and ferrokinetic characteristics of this anemia have been described. 5. The anemia was reversed by riboflavin administration.

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 Morphological changes in the rat small intestine in response to riboflavin depletion

1995 ◽  
Vol 73 (1) ◽  
pp. 141-146 ◽  
Author(s):  
E. A. Williams ◽  
H. J. Powers ◽  
R. D. E. Rumsey
Keyword(s):  
Small Intestine ◽  
Wistar Rats ◽  
Morphological Changes ◽  
Goblet Cells ◽  
Cell Number ◽  
Riboflavin Deficiency ◽  
Functional Changes ◽  
Female Wistar Rats ◽  
Proportional Increase ◽  
Total Dna

Female Wistar rats were weaned onto a diet deficient in riboflavin and compared with weight-matched and ad lib.-fed controls. The effects of riboflavin deficiency on villus morphometry and enterocyte number on the villi in the upper small intestine were studied. Riboflavin depletion was associated with increased villus length and a proportional increase in the number of cell positions along the villi. The total DNA, RNA and protein contents in the intestinal mucosa were not significantly different between any of the groups. Villus hypertrophy in the absence of increased cell number in the small intestine suggests that villus number may be reduced in riboflavin deficiency. Riboflavin deficiency did not influence the number of mucus-producing goblet cells or the amount of mucosal glycoprotein in the small intestine. Impaired production of mucus appeared not to be involved in the structural and functional changes seen in riboflavin deficiency.

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