scholarly journals Effects of dietary iron deficiency and tungsten supplementation on59Fe absorption and gastricretention from59Fe compounds in rats

1989 ◽  
Vol 61 (3) ◽  
pp. 573-581 ◽  
Author(s):  
Gillian E. Shears ◽  
R. J. Neale ◽  
D. A. Ledward
Keyword(s):  
Iron Deficiency ◽  
Xanthine Oxidase ◽  
Gastric Retention ◽  
Dietary Iron ◽  
Digestion Time ◽  
Mucosal Cells ◽  
Ferroxidase Activity ◽  
Intestinal Mucosal Cells ◽  
Absorption Characteristics

1. In vivo59Fe absorption from intrinsically labelled Fe-containing fractions of liver and blood were measured in rats by intragastric dosing. All rats were fed on a low-Fe diet for 3 d before dosing in order to standardize the Fe status of the intestinal mucosal cells.2. An increase in digestion time from 2 to 12 h increased59Fe absorption (P< 0.01) from all fractions except ferritin.3. Fe-deficient rats when compared with essentially Fe-replete rats showed decreased gastric retention for all fractions, but increased59Fe absorption over 2 h only from ferritin. Ferritin showed several unusual absorption characteristics.4. Dietary tungsten supplementation of Fe-deficient rats reduced the ferroxidase activity of intestinal mucosal xanthine oxidase. In addition, gastric retention and59Fe absorption (P< 0.05) from all fractions were increased.

Demonstration of methionine synthetase in intestinal mucosal cells of the rat

1985 ◽  
Vol 69 (3) ◽  
pp. 287-292 ◽  
Author(s):  
J. N. Keating ◽  
D. G. Weir ◽  
J. M. Scott
Keyword(s):  
Crypt Cell ◽  
Cell Populations ◽  
Buffer System ◽  
Mucosal Cell ◽  
Mucosal Cells ◽  
Rat Duodenum ◽  
Small Intestinal ◽  
Intestinal Mucosal Cells ◽  
Crypt Cells

1. Methionine synthetase was measured in the mucosal cells of the rat duodenum, jejunum and ileum by a previously employed method for mucosal cell isolation. No activity was found in these cells. 2. When a dual buffer system for the isolation of villous and crypt cell population was substituted, however, methionine synthetase was found to be active in the duodenum, jejunum and ileum, both in the villous and crypt cell populations. The activity was significantly higher in the crypt cells than in the villous cells throughout the intestine, and higher levels were found in the ileum than in the duodenum or jejunum. 3. As had been previously reported for the rat liver, nitrous oxide in vivo reduced the enzyme activity in both the villous and crypt cell populations, suggesting a role in vivo for the enzyme. We conclude that methionine synthetase is both present and active in the small intestinal mucosal cells of the rat.

scholarly journals Low Phytate Peas (Pisum sativum L.) Improve Iron Status, Gut Microbiome, and Brush Border Membrane Functionality In Vivo (Gallus gallus)

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2563 ◽  
Author(s):  
Tom Warkentin ◽  
Nikolai Kolba ◽  
Elad Tako
Keyword(s):  
Iron Deficiency ◽  
Gut Microbiota ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Iron Status ◽  
Gallus Gallus ◽  
Intestinal Microbiome ◽  
Physiological Status ◽  
Dietary Iron

The inclusion of pulses in traditional wheat-based food products is increasing as the food industry and consumers are recognizing the nutritional benefits due to the high protein, antioxidant activity, and good source of dietary fiber of pulses. Iron deficiency is a significant global health challenge, affecting approximately 30% of the world’s population. Dietary iron deficiency is the foremost cause of anemia, a condition that harms cognitive development and increases maternal and infant mortality. This study intended to demonstrate the potential efficacy of low-phytate biofortified pea varieties on dietary iron (Fe) bioavailability, as well as on intestinal microbiome, energetic status, and brush border membrane (BBM) functionality in vivo (Gallus gallus). We hypothesized that the low-phytate biofortified peas would significantly improve Fe bioavailability, BBM functionality, and the prevalence of beneficial bacterial populations. A six-week efficacy feeding (n = 12) was conducted to compare four low-phytate biofortified pea diets with control pea diet (CDC Bronco), as well as a no-pea diet. During the feeding trial, hemoglobin (Hb), body-Hb Fe, feed intake, and body weight were monitored. Upon the completion of the study, hepatic Fe and ferritin, pectoral glycogen, duodenal gene expression, and cecum bacterial population analyses were conducted. The results indicated that certain low-phytate pea varieties provided greater Fe bioavailability and moderately improved Fe status, while they also had significant effects on gut microbiota and duodenal brush border membrane functionality. Our findings provide further evidence that the low-phytate pea varieties appear to improve Fe physiological status and gut microbiota in vivo, and they highlight the likelihood that this strategy can further improve the efficacy and safety of the crop biofortification and mineral bioavailability approach.

Iron deficiency decreases gluconeogenesis in isolated rat hepatocytes

1989 ◽  
Vol 67 (5) ◽  
pp. 1868-1872 ◽  
Author(s):  
K. L. Klempa ◽  
W. T. Willis ◽  
R. Chengson ◽  
P. R. Dallman ◽  
G. A. Brooks
Keyword(s):  
Iron Deficiency ◽  
Glucose Production ◽  
Rat Hepatocytes ◽  
Female Rats ◽  
Glucose Turnover ◽  
Dietary Iron ◽  
Isolated Rat Hepatocytes ◽  
Iron Deficient ◽  
Isolated Rat

Dietary iron deficiency in rats results in increased blood glucose turnover and recycling. We measured the rates of glucose production in isolated hepatocytes from iron-sufficient (Fe+) and iron-deficient (Fe-) rats to assess the intrinsic capacity of the Fe- liver to carry out gluconeogenesis. Low-iron and control diets were given to 21-day-old female rats. After 4-5 wk, hemoglobin concentrations averaged 4.1 g/dl in the Fe- and 14.3 g/dl in the Fe+ animals. In the hepatocytes from Fe- rats, there was a 35% decrease in the rate of glucose production from 1 mM pyruvate + 10 mM lactate, a 48% decrease from 0.1 mM pyruvate + 1 mM lactate, a 39% decrease from 1 mM alanine, and a 48% decrease from 1 mM glycerol. The addition of 5 microM norepinephrine or 0.5 microM glucagon to the incubation media produced stimulatory effects on hepatocytes from both Fe- and Fe+ rats, resulting in the maintenance of an average difference of 38% in the rates of gluconeogenesis between the two groups. Studies on isolated liver mitochondria and cytosol revealed alpha-glycerophosphate-cytochrome c reductase and phospho(enol)pyruvate carboxykinase activities to be decreased by 27% in Fe- rats. We conclude that because severe dietary iron deficiency decreases gluconeogenesis in isolated rat hepatocytes, the increased gluconeogenesis demonstrated by Fe- rats in vivo is attributable to increased availability of gluconeogenic substrates and upregulation of the pathway.

scholarly journals Studies on the effect of vitamin D on calcium absorption and transport

1969 ◽  
Vol 112 (3) ◽  
pp. 275-283 ◽  
Author(s):  
George Hashim ◽  
Irwin Clark
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Absorption ◽  
Active Process ◽  
Hypervitaminosis D ◽  
Glycolytic Activity ◽  
Mucosal Cells ◽  
Intestinal Mucosal Cells ◽  
Uptake And Release

1. Mucosal cells of the small intestine obtained from rats deprived of vitamin D or given excessive amounts of the vitamin accumulated significantly more calcium than did cells from control animals. 2. Mucosal cells from vitamin D-deficient rats released less calcium than did cells from normal or hypervitaminotic D animals. 3. Studies in vivo showed that the transfer of 45Ca from the intestine to the blood was delayed in vitamin D deficiency, but was accelerated in hypervitaminosis D. 4. The findings support the thesis that vitamin D is involved in the release of calcium rather than in its uptake by mucosal cells. 5. Further evidence is presented suggesting that uptake of calcium by intestinal mucosal cells at 0° is primarily passive, whereas at 38° uptake and release are effected by an active process that depends on energy derived from glycolytic activity.

Bacterial-Mucosal Cell Junctional Complexes

1974 ◽  
Vol 32 ◽  
pp. 144-145
Author(s):  
Roger C. Wagner
Keyword(s):  
Intestinal Wall ◽  
Rat Colon ◽  
Mucosal Cell ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Mucosal Cells ◽  
Mucosal Lining ◽  
Degenerative Alterations ◽  
Junctional Complexes ◽  
Intestinal Mucosal Cells

Bacteria exhibit the ability to adhere to the apical surfaces of intestinal mucosal cells. These attachments either precede invasion of the intestinal wall by the bacteria with accompanying inflammation and degeneration of the mucosa or represent permanent anchoring sites where the bacteria never totally penetrate the mucosal cells.Endemic gram negative bacteria were found attached to the surface of mucosal cells lining the walls of crypts in the rat colon. The bacteria did not intrude deeper than 0.5 urn into the mucosal cells and no degenerative alterations were detectable in the mucosal lining.

Fine Structural Localization of Acyltransferases Involved in Lipid Synthesis in Intestinal Mucosa.

1970 ◽  
Vol 28 ◽  
pp. 54-55
Author(s):  
R. J. Barrnett ◽  
J. A. Higgins
Keyword(s):  
Smooth Endoplasmic Reticulum ◽  
Lipid Synthesis ◽  
Mucosal Cell ◽  
Structural Localization ◽  
Morphological Studies ◽  
Mucosal Cells ◽  
Initial Appearance ◽  
Sh Group ◽  
Hydrolysis Of ◽  
Intestinal Mucosal Cells

The main products of intestinal hydrolysis of dietary triglycerides are free fatty acids and monoglycerides. These form micelles from which the lipids are absorbed across the mucosal cell brush border. Biochemical studies have indicated that intestinal mucosal cells possess a triglyceride synthesising system, which uses monoglyceride directly as an acylacceptor as well as the system found in other tissues in which alphaglycerophosphate is the acylacceptor. The former pathway is used preferentially for the resynthesis of triglyceride from absorbed lipid, while the latter is used mainly for phospholipid synthesis. Both lipids are incorporated into chylomicrons. Morphological studies have shown that during fat absorption there is an initial appearance of fat droplets within the cisternae of the smooth endoplasmic reticulum and that these subsequently accumulate in the golgi elements from which they are released at the lateral borders of the cell as chylomicrons.We have recently developed several methods for the fine structural localization of acyltransferases dependent on the precipitation, in an electron dense form, of CoA released during the transfer of the acyl group to an acceptor, and have now applied these methods to a study of the fine structural localization of the enzymes involved in chylomicron lipid biosynthesis. These methods are based on the reduction of ferricyanide ions by the free SH group of CoA.

Superoxide, Xanthine Oxidase and Platelet Reactions: Further Studies on Mechanisms by which Oxidants Influence Platelets

1981 ◽  
Vol 45 (03) ◽  
pp. 290-293 ◽  
Author(s):  
Peter H Levine ◽  
Danielle G Sladdin ◽  
Norman I Krinsky
Keyword(s):  
Superoxide Dismutase ◽  
Cytochrome C ◽  
Xanthine Oxidase ◽  
Direct Effect ◽  
Platelet Function ◽  
Experimental Conditions ◽  
Release Reaction

SummaryIn the course of studying the effects on platelets of the oxidant species superoxide (O- 2), Of was generated by the interaction of xanthine oxidase plus xanthine. Surprisingly, gel-filtered platelets, when exposed to xanthine oxidase in the absence of xanthine substrate, were found to generate superoxide (O- 2), as determined by the reduction of added cytochrome c and by the inhibition of this reduction in the presence of superoxide dismutase.In addition to generating Of, the xanthine oxidase-treated platelets display both aggregation and evidence of the release reaction. This xanthine oxidase induced aggreagtion is not inhibited by the addition of either superoxide dismutase or cytochrome c, suggesting that it is due to either a further metabolite of O- 2, or that O- 2 itself exerts no important direct effect on platelet function under these experimental conditions. The ability of Of to modulate platelet reactions in vivo or in vitro remains in doubt, and xanthine oxidase is an unsuitable source of O- 2 in platelet studies because of its own effects on platelets.

An overview on mechanism, cause, prevention and multi-nation policy level interventions of dietary iron deficiency

2021 ◽  
pp. 1-15
Author(s):  
Abhishek Kulkarni ◽  
Monika Khade ◽  
Sharadha Arun ◽  
Pranesh Badami ◽  
G. Raja Krishna Kumar ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Dietary Iron ◽  
Policy Level

Maturation, iron deficiency, and ligands in enteric radioiron transport in vitro

1963 ◽  
Vol 204 (1) ◽  
pp. 171-175 ◽  
Author(s):  
W. S. Ruliffson ◽  
J. M. Hopping
Keyword(s):  
Ascorbic Acid ◽  
Iron Deficiency ◽  
Iron Absorption ◽  
Deficiency Anemia ◽  
Anaerobic Incubation ◽  
Reverse Effect ◽  
Factors Affecting ◽  
Everted Gut Sac

The effects in rats, of age, iron-deficiency anemia, and ascorbic acid, citrate, fluoride, and ethylenediaminetetraacetate (EDTA) on enteric radioiron transport were studied in vitro by an everted gut-sac technique. Sacs from young animals transported more than those from older ones. Proximal jejunal sacs from anemic animals transported more than similar sacs from nonanemic rats, but the reverse effect appeared in sacs formed from proximal duodenum. When added to media containing ascorbic acid or citrate, fluoride depressed transport as did anaerobic incubation in the presence of ascorbic acid. Anaerobic incubation in the presence of EDTA appeared to permit elevated transport. Ascorbic acid, citrate, and EDTA all enhanced the level of Fe59 appearing in serosal media. These results appear to agree with previously established in vivo phenomena and tend to validate the in vitro method as one of promise for further studies of factors affecting iron absorption and of the mechanism of iron absorption.

Dietary iron deficiency in the rat. I. Abnormalities in energy metabolism of the hepatic tissue

1994 ◽  
Vol 1188 (1-2) ◽  
pp. 46-52 ◽  
Author(s):  
Alberto Masini ◽  
Gianfranco Salvioli ◽  
Piero Cremonesi ◽  
Barbara Botti ◽  
Daniela Gallesi ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Iron Deficiency ◽  
Hepatic Tissue ◽  
Dietary Iron
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