Factors affecting the Metabolic Production of Methylguanidine

1975 ◽  
Vol 48 (5) ◽  
pp. 341-347 ◽  
Author(s):  
M. Gonella ◽  
G. Barsotti ◽  
S. Lupetti ◽  
S. Giovannetti
Keyword(s):  
Carbon Dioxide ◽  
Renal Failure ◽  
Gastrointestinal Tract ◽  
Urinary Excretion ◽  
The Body ◽  
Urinary Output ◽  
Solution Ph ◽  
Factors Affecting ◽  
Normal Volunteers

1. Methylguanidine administered orally to normal volunteers was almost completely recovered in the urine, indicating that it is absorbed in the gastrointestinal tract and is not converted into other compounds. In normal persons at least, its urinary output therefore corresponds to its metabolic production rate plus the amount ingested. 2. In normal persons, diets based on foods not containing methylguanidine (e.g. vegetarian, protein-free and milk-egg diets) caused a fall in the urinary output of methylguanidine as compared with the output of the same subjects on a free diet. Conversely, higher amounts of methylguanidine were excreted on a diet rich in broth and in boiled beef, which contain large amounts of methylguanidine formed from the oxidation of creatinine, caused by boiling. 3. Oral administration of creatinine to normal volunteers induced an immediate and marked increase in urinary excretion of methylguanidine, and the ingestion of [methyl-14C]creatinine by uraemic patients was followed by the urinary excretion of labelled methylguanidine. These findings indicate that creatinine is partly converted into methylguanidine in both normal and uraemic subjects and accounts for the high metabolic production of methylguanidine in patients with renal failure, in whom the body pool of creatinine is high. 4. Creatinine, incubated at 38°C for 24 h in Krebs bicarbonate solution (pH 7.38) through which was bubbled oxygen with 15% carbon dioxide, was partially oxidized to methylguanidine. This raises the possibility that even in vivo such a conversion may occur ‘non-enzymatically’.

scholarly journals Procyanidins are not bioavailable in rats fed a single meal containing a grapeseed extract or the procyanidin dimer B3

2002 ◽  
Vol 87 (4) ◽  
pp. 299-306 ◽  
Author(s):  
Jennifer L. Donovan ◽  
Adam Lee ◽  
Claudine Manach ◽  
Laurent Rios ◽  
Christine Morand ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Urinary Excretion ◽  
Ring Structure ◽  
Future Research ◽  
Human Gastrointestinal Tract ◽  
Human Diet ◽  
Single Meal ◽  
Nutritional Effects ◽  
Grapeseed Extract

Flavanols are the most abundant flavonoids in the human diet where they exist as monomers, oligomers and polymers. In the present study, catechin, the procyanidin dimer B3 and a grapeseed extract containing catechin, epicatechin and a mixture of procyanidins were fed to rats in a single meal. After the meals, catechin and epicatechin were present in conjugated forms in both plasma and urine. In contrast, no procyanidins or conjugates were detected in the plasma or urine of any rats. Procyanidins were not cleaved into bioavailable monomers and had no significant effects on the plasma levels or urinary excretion of the monomers when supplied together in the grapeseed extract. We conclude that the nutritional effects of dietary procyanidins are unlikely to be due to procyanidins themselves or monomeric metabolites with the intact flavonoid-ring structure, as they do not exist at detectable concentrations in vivo. Future research should focus on other procyanidin metabolites such as phenolic acids and on the effects of the unabsorbed oligomers and polymers on the human gastrointestinal tract.

Food supplement “carrageenan” and its effect on the organism

2020 ◽  
Author(s):  
O.E. Luneva ◽  
Keyword(s):  
Gastrointestinal Tract ◽  
Food Additives ◽  
Food Supplement ◽  
The Body ◽  
Laboratory Rats ◽  
Experimental Part ◽  
In Vivo Experiments ◽  
Physiological Processes

Food additives are positioned as harmless, although, their components affectthe physiological processes associated with the permeability of the wall of the gastrointestinal tract (GIT) and intestinal microbiota. This article describes thecarrageenan supplement and its effects on the body in in vitro and in vivo experiments. The experimental part is devoted to analysis of the intestinalmicrobiota of laboratory rats with the consumption of the carrageenan dietary supplement in the amount of about 4,4 % of the standard feed.

OBSERVATIONS ON PROTEIN DIGESTION IN VIVO: II. DIETARY FACTORS AFFECTING THE RATE OF DISAPPEARANCE OF CASEIN FROM THE GASTROINTESTINAL TRACT

1959 ◽  
Vol 37 (12) ◽  
pp. 1475-1491 ◽  
Author(s):  
Carl Peraino ◽  
Quinton R. Rogers ◽  
Minoru Yoshida ◽  
Mou-Liang Chen ◽  
Alfred E. Harper
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Dietary Factors ◽  
Protein Digestion ◽  
Dietary Carbohydrate ◽  
Factors Affecting ◽  
Single Meal ◽  
Protein Free Diet ◽  
Stomach Emptying

The effects of various dietary changes on the emptying of solids and nitrogen from the stomach and on the disappearance of nitrogen from the gastrointestinal tract of rats trained to consume a single meal daily are described. When the animals were fed 5 g of food the presence of casein in the diet caused a general deceleration of stomach-emptying and altered the shape of the stomach-emptying curve. The presence of 50% of casein in the diet did not result in an accumulation of nitrogen in the intestine much above the amount found when a protein-free diet was fed. When dextrin was the dietary carbohydrate the diet emptied from the stomach as a homogeneous mixture, whereas when sucrose was the dietary carbohydrate the casein emptied from the stomach more slowly than did the other components of the diet. Raising the dietary level of fat to 50% caused a general deceleration of emptying and abolished the above-mentioned carbohydrate effect. No delay in stomach-emptying due to the presence of casein in the diet was noted when only 1.5 g of diet was fed. As the level of food intake was raised the total quantity of nitrogen emptying from the stomach per unit time increased although a greater percentage of the amount ingested emptied from the stomach when the level of food intake was low.

scholarly journals Candida albicans Isolates 529L and CHN1 Exhibit Stable Colonization of the Murine Gastrointestinal Tract

2021 ◽  
Author(s):  
Liam McDonough ◽  
Animesh Anand Mishra ◽  
Nicholas Tosini ◽  
Pallavi Kakade ◽  
Swathi Penumutchu ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Gastrointestinal Tract ◽  
The Body ◽  
Gi Tract ◽  
Phenotypic Differences ◽  
Reference Isolate ◽  
Bacterial Microbiota ◽  
Systemic Infections ◽  
Deficient Mice

Candida albicans is a pathobiont that colonizes multiple niches in the body including the gastrointestinal (GI) tract, but is also responsible for both mucosal and systemic infections. Despite its prevalence as a human commensal, the murine GI tract is generally refractory to colonization with the C. albicans reference isolate SC5314. Here, we identify two C. albicans isolates, 529L and CHN1, that stably colonize the murine GI tract in three different animal facilities under conditions where SC5314 is lost from this niche. Analysis of the bacterial microbiota did not show notable differences between mice colonized with the three C. albicans strains. We compared the genotypes and phenotypes of these three strains and identified thousands of SNPs and multiple phenotypic differences, including their ability to grow and filament in response to nutritional cues. Despite striking filamentation differences under laboratory conditions, however, analysis of cell morphology in the GI tract revealed that the three isolates exhibited similar filamentation properties in this in vivo niche. Notably, we found that SC5314 is more sensitive to the antimicrobial peptide CRAMP, and the use of CRAMP-deficient mice increased the ability of SC5314 to colonize the GI tract relative to CHN1 and 529L. These studies provide new insights into how strain-specific differences impact C. albicans traits in the host and advance CHN1 and 529L as relevant strains to study C. albicans pathobiology in its natural host niche.

A Method for the Study of Cation Transport in vivo: Effects of Digoxin Administration and of Chronic Renal Failure on the Disposition of An Oral Load of Rubidium Chloride

1984 ◽  
Vol 66 (5) ◽  
pp. 569-574 ◽  
Author(s):  
N. A. Boon ◽  
J. K. Aronson ◽  
K. F. Hallis ◽  
N. J. White ◽  
A. E. G. Raine ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cation Transport ◽  
The Body ◽  
Control Group ◽  
Loading Dose ◽  
Rubidium Chloride ◽  
Body Tissues

1. In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations following an oral load of rubidium chloride. The changes in plasma rubidium concentration are related to the distribution of rubidium to all the body tissues and the changes in intra-erythrocytic rubidium concentrations provide an example of rubidium uptake by one particular tissue. 2. In eight healthy volunteers pretreatment with a loading dose of digoxin (20 μg/kg) enhanced the rise in plasma rubidium concentrations and attenuated the rise in intra-erythrocytic rubidium concentrations after the oral load of rubidium chloride. 3. Ten patients with chronic renal failure, compared with a well-matched control group, were found to have changes similar to, but more marked than, those caused by digoxin, i.e. a much greater rise in plasma rubidium concentrations and a much smaller rise in intra-erythrocytic rubidium concentrations, after the oral load of rubidium chloride. 4. These findings are consistent with widespread reduction in Na+,K+-ATPase activity in subjects who have taken a loading dose of digoxin and patients with chronic renal failure. They are, therefore, consistent with the findings of previous studies in vitro and show that it is possible to demonstrate changes in cation transport in vivo.

Effect of changes in the red cell volume on the carbon dioxide titration curve in vivo in the rat

1981 ◽  
Vol 59 (5) ◽  
pp. 500-503
Author(s):  
S. Kaufman ◽  
C. T. Kappagoda
Keyword(s):  
Carbon Dioxide ◽  
Cell Volume ◽  
Titration Curve ◽  
The Body ◽  
Red Cell ◽  
Red Cell Volume ◽  
Titration Curves

Acute in vivo CO2 titration curves were performed on rats anaesthetized with pentobarbitone. The slope of the in vivo CO2 titration curve in the rat was found to be similar to that previously reported in the dog and in man. Removal of approximately 30% of the haemoglobin of the body did not influence significantly the slope of the in vivo CO2 titration curve in the rat.

OBSERVATIONS ON PROTEIN DIGESTION IN VIVO: II. DIETARY FACTORS AFFECTING THE RATE OF DISAPPEARANCE OF CASEIN FROM THE GASTROINTESTINAL TRACT

1959 ◽  
Vol 37 (1) ◽  
pp. 1475-1491 ◽  
Author(s):  
Carl Peraino ◽  
Quinton R. Rogers ◽  
Minoru Yoshida ◽  
Mou-Liang Chen ◽  
Alfred E. Harper
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Dietary Factors ◽  
Protein Digestion ◽  
Dietary Carbohydrate ◽  
Factors Affecting ◽  
Single Meal ◽  
Protein Free Diet ◽  
Stomach Emptying

The effects of various dietary changes on the emptying of solids and nitrogen from the stomach and on the disappearance of nitrogen from the gastrointestinal tract of rats trained to consume a single meal daily are described. When the animals were fed 5 g of food the presence of casein in the diet caused a general deceleration of stomach-emptying and altered the shape of the stomach-emptying curve. The presence of 50% of casein in the diet did not result in an accumulation of nitrogen in the intestine much above the amount found when a protein-free diet was fed. When dextrin was the dietary carbohydrate the diet emptied from the stomach as a homogeneous mixture, whereas when sucrose was the dietary carbohydrate the casein emptied from the stomach more slowly than did the other components of the diet. Raising the dietary level of fat to 50% caused a general deceleration of emptying and abolished the above-mentioned carbohydrate effect. No delay in stomach-emptying due to the presence of casein in the diet was noted when only 1.5 g of diet was fed. As the level of food intake was raised the total quantity of nitrogen emptying from the stomach per unit time increased although a greater percentage of the amount ingested emptied from the stomach when the level of food intake was low.

Evaluation of mannitol, lactulose and 51Cr-labelled ethylenediaminetetra-acetate as markers of intestinal permeability in man

1987 ◽  
Vol 73 (2) ◽  
pp. 197-204 ◽  
Author(s):  
M. Elia ◽  
R. Behrens ◽  
C. Northrop ◽  
P. Wraight ◽  
G. Neale
Keyword(s):  
Urinary Excretion ◽  
Intestinal Permeability ◽  
Large Bowel ◽  
Normal Subjects ◽  
Distribution Volume ◽  
The Body ◽  
Factors Affecting ◽  
51Cr Edta ◽  
Small Intestinal ◽  
Radionuclide Scanning

1. Factors affecting the intestinal uptake and urinary excretion of mannitol, lactulose and 51Cr-labelled ethylenediaminetetra-acetate (51Cr-EDTA), have been investigated in normal subjects and three patients with ileostomy. 2. The distribution volume of markers within the body, the rate of disappearance from plasma and renal clearance were assessed after an intravenous injection of a mixture of mannitol (2 g), [14C]mannitol (10 μCi), lactulose (0.1 g) and 51Cr-EDTA (5 μCi). 3. The urinary recovery of all the intravenously administered markers was close to 100%. Distribution volumes and patterns of excretion were virtually identical. Oxidation of intravenously administered mannitol accounted for only about 1% of the dose. 4. The passage of an orally administered mixture of markers was traced through the intestine and into urine. Transit time through the gastrointestinal tract was measured by the breath hydrogen method and by radionuclide scanning. 5. The passage of markers from mouth to the large bowel was essentially complete by 3.5 h. In some subjects the marker appeared in the large bowel as early as 30–40 min but in others it took three times as long. 6. After an oral dose the urinary excretion of mannitol fell progressively from 2 to 6 h, whereas the excretion of lactulose and 51Cr-EDTA increased slightly. As a consequence the lactulose/mannitol and 51Cr-EDTA/mannitol ratios in urine collected between 0 and 2 h were more than twofold higher than in urine collected between 4 and 6 h (P < 0.001). After 6 h, the urinary excretion of mannitol and lactulose declined rapidly in all subjects, and was similar to the pattern of excretion of 51Cr-EDTA in subjects with an ileostomy. In contrast, in normal subjects, the excretion of 51Cr-EDTA did not decline rapidly but continued for 24–48 h. 7. Differences in the excretion of mannitol, lactulose and 51Cr-EDTA after oral dosing is due to differences in the temporal pattern of absorption of these markers and not to differences in their distribution volume, oxidation or their clearance by the kidney. 8. The data suggest that the uptake of lactulose by the small intestine persists for longer than the uptake of mannitol, and show that 51Cr-EDTA is readily absorbed in the colon. This study indicates factors which must be considered in the design and interpretation of tests of small intestinal permeability.

The Metabolism of Tartrate in Man and the Rat

1978 ◽  
Vol 54 (3) ◽  
pp. 273-281
Author(s):  
V. S. Chadwick ◽  
A. Vince ◽  
M. Killingley ◽  
O. M. Wrong
Keyword(s):  
Carbon Dioxide ◽  
Urinary Excretion ◽  
Direct Injection ◽  
Intestinal Bacteria ◽  
The Body ◽  
Sodium Tartrate ◽  
Main Site ◽  
Body Tissues ◽  
System L ◽  
The Difference

1. Sodium tartrate labelled with 14C was given orally and parenterally to man and rats, and by direct injection into the caecum in rats. From the differences in urinary excretion after oral and parenteral administration intestinal absorption of tartrate was calculated as 18% of the dose in man and 81% in rats. Urinary tartrate was equivalent to 14% of the dose in man and 70% in rats, the difference between absorption and urinary excretion representing metabolism in body tissues. 2. Both man and the rat excreted part of the 14C as respiratory carbon dioxide. This occurred to a small extent after parenteral injection, suggesting metabolism of tartrate by body tissues, but was greater after oral or intracaecal administration, indicating that the main site of tartrate metabolism is the intestine. 3. Several genera of intestinal bacteria were shown to liberate [14C]carbon dioxide from labelled tartrate, and in a faecal incubation system l-tartrate, the natural isomer, was metabolized five times as rapidly as d-tartrate. 4. Oral sodium l-tartrate, 1·5 mmol day—1 kg—1, was given to two subjects and was shown to alkalinize the urine like sodium salts of other organic acids which are metabolized in the body. The reduction in renal hydrogen ion excretion showed that an average of 84% of the dose was metabolized. 5. Only 5% of labelled tartrate given by mouth appeared in faeces, and pharmacological doses of unlabelled l-tartrate had little or no aperient effect. 6. No evidence of toxicity of l-tartrate was encountered.

scholarly journals Polypeptide hormone receptors in vivo: demonstration of insulin binding to adrenal gland and gastrointestinal epithelium by quantitative radioautography.

1980 ◽  
Vol 28 (8) ◽  
pp. 824-835 ◽  
Author(s):  
J J Bergeron ◽  
R Rachubinski ◽  
N Searle ◽  
D Borts ◽  
R Sikstrom ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Adrenal Gland ◽  
Insulin Receptor ◽  
Insulin Action ◽  
Hormone Receptors ◽  
Specific Interaction ◽  
Insulin Binding ◽  
The Body ◽  
Quantitative Radioautography

A tissue-screening survey employing quantitative radioautography was carried out at 2 min after the intravascular injection of 125I-insulin into laboratory rats. The results revealed a substantial binding of insulin to cells forming the proximal convoluted tubule in kidney, hepatocytes of liver, acinar cells of the pancreas, parenchymal cells of the adrenal cortex and medulla, and epithelial cells of the gastrointestinal tract. Control experiments indicated that this binding was due to a specific interaction with the insulin receptor, except in the case of kidney where the binding was shown to be nonspecific. Although the major target for insulin action (liver) clearly demonstrated specific insulin binding, several other classical targets (adipocytes, skeletal, cardiac, and smooth muscle cells) showed no specific 125I-insulin binding and therefore indicated the limits of sensitivity of the in vivo radioautographic method. Nevertheless, the working hypothesis of a direct correlation of insulin receptor density with insulin action points to the hitherto unemphasized targets of pancreas, adrenal gland, and gastrointestinal tract as major sites of insulin action in the body.

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