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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General evidence of malnutrition such as loss in body weight associated with intestinal parasitism has been attributed to decreased food intake, to intestinal malabsorption, and to change in host basal metabolism. To establish the relative importance of these factors in this regard, rats with trichinosis were studied. The weights of infected and uninfected animals were followed after being placed on one of three feeding regimens for 1 week--stock diet ad libitum, intraduodenal nutrition, and intravenous nutrition. Infected rats on a stock diet lost weight whereas those on the other two regimens maintained the same weight pattern as uninfected counterparts. The maintainance of body weight occurred despite alterations at the level of the intestinal brush border as indicated by a depression of intestinal disaccharidase activities (sucrase and lactase) and by reduction of monosaccharide absorption (measured as accumulation of beta-methyl glucoside) in the proximal, heavily infected region of the small intestine. There was no compensatory increase in enzyme activity nor in the absorptive capacity in the distal gut. Results support the conclusion that inadequate oral food intake rather than changes in basal metabolism or intestinal pathophysiology accounts for weight loss during the intestinal phase of infection.
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PMID:Enteral and parenteral feeding to evaluate malabsorption in intestinal parasitism. 11 Jan 62

A phytohemagglutinin extract is prepared from raw kidney beans (Phaseolus vulgaris) and incorporated at a level of 1% (dry matter) in the diet of young growing rats. Beside a decrease of feed intakes, the main effects of the experimental diet are the following : growth depression, decrease of dry matter and protein digestibility and hypoglycemia. Biological value, organs weight (liver, kidneys, spleen) did not change significantly. The hemagglutinin extract induces an inhibition of saccharase activity whereas (Na+-K+)-ATPase remains unchanged. Growth depressing effect may be due to an alteration of hydrolysis and absorption mechanisms at the level of brush border of enterocytes.
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PMID:[Effects of a phytohemagglutinin extract on growth, nitrogen digestibility and the activity of invertase and (Na+-K+)-ATPase in the intestinal mucosa of the rat]. 23 10

Lactase deficiency, manifested clinically by lactose malabsorption, is often the only biochemical evidence of a residual disturbance of jejunal mucosal function after Escherichia coli enteropathy in the infant. Villous morphology is usually normal. A sustained depression of the processes of biochemical differentiation of lactase biosynthesis has been postulated to explain similar states of lactase deficiency, but a possible influence of altered epithelial cell turnover on the mucosal lactase levels has not been investigated. In ten infants with a residual lactose malabsorption, after E. coli infection, jejunal cell renewal activity and disaccharidase activities were studied by analysis of the exfoliated cells collected by lumenal perfusion. Significant increases in DNA and protein exfoliation and in the brush border activities of sucrase and lactase were observed during recovery from the malabsorptive disturbance. DNA and protein efflux increased almost linearly during a 20-day period. Lactase was initially four times more deficient than sucrase activity in the exfoliated cells. Both enzyme activities increased at almost identical rates. Therefore, it took longer for lactase activity to return to normal levels. The lactase/sucrase ratios approached normal at the end of the 20-day period. The changes in the exfoliating levels of the two enzymes, when analysed in relation to the increases in cell renewal activity, suggested a relationship between sucrase and lactase levels and cell age.
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PMID:Intestinal exfoliated cells in infant diarrhoea: changes in cell renewal and disaccharidase activities. 104 54

Although it is generally agreed that active sugar absorption in vitro is absolutely dependent on the presence of sodium ions on the luminal side of the mucosa, previous in vivo studies in the ileum of rat, dog and man have shown that active glucose absorption is almost as rapid from a sodium-free mannitol solution as from a sodium chloride solution. These experiments were performed in hopes of reconciling this discreptancy. Absorption of three actively transported sugars (glucose, galactose, and 3-O-methylglucose) having different apparent Km's, and of fructose (absorbed by a separate carrier-mediated process) were measured in the human ileum in vivo. The following observations were made: (1) Mannitol substitution for sodium results in only a slight reduction (23%) in the active absorption of glucose. (2) Magnesium substitution for sodium results in a greater depression (45%) of glucose absorption. (3) The apparent Km for glucose absorption is increased when sodium is replaced by magnesium, but the Vmax is not altered. (4) Magnesium does not depress glucose absorption or the apparent Km for glucose transport when sodium is present in the perfusing solution. (5) Neither sodium removal nor magnesium has any effect on fructose absorption. (6) Absorption of galactose and 3-O-methylglucose (low affinity sugars for the glucose carrier) is reduced by about 40 to 50% when mannitol replaces sodium, but magnesium substitution for mannitol in a sodium-free medium does not further depress absorption of these sugars. The following conclusions are suggested by these results: First, part of the discrepancy between previous in vitro and in vivo experiments was due to the type of test sugar (glucose versus glucose analogue) and the solute used to replace sodium in the luminal solution. Second, magnesium is more effective than mannitol in reducing sodium concentration at the glucose transport site on the brush border. Third, luminal sodium ions have an important effect on active sugar absorption in the human small intestine in vivo, as they do in vitro. And, fourth, there is a component of active sugar absorption (about one-half) which appears to be independent of luminal sodium ions in vivo.
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PMID:Effect of sodium, mannitol, and magnesium on glucose, galactose, 3-O-methylglucose, and fructose absorption in the human ileum. 111 66

The objective of this study was to investigate the mechanism by which ethanol inhibits intestinal absorption of sugars. In vitro experiments on hamster jejunum have shown that the presence of ethanol in the mucosal solution caused an inhibition of the net transport of water and glucose. There was also a decrease in the intracellular water content and an increase in the intracellular sodium and potassium concentration of the gut tissue. In contrast, the intracellular glucose concentration decreased in the presence of ethanol. These ethanol-induced changes were directly related to the ethanol concentration of the mucosal solution. In the presence of 450 mM (2%) ethanol in the mucosal solution, there was also a significant inhibition of transmural potential difference, estimated glucose metabolism, and both unidirectional fluxes of sodium. The net flux of sodium to the serosal side however did not decrease significantly. These effects of ethanol cannot be fully explained by its osmotic action, and it is suggested that the ethanol-induced reduction in glucose transport could be mainly the result of an interference with the carrier-mediated coupled entrance of glucose and sodium across the brush border. A depression of cellular metabolism could also have played a role in this process.
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PMID:Effect of ethanol on sodium-dependent glucose transport in the small intestine of the hamster. 113 33

Feeding sodium deoxycholate orally to rats for four days caused depression of the activity of the small intestinal enzymes lactase, sucrase, maltase, alkaline phosphatase, and N-acetyl-beta-glucosaminidase. The first four are brush border enzymes, the last a lysosomal enzyme. Alkaline phosphatase activity recovered very rapidly and rebounded to above the normal level within 24 hours. The activity of the three disaccharidases returned to normal within seven days while no recovery was observed within 96 hours of the activity of the lysosomal enzyme, N-acetyl-beta-glucosaminidase, after removing the bile salt from the diet.
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PMID:Deoxycholate depresses small-intestinal enzyme activity. 114 Jun 27

Polyamino acids including polyaspartic acid (PAA) have been reported to provide protection against the development of aminoglycoside-induced nephrotoxicity in the rat as assessed by histopathology scoring. We sought to confirm and extend these observations by determining whether PAA also prevented functional and biochemical lesions of gentamicin-nephrotoxicity in an animal model studied extensively in our laboratory. Rats were given injections of: 1) 0.9% NaCl at 2.5 ml/kg b.wt. per day; 2) PAA (mol.wt. 15,000) at 500 mg/kg per day; 3) gentamicin at 100 mg/kg per day or 4) gentamicin at 100 mg/kg per day and PAA at 500 mg/kg per day for 6 days. Rats injected with gentamicin exhibited: 1) increased urinary excretion of the brush border membrane enzyme alanine aminopeptidase and the lysosomal enzyme N-acetyl-beta-d-glucosaminidase after the first injection; 2) increased total phospholipid and malondialdehyde but decreased catalase activity in the renal cortex; 3) elevation of serum creatinine and depression of creatinine clearance and 4) extensive proximal tubular cell necrosis all determined 24 hr after the last injection of gentamicin. Rats injected with gentamicin plus PAA also exhibited increased urinary excretion of alanine aminopeptidase not different in magnitude from that of rats injected with gentamicin alone, whereas N-acetyl-beta-d-glucosaminidase rose more slowly and returned to base line by day 4. Total renal cortical phospholipid was elevated to the same extent in the two groups. Malondialdehyde was not different from control and catalase activity was significantly less depressed in rats injected with gentamicin plus PAA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Polyaspartic acid protects against gentamicin nephrotoxicity in the rat. 274 94

A total of 568 strains of Escherichia coli isolated from healthy and diarrheic rabbits were separated into 11 different biotypes according to the fermentation patterns of four carbohydrates. Strains belonging to biotypes 1 to 3, 6, and 8 induced lesions characteristic for attaching and effacing E. coli (AEEC). They attached to the intestinal epithelium of the terminal small intestine and the large intestine of 5-week-old rabbits after experimental infection and caused effacement of the microvillous brush border. However, pathogenicity for weaned rabbits, as judged by diarrhea score, anorexia, and reduced weight gain, varied according to the biotypes of the strains. Strains belonging to biotypes 1 and 6 produced only discrete clinical signs, strains belonging to biotypes 2 and 3+ (motile) induced diarrhea and growth depression, whereas strains belonging to biotypes 3- (immotile) and 8 caused severe clinical signs and high mortality. This confirms evidence from the field. Biotypes 3- and 8, accounting for 35.5 and 7.1% of AEEC strains in weaned diarrheic rabbits, respectively, were not detected in weaned healthy rabbits, while biotype 2 was the predominant strain in weaned healthy rabbits (62.3%). Finally, serotyping showed a close relationship between biotype and serotype of the AEEC examined. Most strains of biotypes 1+ and 2+ tested were O109:K-:H2 and O132:K-:H2, respectively, whereas all strains tested of biotype 3- were O15:K-:H- and those of biotype 8 were O103:K-:H2. These data indicate that specific clones of AEEC might be involved in juvenile rabbit enteritis. It was concluded that determination of biotypes allows the screening of highly pathogenic AEEC in weaned rabbits (biotypes 3- and 8).
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PMID:Biotype, serotype, and pathogenicity of attaching and effacing enteropathogenic Escherichia coli strains isolated from diarrheic commercial rabbits. 328 97

A case of prolonged diarrhoea following Escherichia coli 0111 gastroenteritis is reported. Electron microscopy of the jejunal biopsy revealed effacement of the brush border and attachment of bacteria by pedestal formation. Specific activities of brush border enzymes showed marked depression of disaccharidases, zinc-resistant alpha-glucosidase, and alkaline phosphatase. In contrast, marker enzymes for basolateral membranes and endoplasmic reticulum were unaffected. The biochemical changes support the pathogenic mechanism suggested by ultrastructural studies previously reported.
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PMID:Ultrastructural and biochemical changes in human jejunal mucosa associated with enteropathogenic Escherichia coli (0111) infection. 351 Dec 12

Dietary calcium (CA++) supplementation attenuates gentamicin nephrotoxicity in rats. It has been proposed that this protective effect results from the ability of Ca++ to interfere with gentamicin binding to renal cell membranes. However, calcium supplementation also suppresses parathyroid hormone (PTH) activity, which may affect gentamicin nephrotoxicity by altering renal brush border phospholipid composition or renal calcium handling. We therefore compared gentamicin nephrotoxicity in PTH-stimulated control rats and parathyroidectomized (PTX) rats. Although their pretreatment serum ionized calcium concentration was significantly higher (1.27 +/- 0.01 vs. 0.88 +/- 0.06 mmol/L; P less than 0.001), PTH-stimulated rats had higher peak renal cortical gentamicin concentrations (543 +/- 20 vs. 395 +/- 49 micrograms/gm; P less than 0.025) and serum creatinine concentrations (3.0 +/- 0.8 vs. 0.9 +/- 0.3 mg/dl; P less than 0.05). Structural injury and depression of renal cortical slice uptake of p-aminohippurate were also less severe in PTX rats. Gentamicin treatment also caused increased urinary Ca++ excretion in control rats (from 2.12 +/- 0.64 mumol/mg creatinine per day [pretreatment] to 16.86 +/- 2.07 mumol/mg creatinine per day; P less than 0.001) but not in PTX rats. Control rats ingesting chow containing a standard Ca++ content (1.2%) resembled PTX rats. These results indicate that PTH stimulation exacerbates gentamicin nephrotoxicity. Increased peak renal cortical gentamicin concentrations in PTH-stimulated rats may be caused by increased gentamicin transport across the brush border as a consequence of PTH-mediated alteration of plasma membrane phospholipid composition, turnover, or both.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone activity on gentamicin nephrotoxicity. 379 14


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