Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A secondary hyperparathyroidism resulting from decreased intestinal calcium (Ca) absorption has been proposed as a contributory factor to glucocorticoid-induced osteoporosis. Inhaled steroids do not usually suppress adrenal gland function unless daily doses above 1,500 microgram are used. A recent study, however, has shown a reduced total body calcium in patients on regular beclomethasone treatment. In theory, osteopenia in these patients could be due to a direct effect of inhaled steroids on bone or due to an impaired intestinal calcium absorption. In this study, Ca absorption and parathyroid hormone (PTH) secretion were evaluated in three groups: 1) asthmatics on continuous oral and inhaled steroid treatment (11.3 +/- 4.4, range 5-33.5 mg.day-1 prednisone and 660 +/- 265, range 400-1,600 microgram.day-1 beclomethasone, respectively); 2) asthmatics on regular beclomethasone therapy (585 +/- 210, range 400-1,200 microgram.day-1); and 3) healthy subjects. The prevalence of vertebral fractures was evaluated by a spinal X-ray. No differences were found in either Ca absorption or PTH serum levels between asthmatics and healthy subjects (analysis of variance-ANOVA). Vertebral fractures were significantly more frequent in patients from group 1 (14 of 25) than in those from group 2 (2 or 25). We conclude that both prolonged oral steroid treatment and inhaled steroids, at doses lower than 1,600 microgram.day-1 do not cause Ca malabsorption, and that hyperparathyroidism does not contribute to osteoporosis in these patients.
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PMID:Intestinal calcium absorption and parathyroid hormone secretion in asthmatic patients on prolonged oral or inhaled steroid treatment. 185 73

Short bowel syndrome (SBS) in the newborn results in limited intestinal absorptive capacity, leading especially to fatty acid (FA) malabsorption. It is unknown whether adaptation occurs in time in FA absorption, and whether this adaptation is chain-length dependent. The aid of the present study was to prospectively evaluate FA absorption and excretion during SBS in the newborn. Twenty-one neonates who underwent small bowel resection (of variable length) for various reasons (necrotizing enterocolitis, intestinal atresia, meconium peritonitis, cloacal extrophy, etc) were studied. Eight neonates had SBS, defined as a small bowel remnant of less than 50% of the original small bowel length related to gestational age. The mean remaining small bowel length in the SBS group was 34% (24% to 42%). The non-SBS control group consisted of 13 neonates who had only minor small bowel resections. The mean remaining bowel length for the non-SBS group was 95% (70% to 100%). The results show that the total fractional excretion of FA (FE-FA) at 2 weeks and 1, 2, 3, and 4 months postsurgery was 51% +/- 37%, 33% +/- 24%, 51% +/- 65%, 53% +/- 27%, and 7% +/- 2% in patients with SBS, versus 12% +/- 8%, 24% +/- 10%, 9% +/- 3%, 8% +/- 3% and 17% +/- 14% in the non-SBS controls, respectively (P < .05 by ANOVA). There appeared to be an amelioration in time in FA absorption, especially in the SBS group, after 3 months. FE-FA was chain-length related, being considerably less for C10 and C12 than for C14 and longer amounts. An amelioration of absorption occurred in the SBS patients, especially with the longer-chain FA. On the basis of the study data, the authors conclude that in the initial adaptation phase shorter chain lengths are better absorbed than longer chain lengths; however, in the latter FA group, substantial adaptation occurs with time.
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PMID:Prospective evaluation of faecal fatty acid excretion in short bowel syndrome in newborns. 880 4

Alagille syndrome (AGS) is frequently associated with growth failure, which has been attributed to concurrent congenital anomalies, cholestasis, and malabsorption and/or malnutrition. However, the underlying cause of the growth failure is not well understood. Our objective is to analyze the growth pattern in 26 patients with AGS and the possible effect that orthotopic liver transplantation (OLT) may have on this pattern. The standardized height, weight, and growth velocity of 26 pair-matched patients with AGS were compared. Thirteen patients underwent OLT. Repeated-measure ANOVA methods were used for the statistical analysis. The overall mean standardized height (z score) was -2.92 in the OLT group versus -1.88 in the non-OLT group (P =.03). The overall mean standardized weight was -1. 21 in the non-OLT group and -1.67 in the OLT group (P =.23). In 15 patients, birth weight was 2.82 +/- 0.4 kg, for a mean standardized weight of -0.95, and weight at diagnosis was 4.53 +/- 2.12 kg, for a mean standardized weight of -1.56. Bone age was delayed in the 9 patients who underwent bone-age analysis. Growth hormone therapy administered to 2 patients did not improve growth. Patients with AGS had growth failure secondary to other factors in addition to liver disease. Growth failure beginning in the prenatal period supports a genetic basis for this feature. Growth improvement up to normal levels should not be expected as a benefit of OLT in these patients. Growth failure as a primary indication for OLT should be cautiously examined in patients with AGS.
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PMID:Does liver transplantation affect growth pattern in Alagille syndrome? 1098 57

Enteral probiotics such as Lactobacillus casei GG (LGG) have been used in the treatment of a variety of intestinal disorders in infants and children, including diarrhea, malabsorption, and Clostridium difficile colitis. We have previously demonstrated that the probiotic bacterium LGG has an inhibitory effect on bacterial translocation (BT) in a neonatal rabbit model. However, this in-vivo model is limited for investigating the cellular and molecular mechanisms responsible for probiotic inhibition of BT. The purpose of this study was to determine the efficacy of LGG in reducing the rate of Escherichia coli C25 (E. coli C25) translocation using an in-vitro enterocyte cell-culture model. Human colonic carcinoma (Caco-2) enterocytes were seeded in porous filters in the apical chamber of a two-chamber cell-culture system and grown for 14 days to confluence. The monolayers were incubated at 37 degrees C with LGG for 180 min. Non-adherent LGG was washed away prior to a 120-min incubation period with 10(5) CFU E. coli C25. E. coli that had translocated across the enterocyte monolayer were quantified by growing basal-chamber media samples on gram-negative bacteria-specific MacConkey's agar. In order to determine monolayer integrity, transepithelial electrical resistance (TEER) was measured across Caco-2 cells treated with LGG and E. coli. Statistical analysis was by ANOVA with P < 0.05 considered significant. LGG inhibited E. coli translocation at all LGG concentrations tested. The TEER ratio was not significantly altered by addition of LGG or E. coli (0.9 +/- 0.03 vs 0.8 +/- 0.05). These results demonstrate that the probiotic bacterium LGG inhibits BT of E. coli C25 in a dose-dependent manner in an in-vitro cell-culture model. This model should be valuable in investigating the cellular and molecular mechanisms involved in the inhibition of pathological enteral bacteria by probiotic agents.
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PMID:Effect of probiotics on enterocyte bacterial translocation in vitro. 1140 59

The objective of this study was to investigate whether folinic acid supplementation would protect young mice against suppression of growth by methotrexate (MTX). Four equal groups of Balb/c young male mice (5 animals in each group; mean+/-SD body weight 9.64+/-0.85 g, in their rapid growth phase) were subjected to the following drug treatment: One group was given MTX (3.5 mg/kg body weight) intraperitoneally on every 2nd day, another received folinic acid (7.0 mg/kg body weight) intraperitoneally every 2nd day. The third group was given both of these drugs (MTX on every 2nd day and folinic acid 8 h post-MTX injection). The fourth group was injected with physiological saline every other day to serve as a control group. Total body weight, food and water consumption by animals in each group were monitored every second day for a period of 3 weeks. After this period mice were sacrificed and liver, spleen and kidneys were excised, weighed and analyzed for MTX and dihydrofolate reductase activity. A small segment of the proximal part of small intestine and small pieces of liver and kidney were also removed to study morphological changes. Compared to the groups, which received folinic acid alone, folinic acid plus MTX or physiological saline, mean increase in body weight (6.8+/-0.8 g) of mice over a period of 3 weeks was minimal in the group receiving MTX alone (one-way ANOVA p=0.0001). The mean weights of liver and kidney in this group receiving MTX alone were also found to be significantly less than the mean weights of these organs in the 3 groups (p<0.001). The negative effect on growth of animals appears not only due to malabsorption but inhibition of pathway of de novo DNA synthesis may also be involved. This is supported by loss of villous pattern in small intestine of mice treated with MTX alone and increased accumulation of free MTX and decreased dihydrofolate reductase in the liver of the group receiving MTX alone as compared with the group receiving MTX plus folinic acid. The data indicate that the administration of folinic acid protects mice against suppression of growth by MTX. On the basis of these observations it can be deduced that patients suffering from juvenile rheumatoid arthritis or acute lymphoblastic leukaemia receiving MTX over a long period of time might be at a risk of experiencing short-term suppression of growth, however they could benefit from supplementation with folinic acid.
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PMID:Folinic acid protects against suppression of growth by methotrexate in mice. 1174 19

Long chain fatty acids (LCFAs) appear to be powerful stimulants for small bowel adaptation in patients with short bowel syndrome (SBS). However, the dietary lipid content may alter intestinal lipid transport. The aim of this study was to investigate the effects of a high fat diet (HFD) on in vivo lipid absorption and molecular and cellular mechanisms of LCFAs uptake by the remaining bowel. Male Sprague-Dawley rats (240-280) were randomly assigned to one of three groups: sham rats fed normal chow (sham-NC), SBS rats fed NC (SBS-NC) and SBS rats fed HFD (SBS-HFD). SBS rats underwent a 75% small bowel resection. Rats were sacrificed on day 3 or 14. Body weight, fat intake and fat clearance (total fecal fat) were measured twice a week. Fat absorbability was calculated as intake minus clearance and was expressed as percent of intake. Total RNA from the mucosa of duodenum, jejunum and ileum was extracted using TRIZOL Reagent. Northern blot analysis was performed to determine FAT/CD36 mRNA levels. Enterocyte LCFA transport was measured on day 14. LCFA uptake was determined by measuring cellular [3H]-oleate uptake over time (4-120 s). Mean (+/-SE) FAT/CD36 mRNA levels and oleate uptake kinetic parameters were analyzed using ANOVA. Fat absorbability diminished after bowel resection, suggesting fat malabsorption. Remaining bowel in SBS-NC rats responded by an increase in FAT/CD36 mRNA levels in the duodenum and ileum on day 3, and the duodenum and jejunum on day 14 compared to sham-NC animals, and was accompanied by an increase in enterocyte LCFA transport in all segments. Exposure to a HFD for 14 days resulted in significantly increased fat absorbability after 3 days compared to SBS-NC rats. However, FAT/CD36 mRNA levels (vs. SBS-NC) decreased in all segments on day 3. On day 14, FAT/CD36 mRNA levels were decreased in the duodenum and ileum and were accompanied by reduced oleate uptake by isolated enterocytes in the ileum (vs. SBS-NC). In a rat model of SBS, early high fat diet increased lipid absorptive capacity of the intestinal remnant as seen by increased fat absorbability. The main mechanisms of this effect may be an acceleration of structural intestinal adaptation resulting in an increased number of enterocytes. However, at molecular and cellular levels HFD decreased mucosal FAT/CD36 mRNA levels and oleic acid uptake by isolated enterocytes.
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PMID:Effect of a high fat diet on lipid absorption and fatty acid transport in a rat model of short bowel syndrome. 1272 10

Obesity is considered a primary risk factor for cardiovascular disease and related mortality. The current study aimed to investigate the efficacy of minimal invasive gastric banding (GB) surgery for reducing caloric intake in morbid obesity, and to analyze the effects of weight loss on body composition and metabolic and psychosocial outcomes. Twenty-six adult severely obese patients (mean body mass index [BMI], 48.1 kg/m(2); range, 42 to 56) underwent adjustable silicone laparoscopic GB. Nine additional obese patients who declined surgery were treated with metformin (2 g daily) and served as a small additional group (BMI, 50.5 kg/m(2); range, 41 to 68). Presurgery and 17 +/- 2.2 months postoperatively, body composition (fat mass [FM], lean body mass [LBM], body water) and serum parameters (lipids, glucose, thyrotropin-stimulating hormone [TSH]) were determined. Quality of life (QoL) was evaluated by a standardized self-rating questionnaire (Short Form-36 [SF-36]), and supplemented by measures of physical complaints and psychological distress. After GB, weight loss was 21 +/- 14.9 kg (14%, P <.001). It was associated with a decrease in FM by 14 +/- 8.6 kg (18%, P <.001), LBM by 4 +/- 2.7 kg (5%, P <.001), body water by 4 +/- 3.4 L (7%, P <.01), systolic blood pressure by 16 +/- 26.3 mm Hg (10%, P <.05), total cholesterol by 0.69 +/- 1.29 mmol/L (12%, P <.05), and low-density lipoprotein cholesterol (LDL-C) by 0.38 +/- 0.39 mmol/L (10%, P <.05). Highly significant interactions between surgery and time were noted for weight (P <.005), BMI (P <.005), and FM (P <.007, analysis of variance [ANOVA]). Preoperatively, 14 of 26 patients (54%) had high fasting blood sugar levels (type 2 diabetics) and 11 (42%) had impaired glucose tolerance, whereas postoperatively, for baseline glucose levels a trend to decrease was noted. Neither malabsorption nor anemia was observed. QoL improved after GB; in particular, physical functioning and well being increased (P <.01), and somatic complaints (eg, dyspnea and heart complaints, pain in legs and arms) markedly decreased (P =.008). In the metformin group, neither relevant weight loss nor a significant decrease of biochemical values was observed. Minimal invasive GB is a successful therapeutic tool for reducing FM in morbidly obese patients. Weight loss resulted in improved metabolic parameters, suggesting a lowered atherogenic risk.
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PMID:Metabolic and psychosocial effects of minimal invasive gastric banding for morbid obesity. 1466 54

Contrary to frequent claims, vitamin D insufficiency does not generally cause malabsorption of calcium because serum 1,25(OH)(2)D, which is the major determinant of calcium absorption, is maintained by secondary hyperparathyroidism. Nevertheless, because malabsorption of calcium has been described in osteomalacia, there must be a 25(OH)D level below which the serum 1,25(OH)(2)D can no longer be sustained, although it has never been defined. This paper seeks to define it. We examined the records of 3661 patients and found 319 with a serum 25(OH)D < or = 40 nM, in whom calcium absorption, serum calcium, PTH, bone markers, and vitamin D metabolites had been measured. They were grouped according to their serum 25(OH)D into four categories, 0-10, 11-20, 21-30, and 31-40 nM, and differences between the groups were tested by ANOVA. Correlations between the variables were also examined. Serum calcium, 1,25(OH)(2)D, and calcium absorption were significantly decreased and serum PTH and alkaline phosphatase (ALP) and urine hydroxyproline were increased in those with 25(OH)D < or = 10 nM. Serum ALP and urine hydroxyproline were more strongly related, inversely, to calcium absorption than to the vitamin D metabolites. We conclude that vitamin D deficiency does not reduce serum 1,25(OH)(2)D, and therefore calcium absorption, until the serum 25(OH)D falls to approximately 10 nM. At this level, the substrate concentration seems to be insufficient to maintain the level of the dihydroxy metabolite despite secondary hyperparathyroidism. Further studies are needed to see how these changes correlate with the histological changes of osteomalacia.
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PMID:Vitamin D metabolites and calcium absorption in severe vitamin D deficiency. 1859 33