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Biomedical subjects

C C Roy

Publications and source records attributed to C C Roy.

At least 19 recordsLinked to original sources
PubMed1992

Intraluminal and intracellular phases of fat absorption are impaired in essential fatty acid deficiency.

The structure and function of enterocyte membranes are particularly sensitive to the degree of fatty acid saturation. The objective of the present study was to assess intestinal fat transport in essential fatty acid (EFA)-deficient animal models. Both the digestive and absorptive phases leading to the formation and the secretion of triglyceride (TG)-rich lipoproteins were investigated. After an intraduodenal fat infusion, the percentage increase of plasma TG over fasting values was examined over a period of 4 h in two groups of control and EFA-deficient rats. Lower values at 1 and 2 h (P less than 0.05) were observed in EFA-deficient rats, suggesting fat malabsorption. Likewise, postprandial chylomicronemia was diminished. In a separate group of rats, EFA deficiency was associated with reduced TG and chylomicron-TG transport into lymph. Although pancreatic lipase activity did not change (47.1 vs. 46.2 mumol free fatty acids.mg protein-1.h-1), bile flow was decreased over the 8-h period of collection. Concomitantly, a significant decline (nmol.min-1.g liver-1, P less than 0.05) was discernible in the biliary secretory rate of bile salts (14.09 +/- 2.13 vs. 35.09 +/- 3.73), phospholipids (7.01 +/- 0.61 vs. 11.79 +/- 1.65) and cholesterol (0.19 +/- 0.01 vs. 0.83 +/- 0.06). In vitro studies, utilizing everted sacs incubated with mixed micelles, revealed that EFA-deficient jejunal segments of rats incorporated and esterified less [14C]oleic acid (21 and 32%, respectively). Moreover, the synthesis and secretion of TG-rich lipoproteins were found markedly reduced in mouse jejunal explant cultures. We conclude that EFA deficiency modifies both the intraluminal and intracellular phases of fat absorption.

Absorption↗
PubMed1992

The hydrocarbon breath test in the study of lipid peroxidation: principles and practice.

Lipid peroxidation has gained increasing interest in recent years as one of the more prominent features of free radical-induced damage in biology. The study of lipid peroxidation might increase our understanding of the etiology and pathophysiology of a great number of diseases. Ethane and pentane are among the numerous end-products of lipid peroxidation and although they represent only a small and possibly variable proportion of the total amount of peroxidized polyunsaturated fatty acids, their determination in head space or exhaled breath enables accurate assessment of oxidative stress both in vitro and in vivo. To date, the number of studies utilizing the hydrocarbon breath test as a marker of lipid peroxidation in humans is small. Technical difficulties are among the main reasons for the limited use of this method. An appropriate washout period, the use of the right materials, the scrupulous avoidance of air contamination, adequate preinjection concentrations of the samples, and a sensitive gas chromatographic technique enable the accurate and reproducible measurement of hydrocarbons in human breath. The hydrocarbon breath test provides a noninvasive and extremely sensitive instrument for the assessment of oxidative stress status in adults as well as in children.

Breath Tests↗
PubMed1991

Preparative steps necessary for the accurate measurement of malondialdehyde by high-performance liquid chromatography.

The need for a more specific, reliable, and reproducible technique for the measurement of malondialdehyde (MDA) has prompted modifications of currently available methods based on the formation and recovery of the complex between MDA and thiobarbituric acid (TBA). To 500 microliters of plasma or to 300 mg of liver homogenate, 2 ml of H2O and 500 microliters of 0.5% butylated hydroxytoluene in methanol were added to prevent further formation of MDA. Precipitation of proteins carried out with 200 microliters of 0.66 N H2SO4 and 150 microliters of 10% Na2WO4 (w/v) led to complete recovery of the MDA standard. Maximum formation of the MDA-TBA complex was obtained by adjusting the pH between 2.5 and 4.5 and heating the MDA-TBA mixture at 100 degrees C for 60 min. Extraction of the MDA-TBA complex was a critical step and proved complete with n-butanol at pH less than 0.75. It was then evaporated at 37 degrees C under nitrogen. The MDA-TBA complex solubilized in H2O was shown to be stable for at least 7 days. These preparative steps led to the detection of a single peak that on spectral analysis was identified as pure MDA-TBA. This procedure offers several advantages in terms of specificity, recovery, and reproducibility.

1-Butanol↗
PubMed1991

Taurine decreases fecal fatty acid and sterol excretion in cystic fibrosis. A randomized double-blind trial.

Patients with cystic fibrosis may still have a significant degree of steatorrhea despite adequate pancreatic enzyme supplementation. Taurine is a conditionally essential amino acid that possibly improves the micellar phase of fat digestion. Thirteen children with cystic fibrosis and a significant degree of steatorrhea (> 13 g/d) were enrolled in a randomized double-blind crossover study of taurine (30 mg/kg per day) in contrast to placebo for two successive 4-month periods. No difference was noted in height and weight velocity, lung function, vitamin A level, and essential fatty acid status. Twelve of the 13 patients showed a decrease in fecal fatty acid excretion (26.5 +/- 2.6 g/24 h vs 15.4 +/- 2.5 g/24 h), affecting mainly saturates and monounsaturates, and a decrease in total sterol excretion (1492.6 +/- 303 mg/24 h vs 1211.7 +/- 213.8 mg/24 h) while ingesting taurine. Taurine may be a useful adjunct in patients with cystic fibrosis and severe steatorrhea.

Adolescent↗
PubMed1991

Pneumatosis and pneumoperitoneum in chronic idiopathic intestinal pseudoobstruction.

Chronic idiopathic intestinal pseudoobstruction is a diagnosis of exclusion for the rare patient with severe small bowel atony without any demonstrable organic cause. The very poor prognosis associated with this disease has been somewhat improved with the advent of parenteral nutrition; nevertheless, these patients follow a stormy course characterized by malnutrition, recurrent obstruction, infection, hemorrhage, and perforation. We describe a 16-year-old boy with this disease who presented to us with vague abdominal pain and pneumoperitoneum. Laparotomy showed pneumatosis cystoides intestinalis without intestinal perforation. The presence of free air in the abdominal cavity is an almost pathognomonic sign of intestinal perforation. Pneumatosis cystoides intestinalis is one of the very few nonsurgical causes of pneumoperitoneum. Beyond the neonatal period, in which it is the hallmark of necrotizing enterocolitis, it has been described in patients with severe obstructive lung disease, in collagenous disorders, and in the short-bowel syndrome. In the present case, it may have resulted from chronic intestinal distension, allowing air under pressure to dissect through the bowel wall. The challenge of such a unique association of conditions lies in the avoidance of unnecessary surgery in a chronic, essentially nonsurgical disease while avoiding unnecessary delay in a possibly acute surgical event.

Child↗
PubMed1991

Metabolic fate of chylomicrons obtained from rats maintained on diets varying in fatty acid composition.

The importance of the fatty acid component in the metabolism of chylomicrons was demonstrated by feeding diets varying in fatty acid composition which resulted in chylomicrons of different sizes. On a diet rich in polyunsaturated fatty acids (PUFA) from safflower oil, chylomicrons of diameter 1853 +/- 192 A were harvested from the mesenteric lymph, whereas on coconut oil and medium-chain triglyceride diets the chylomicron size was 1403 +/- 83 and 604 +/- 40 A, respectively. When the isolated chylomicrons were injected into recipient rats maintained on a regular diet, their half-life (t1/2) decreased from 5.4 +/- 0.4 to 1.8 +/- 0.3 min with the increase in particle size. No significant difference in the apolipoprotein profile of chylomicrons of various sizes was noted, indicating that alterations of chylomicron removal are not related to apolipoprotein composition. Rats maintained on PUFA diets showed a marked increase in their adipose tissue lipoprotein lipase activity. The fast removal of large chylomicrons and increased tissue lipoprotein lipase activity, together with suppression of hepatic lipogenesis on this diet, apparently explains the low plasma triglyceride level in rats maintained on diets rich in PUFAs.

Animals↗
PubMed1991

The effect of taurine on the cholestatic potential of sulfated lithocholate and its conjugates.

The present study was aimed at determining whether the protection by taurine of lithocholate-sulfate-induced cholestasis is mediated by conjugation or by direct effect of the amino acid on bile formation. Injection of free and conjugated (glycine and taurine) sulfated lithocholate in guinea pigs significantly reduced the secretion rate of non-sulfated bile acids in bile. There was no decrease in bile flow after the injection of taurine-conjugated sulfated lithocholate, which was completely recovered in bile within 60 min. In contrast, injection of sulfated lithocholate and its glycine conjugate led to a marked decrease in bile flow, and neither one was significantly recovered in bile. In addition, both caused morphological changes in the liver, characterized by the accumulation of cytoplasmic vacuoles with lamellated myelin figures characteristic of phospholipidosis. Pretreatment with taurine (0.5% in drinking water for 3 days) prevented both the drop in bile flow and the histological changes in the liver, suggesting that conjugation with taurine removed the cholestatic potential of sulfated lithocholate. However, since taurine was effective not only in preventing cholestasis induced by the free form of sulfated lithocholate but also against its glycine conjugate, these results suggest that other mechanisms in addition to conjugate must be involved.

Animals↗
PubMed1990

Mechanisms of hypercholesterolaemia in glycogen storage disease type I: defective metabolism of low density lipoprotein in cultured skin fibroblasts.

Hyperlipidaemia is a feature of glycogen storage disease type I (GSD-I) (Levy et al.). High levels of LDL cholesterol (200 +/- 25 mg dl-1) and apo B (387 +/- 44 mg dl-1) were found in association with hypercholesterolaemia in GSD-I. Related causative factors might be attributed to overproduction and/or delayed removal of LDL. In this study, a possible alteration in the clearance of LDL was examined. Using cultured fibroblasts for LDL receptor activity, the following observations were made: 1. GSD-I fibroblasts revealed only a slight decrease in LDL binding (65 +/- 7) when compared with controls (74 +/- 4 ng mg-1 protein), however, LDL internalization (382 +/- 24 vs. 570 +/- 52 ng mg-1 protein) and proteolytic degradation (2082 +/- 280 vs. 2916 +/- 12.5 ng mg-1 protein) were significantly affected (P less than 0.01). 2. Binding, internalization and proteolytic degradation of LDL from GSD-I were compared with that of controls, and were found to be significantly lower (P less than 0.01). 3. Substitution of control lipoprotein-deficient serum (LPDS) by GSD-I LPDS further diminished the above processes (P less than 0.05). Our results demonstrate that increased plasma cholesterol in GSD-I is due to a decreased catabolism of LDL. The data suggest that the problem may well be multifactorial, due to diminished receptor expression, abnormal LDL composition and impaired LDL receptor interaction due to a circulating inhibitory factor.

Adolescent↗
PubMed1990

In vitro remodelling of plasma lipoproteins in whole plasma by lipoprotein lipase in primary and secondary hypertriglyceridaemia.

In patients with familial lipoprotein lipase deficiency (FLPL-d) and glycogen storage disease type I (GSD-I), hypertriglyceridaemia (1445 +/- 247 and 1082 +/- 312 mg dl-1, n = 5 per group) was associated primarily with reduced extrahepatic lipoprotein lipase (LPL) activity (0.33 +/- 0.33 and 1.69 +/- 0.38 mumol FFA ml-1 h-1) when compared with controls (4.83 +/- 0.90). Hypercholesterolaemia was characterized by elevated LDL cholesterol (191 +/- 30 and 344 +/- 34 vs. 115 +/- 5 mg dl-1 in controls P less than 0.01) and low HDL cholesterol (12 +/- 2 and 22 +/- 2 vs. 56 +/- 3 in controls, P less than 0.001). In order to ascertain the role of LPL in the interconversion and remodelling of lipoproteins in these disorders, we analysed lipid and lipoprotein profiles before and following in vitro incubation of patient plasma with purified milk LPL (EC 3.1.1.34) for 6 h at 37 degrees C. The efficiency of exogenous LPL in vitro was demonstrated by the extent of hydrolysis of chylomicrons and of VLDL-TG in both groups. Concomitant with the disappearance of TG-rich lipoprotein particles, a consistent per cent increment of IDL (99.2 +/- 30.8 and 43.9 +/- 70.5), LDL (152.8 +/- 36.2 and 137.0 +/- 36.1) and of HDL2 (144.8 +/- 29.4 and 99.8 +/- 18.7) was observed in both groups of patients. The enhancement of the latter fractions contrasted with the decline of HDL3 mass concentration (25.4 +/- 7.7 and 51.4 +/- 5.8%), suggesting that a major shift of HDL3----HDL2 occurs following in vitro lipolysis by LDL. Simultaneous compositional and morphological changes of individual lipoprotein particles were noted, confirming the dynamic movement and exchange of neutral lipids and proteins. Specificity of LPL results was demonstrated by experiments in which incubation of the whole plasma at 37 degrees C without exogenous lipolytic enzyme did not cause any substantial changes. The present study, therefore, demonstrates a correction of the major lipoprotein abnormalities associated with FLPL-d and GSD-I by exogenous LPL. No substantial difference was noted between primary (FLPL-d) and secondary (GSD-I) hyperlipidaemias. These studies allow us to conclude that a simple in vitro system, utilizing an exogenous source of LPL and plasma from patients, may serve as a suitable model for the study of the metabolic relationships of lipoproteins. However, in view of the fact that the extent of lipolysis achieved in vitro did not differ between FLPL-d and GSD-I, it may not be able to separate primary from secondary hyperlipaemias.

Adolescent↗
PubMed1990

Apolipoprotein B-100: immunolocalization and synthesis in human intestinal mucosa.

Despite the evidence that the human small intestine produces two separate species of apoB mRNA encoding for B-100 and B-48, there is a paucity of data concerning the expression of the latter form in this organ. Using a high resolution immunogold approach, with specific polyclonal antibodies and a panel of monoclonal antibodies (2D8, 3A10, 4G3), both forms of apoB (B-48 and B-100) were revealed over enterocytes of pediatric intestinal samples. Intense labeling was observed over microvilli, apical smooth membrane vesicles, multivesicular bodies, the basolateral membrane, as well as the trans Golgi region. Only low labeling was found over the rough endoplasmic reticulum (rER). Similar patterns of apoB distribution characterized both duodenal and jejunal regions. The presence of labeling over the Golgi apparatus and rER suggests a synthetic activity of both forms of apoB by the epithelial cells. To test this hypothesis, human intestine was incubated with [3H]leucine, homogenized, and subjected to immunoprecipitation for apoB. Immunoprecipitates contained radioactivity mainly in apoB-48 with relatively small amounts in apoB-100 when examined by NaDodSO4-polyacrylamide gel electrophoresis. These findings were further supported by the biochemical determination of apoB-100 and apoB-48 in chylomicron particles isolated from thoracic duct lymph of a human donor. Taken together, our data suggest that the human intestine is able to synthesize and to express the apoB-100.

Apolipoprotein B-100↗
PubMed1990

Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes.

Essential fatty acids (EFA) are important structural and functional components of cell membranes. Their deficiency has been associated with several clinical and biochemical abnormalities. In the present study, the lipid profile as well as the concentration, composition, and metabolism of lipoproteins were examined in rats rendered EFA-deficient over a period of 12 weeks. Changes in plasma fatty acids mainly induced an increase of palmitoleic (16:1 n-7) and eicosatrienoic (20:3 n-9) acids, while linoleic (18:2 n-6), arachidonic (20:4 n-6), linolenic (18:3 n-3), and docosahexaenoic (22:6 n-3) acids were decreased. The results show increased concentrations of free fatty acids (FFA) (P less than 0.001), triglycerides (P less than 0.001), total cholesterol (P less than 0.02), free cholesterol (P less than 0.005), and phospholipids (P less than 0.05) when compared to pair-fed controls. Similar levels of cholesteryl esters were found in the two groups, and lecithin: cholesterol acyltransferase activity (nmol/100 microliters plasma per h) (8.98 +/- 1.44 vs 8.72 +/- 0.50) did not differ. On the other hand, postheparin extrahepatic lipoprotein lipase (LPL) activity was significantly (P less than 0.002) decreased (5.96 +/- 0.29 vs 7.29 +/- 0.68 mumol FFA/ml per h) and could account for the hypertriglyceridemia as well for the relative triglyceride enrichment of very low density lipoprotein, intermediate density lipoprotein, and low density lipoprotein particles. This enzymatic depletion of LPL was mainly due to the adipose tissue, since a higher level (P less than 0.001) of hepatic lipase (325.8 +/- 16.0 vs 130.8 +/- 9.5 nmol FFA/mg protein per h) was found in liver acetone powder extracts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

One-hour blood-xylose test in diagnosis of cow's milk protein intolerance.

In this prospective study, 18 consecutive children suspected of cow's milk protein intolerance (C.M.P.I.) on clinical grounds were investigated before and after challenge with cow's milk. One-hour blood-xylose, serum-IgE, eosinophil count, serum-complement (C3) and a jejunal biopsy specimen for histology and disaccharidase activity were obtained from all patients before challenge. Serum-complement was measured again 24 h after the beginning of the challenge and the first three tests were repeated on the fifth day. A second jejunal biopsy was obtained in 9 of the first 10 children. 15 of the 18 children were considered to have C.M.P.I. The one-hour blood-xylose test emerged as a simple and valuable test in the diagnosis of C.M.P.I. A significant drop (51--81%) in the one-hour blood-xylose level was observed in all 15 patients. In all patients but one it dropped below 25 mg/dl. Mean value (+/- S.D.) for the group was 47.5 +/- 11.1 mg/dl before and 17.2 +/- 4.2 mg/dl after cow's milk ingestion.

Animals↗
PubMed1979

The role of gastric lipolysis on fat absorption and bile acid metabolism in the rat.

In vivo studies were carried out in young Sprague-Dawley rats to examine the role of gastric lipolysis on fat absorption and bile acid metabolism. When fed by gastric perfusion 5 times (corn oil, 4 g/day) their usual dietary intake of fat, rats deprived of lingual lipase by the creation of an esophageal fistula had a significant degree of fat and bile acid malabsorption as well as a shortened bile acid half-life when compared to animals with a gastrostomy. The % fat absorption, bile acid loss and bile acid pool were normal in 2 groups of esophageal fistula rats fed the same quantity of corn oil or twice (8 g/day) that amount as a fine emulsion. In view of a negligible gastric lipase activity in animals with an esophageal fistula and of decreased hydrolysis of a triglyceride test meal, these data suggest that gastric lipolysis is of physiological importance in situations where lipolytic mechanisms are stressed by a large fat intkae. Its principal role is to potentiate intestinal lipolysis by facilitating the emulsification of dietary lipids through its formed products and, therefore, the contact of pancreatic lipase with its substrates.

Animals↗