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gallstones/triglyceride

پیوند در کلیپ بورد ذخیره می شود
صفحه 1 از جانب 323 نتایج

Increased activity of hepatic microsomal triglyceride transfer protein and bile acid synthesis in gallstone disease.

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A strong interrelationship exists between the regulation of bile acid (BA) metabolism and hepatic very low density lipoprotein (VLDL) production. We have recently shown that BA synthesis is increased in gallstone disease. We investigated the activity of hepatic microsomal triglyceride transfer

Inactivation of hepatic microsomal triglyceride transfer protein protects mice from diet-induced gallstones.

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OBJECTIVE Microsomal triglyceride transfer protein (MTTP) is critical for the production of very-low-density lipoproteins (VLDL). The current studies were undertaken to examine the in vivo role of MTTP in hepatic cholesterol and fatty acid metabolism, as well as in biliary lipid secretion. We also

[Influence of the conservative cholelitholytic therapy using chenodesoxycholic acid (CDC) on cholesterol and triglycerides in the blood of patients with gall stones].

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In 11 patients with radiolucent gallstones treated for 3-18 months with chenodeoxycholic acid (CDC) serum cholesterol and triglyceride levels were measured. No significant changes of serum cholesterol and triglycerides could be observed during the course of longterm treatment with CDC. After 3 and 6

The common adiponutrin variant p.I148M does not confer gallstone risk but affects fasting glucose and triglyceride levels.

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Recently the common adiponutrin (PNPLA3) polymorphism p.I148M has been identified as a genetic determinant of severe forms of non-alcoholic fatty liver disease and alcoholic liver disease. Additionally, insulin resistance - linked to the development of non-alcoholic steatohepatitis - increases the

Triglycerides and gallstone formation.

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Changes in bile acid (BA) metabolism and gallbladder function are critical factors in the pathogenesis of gallstones. Patients with hypertriglyceridemia (HTG) - often overweight and insulin resistant - are at risk for gallstone disease. The question arises whether HTG itself contributes to gallstone

Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil.

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OBJECTIVE The aim of this study was to unravel the mechanisms responsible for the increased risk of gall stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride lowering therapy by bezafibrate and fish oil on determinants of cholelithiasis (biliary lipid composition

[A case cirrhosis with gallstone favourably responding to administration of medium chain triglycerides (MCT)].

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Insulin injections enhance cholesterol gallstone incidence by changing the biliary cholesterol saturation index and apo A-I concentration in hamsters fed a lithogenic diet.

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OBJECTIVE A link between insulin and cholesterol gallstone disease has often been suspected but never demonstrated. The aim was to evaluate the direct implication of insulin in the gallbladder cholesterol gallstone formation process. METHODS Hamsters fed with a soft-inducing lithogenic diet,

Risk of gallstone disease in advanced chronic phase of fascioliasis: an experimental study in a rat model.

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In Wistar rats experimentally infected with Fasciola hepatica, the association between time of infection, number of flukes, rat weight, and serum lipid levels and the risk of developing pigment stones in the main bile duct was examined using data obtained at 100, 200, 300, 400, and 500 days

Gallstones in obesity and weight loss.

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The prevalence of cholesterol gallstones is increased in obese persons. The risk is especially high in those with the highest body mass index (relative risk 5-6). Weight loss further increases the risk of gallstones: the prevalence of new gallstones reaches 10-12% after 8-16 weeks of low-calorie

Ursodeoxycholic acid treatment of gallstones. Dose-response study and possible mechanism of action.

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To determine the optimum dose for the medical treatment of gallstones with ursodeoxycholic acid (U.D.C.A.), 11 non-obese patients with radiolucent gallstones were given 5 mg, 10 mg, and 15 mg U.D.C.A. kg body-weight-1 day-1 for 6 weeks each. Apart from 3 patients who required surgery for gallstone

Influence of chenodeoxycholic acid on the kinetics of endogenous triglyceride transport in man.

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Plasma lipids and triglycerides kinetics were studied in ten subjects before and after 6-8 weeks treatment with 1 g/day chenodeoxycholic acid for radiolucent gallstones. Plasma triglyceride concentration fell by 20% and phospholipid concentration rose by 5% on average; there was no change in

An analysis of data on human hepatic bile. Relationship between main bile components, serum cholesterol and serum triglycerides.

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Hepatic bile samples were taken from the common duct during interval operations for gallstone disease, performed under standardized conditions. Prior to operation serum cholesterol and triglycerides levels were determined. The concentrations of Cholesterol (Chol), phospholipids (Lip P) and of the

Factors associated with gallstone disease in the MICOL experience. Multicenter Italian Study on Epidemiology of Cholelithiasis.

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The epidemiological associations of gallstone disease were evaluated in a general population sample of 29,584 individuals (15,910 men and 13,674 women; age range, 30-39 years) belonging to 14 cohorts examined between December 1984 and April 1987. Subjects were screened for the presence of gallstones

The use of simvastatin for the prevention of gallstones in the lithogenic prairie dog model.

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BACKGROUND Surgery for morbid obesity is rapidly increasing. Patients undergoing bariatric surgery are prone to gallstone development during the rapid weight loss. These patients are often given medications such as ursodeoxycholic acid to prevent gallstone formation; however, these medications are
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