Dietary N–3 Polyunsaturated Fatty Acids Decrease Biliary Cholesterol Saturation in Gallstone Disease

Berr, Frieder; Holl, Joseph; Jüngst, Dieter; Fischer, Sven; Richter, Werner; Seifferth, Bernd; Paumgartner, Gustav

doi:10.1002/hep.1840160418

Cited by 59 publications

(24 citation statements)

References 46 publications

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“…34 Fish oil non-significantly decreased biliary cholesterol saturation, corroborating an earlier study by Berr and colleagues. 17 This observation may be linked to fish oil induced changes in the fatty acid distribution of biliary phospholipids: the ω-3 fatty acid fractions increased and partly replaced the linoleic acid fraction. Previously, Berr et al suggested that different biliary phosphatidylcholine species have different cholesterol-phospholipid packaging capacities and demonstrated an inverse correlation between CSI and the eicosapentaenoic acid content of biliary phospholipids.…”

Section: Discussionmentioning

confidence: 99%

“…Fish oil, known for its profound hypotriglyceridaemic capacity, 16 decreases biliary cholesterol saturation in patients with gall stone disease. 17 Thus fish oil may be a therapeutic alternative to fibrates in HTG patients in exerting similar lipid lowering properties without adversely influencing the risk of gall stone formation. Therefore, a second aim of this study was to compare the effects of bezafibrate and fish oil on serum lipids and both biliary lipid composition and gall bladder motility as risk factors for the development of gall stone disease in patients with HTG.…”

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confidence: 99%

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

Jonkers

Smelt²,

Ledeboer³

et al. 2003

Gut

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Background and aim: 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 and gall bladder motility) in HTG patients. Patients and methods: Gall bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between nine HTG patients and 10 age, sex, and body mass index matched normolipidaemic controls. The effects of bezafibrate and fish oil in HTG patients were studied in a randomised cross over trial. Results: HTG patients showed 14-fold higher serum triglyceride (TG) levels than controls. Biliary lipid composition, fasting gall bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall bladder emptying was reduced in HTG patients compared with controls during CCK infusion (−22%) as well as in response to a meal (−37%; both p<0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (−68% and −51% v baseline, respectively; both p<0.01). Fasting CCK levels were not affected whereas CCK induced gall bladder emptying increased during bezafibrate (+29%; p<0.001) and tended to increase on fish oil therapy (+13%; p=0.07). Postprandial gall bladder motility improved on bezafibrate and fish oil (+47 and +25% v baseline, respectively; both p<0.02) at least partly due to increased gall bladder sensitivity to CCK (both p<0.05 v baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p<0.05) but no effects on cholesterol saturation index were seen with either treatment. Conclusions: We suggest that impaired gall bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall stone disease in HTG patients. Triglyceride lowering therapy by both fish oil and bezafibrate improve gall bladder dysmotility without adversely affecting biliary cholesterol saturation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Jonkers

Smelt²,

Ledeboer³

et al. 2003

Gut

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“…Positive associations have also been found for fried food consumption 72 and preference for oily foods 70 . Recent experimental studies have brought attention to fish oils as a protective factor 74,75 . No observational epidemiological studies have specifically investigated the association between fish oils and GBD.…”

Section: Fatty Acidsmentioning

confidence: 99%

Dietary intake and gallbladder disease: a review

Tseng

Everhart

Sandler

1999

Public Health Nutr.

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Objective: Dietary intake has long been looked upon as a potentially modifiable risk factor for gallbladder disease (GBD), here defined as either having gallstones or having had surgery for gallstones. This paper reviews the epidemiological evidence for an association between dietary intake and GBD, focusing on six dietary factors that have received the most attention in studies in this area: energy intake, fatty acids, cholesterol, carbohydrates and fibre, calcium and alcohol. The objectives of this review are to evaluate the potential usefulness of altering the diet to prevent GBD and to consider future research in this area. Design: We reviewed all English-language epidemiological studies on diet and cholelithiasis that were cross-sectional, cohort or case-control in design and that were indexed in the Medline database from 1966 to October 1997. Results: A positive association was suggested with simple sugars and inverse associations with dietary fibre and alcohol. No convincing evidence was found for a role for energy intake or intake of fat or cholesterol. Variable means of ascertaining cases and inaccurate measurement of dietary intake may contribute to variation in results across studies. Conclusions: Some specific components of the diet that may affect GBD include simple sugars, fibre and alcohol, but whether risk for GBD can be reduced by altering intake of a specific dietary factor has not been established. Although no specific dietary recommendations can be made to reduce risk of GBD per se, a 'healthy' diet aimed at reducing risk of other diseases might be expected to reduce risk for GBD as well.

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“…This was due mainly to a decrease in biliary phospholipids. Berr et al (23) recently showed in gallstone patients that after marine fish oil supplementation the proportion of n-3 unsaturated fatty acids in the biliary phospholipids was increased and the cholesterol-to-phospholipid ratio and CSI were increased but that the nucleation time of duodenal bile remained unchanged (23). In rats bean intake increased biliary cholesterol and phospholipid output (11).…”

Section: Discussionmentioning

confidence: 97%

Effect of dietary phospholipids and their constituents on bile composition in rats and hamsters†

Peled

Gilat

1994

Hepatology

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The formation of cholesterol gallstones is a result of an interaction between bile lipid concentration, composition and other factors. The solubilization of cholesterol in bile is affected by the nature of the fatty acids and head groups of biliary phospholipids. In this study we tried to modulate the composition of biliary lipids in the rat and hamster by means of dietary supplementation of whole phospholipids or their constituents (at 3% to 5% of food weight). A striking effect of ethanolamine feeding in rats and hamsters was demonstrated: Biliary cholesterol concentration and cholesterol saturation index were significantly lower (p < 0.03). In rats, bile acid concentration was increased, contributing to decreased bile lithogenicity. Ethanolamine also increased biliary phospholipid output. Other test substances had less marked effects. The addition of lecithin to rat diet significantly increased phospholipid concentration (p < 0.05) compared with controls. Cholesterol and bile acid concentrations were reduced in palmitic acid-fed hamsters (NS). Choline supplementation insignificantly increased the cholesterol saturation index in hamsters. Despite the clear effect of ethanolamine on biliary lipid composition, no change could be demonstrated in the proportion of phosphatidylethanolamine in bile. It is postulated that ethanolamine was methylated in the liver to choline. Our data demonstrate that biliary lipid composition can be modulated by dietary phospholipids or their components.

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Dietary N–3 Polyunsaturated Fatty Acids Decrease Biliary Cholesterol Saturation in Gallstone Disease

Cited by 59 publications

References 46 publications

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

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

Dietary intake and gallbladder disease: a review

Effect of dietary phospholipids and their constituents on bile composition in rats and hamsters†

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