Abstract
Since obese patients form cholesterol gallstones very rapidly after bariatric surgery, in patients who did not form gallstones during preceding years, we hypothesized that gallstone formation follows a different trajectory in bariatric patients compared to nonbariatric patients. We therefore analyzed the lipid composition of gallbladder bile derived from 18 bariatric gallstone patients and 17 nonbariatric gallstone patients (median (IQR) age, 46.0 (28.0–54.0) years; 33 (94%) female) during laparoscopic cholecystectomy using an enzymatic and lipidomics approach. We observed a higher concentration of total lipids (9.9 vs. 5.8 g/dL), bile acids (157.7 vs. 81.5 mM), cholesterol (10.6 vs. 5.4 mM), and phospholipids (30.4 vs. 21.8 mM) in bariatric gallstone patients compared to nonbariatric gallstone patients. The cholesterol saturation index did not significantly differ between the two groups. Lipidomics analysis revealed an interesting pattern. Enhanced amounts of a number of lipid species were found in the gallbladder bile of nonbariatric gallstone patients. Most striking was a fivefold higher amount of triglyceride. A concomitant ninefold increase of apolipoprotein B was found, suggesting secretion of triglyceride-rich lipoproteins (TRLs) at the canalicular pole of the hepatocyte in livers from nonbariatric gallstone patients. These findings suggest that gallstone formation follows a different trajectory in bariatric patients compared to nonbariatric patients. Impaired gallbladder emptying might explain the rapid gallstone formation after bariatric surgery, while biliary TRL secretion might contribute to gallstone formation in nonbariatric patients.
Highlights
Cholesterol gallstone disease is a prevalent and multifactorial disease
Since CE and TG are solubilized in plasma in the form of Finding enhanced amounts of CE and TG in gallbladder biles from nonbariatric lipoproteins, we investigated whether concentrations of apolipoprotein A-1 and gallstone patients was unexpected
Since CE and TG are solubilized in plasma in the form apoB in the gallbladder bile of the two groups associated with the difference in CE and of lipoproteins, we investigated whether concentrations of apolipoprotein A-1 and TG
Summary
Cholesterol gallstone disease is a prevalent and multifactorial disease. The formation of cholesterol gallstones implies a failure of biliary cholesterol homeostasis [1]. Involved factors include unbalanced hepatic biliary lipid secretion leading to bile that is supersaturated with cholesterol, the presence of crystallization-promoting factors, impaired gallbladder contraction, altered intestinal lipid and bile acid absorption, and altered gut microbiota. Multiple lithogenic gene variations are identified that are involved in the regulation of cholesterol homeostasis [2]. Supersaturated bile is a prerequisite for the formation of cholesterol gallstones, it is frequently found in patients without gallstones [3,4]. The nucleation of cholesterol crystals from supersaturated bile is considered to be the critical step in the formation of cholesterol gallstones
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