Display options
Share it on

Metabolites. 2021 Oct 05;11(10). doi: 10.3390/metabo11100682.

Gallstone Formation Follows a Different Trajectory in Bariatric Patients Compared to Nonbariatric Patients.

Metabolites

Sylke Haal, Maimoena S S Guman, Yair I Z Acherman, Johannes P G Jansen, Michel van Weeghel, Henk van Lenthe, Eric J M Wever, Victor E A Gerdes, Rogier P Voermans, Albert K Groen

Affiliations

  1. Department of Internal Medicine, Spaane Gasthuis, 2134 TM Hoofddorp, The Netherlands.
  2. Department of Gastroenterology and Hepatology, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, 1105 AZ Amsterdam, The Netherlands.
  3. Department of Internal and Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, 1105 AZ Amsterdam, The Netherlands.
  4. Department of Surgery, Spaarne Gasthuis, 2134 TM Hoofddorp, The Netherlands.
  5. Laboratory of Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, The Netherlands.
  6. Core Facility Metabolomics, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
  7. Bioinformatics Laboratory, Department of Epidemiology and Data Science, Amsterdam UMC, University of Amsterdam, Amsterdam Public Health, 1105 AZ Amsterdam, The Netherlands.

PMID: 34677397 PMCID: PMC8541369 DOI: 10.3390/metabo11100682

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.

Keywords: bariatric surgery; bile; gallstones; lipidomics; triglyceride-rich lipoproteins

References

  1. Int J Obes Relat Metab Disord. 1993 Mar;17(3):153-8 - PubMed
  2. Nat Biotechnol. 2012 Oct;30(10):918-20 - PubMed
  3. N Engl J Med. 1988 Dec 15;319(24):1567-72 - PubMed
  4. Int J Obes Relat Metab Disord. 1998 Jun;22(6):592-600 - PubMed
  5. Dis Model Mech. 2021 Apr 1;14(4): - PubMed
  6. Surg Obes Relat Dis. 2017 Apr;13(4):681-685 - PubMed
  7. Curr Opin Gastroenterol. 2018 Mar;34(2):71-80 - PubMed
  8. Br J Surg. 2012 Jun;99(6):864-9 - PubMed
  9. Int J Mol Sci. 2018 Oct 16;19(10): - PubMed
  10. J Clin Invest. 1973 Jun;52(6):1467-79 - PubMed
  11. Hepatology. 1995 Dec;22(6):1735-44 - PubMed
  12. Lancet. 2006 Jul 15;368(9531):230-9 - PubMed
  13. Am J Gastroenterol. 1991 Aug;86(8):1000-5 - PubMed
  14. J Lipid Res. 1996 Mar;37(3):606-30 - PubMed
  15. J Clin Invest. 1975 Oct;56(4):996-1011 - PubMed
  16. Hepatology. 2005 Jun;41(6):1322-8 - PubMed
  17. Surg Obes Relat Dis. 2019 Jun;15(6):827-831 - PubMed
  18. Obes Surg. 2016 May;26(5):990-4 - PubMed
  19. J Lipid Res. 1978 Nov;19(8):945-55 - PubMed
  20. Gastroenterology. 1979 Oct;77(4 Pt 1):611-7 - PubMed
  21. J Clin Invest. 1973 Oct;52(10):2389-97 - PubMed
  22. Gastroenterology. 1995 Jun;108(6):1882-8 - PubMed
  23. Gastroenterology. 1991 Aug;101(2):490-6 - PubMed
  24. Hepatology. 1990 Jan;11(1):1-6 - PubMed
  25. Hepatology. 1996 Sep;24(3):544-8 - PubMed
  26. Gastroenterology. 1993 Oct;105(4):1200-8 - PubMed
  27. Gastroenterology. 1992 Aug;103(2):566-70 - PubMed
  28. J Lipid Res. 2019 Mar;60(3):498-505 - PubMed
  29. Eur J Clin Invest. 1986 Apr;16(2):133-42 - PubMed
  30. Surg Obes Relat Dis. 2014 Mar-Apr;10(2):313-21 - PubMed
  31. Yonsei Med J. 2003 Aug 30;44(4):561-70 - PubMed
  32. Obes Surg. 2009 Jan;19(1):22-8 - PubMed
  33. J Lipid Res. 1983 Apr;24(4):391-401 - PubMed
  34. Am J Clin Nutr. 1983 May;37(5):749-54 - PubMed
  35. Surg Obes Relat Dis. 2007 Jul-Aug;3(4):476-9 - PubMed
  36. Cancers (Basel). 2020 Jun 21;12(6): - PubMed
  37. Ann Intern Med. 1995 Jun 15;122(12):899-905 - PubMed
  38. Gastroenterology. 1992 Jul;103(1):214-21 - PubMed
  39. Updates Surg. 2020 Dec;72(4):1125-1133 - PubMed
  40. Surg Obes Relat Dis. 2018 Jul;14(7):992-996 - PubMed
  41. Eur J Clin Invest. 1993 May;23(5):283-8 - PubMed
  42. Gastroenterology. 1995 Dec;109(6):1997-2006 - PubMed

Publication Types