Higher circulating bile acid concentrations in obese patients with type 2 diabetes

Royce Vincent, Sohail Omar, Samer Ghozlan, David R. Taylor, Gemma Cross, Roy Sherwood, Lars Fandriks, Torsten Olbers, Malin Werling, Jamshid Alaghband-Zadeh, Carel W. le Roux

    Research output: Contribution to journalArticlepeer-review

    67 Citations (Scopus)

    Abstract

    Background: Bile acids (BAs) play an important role in releasing incretin hormones via the enteroendocrine L-cell surface TGR5 receptors. The aim of this study was to investigate the difference in BA concentration at baseline and in response to a meal stimulus between type 2 diabetes mellitus (T2DM) and a matched normoglycaemic group.

    Materials and methods: A cross-sectional study of 12 patients with known T2DM and 12 matched normoglycaemic controls compared BA fractions after an overnight fast and following a standard meal.

    Results: The T2DM group had higher baseline glucose (P<0.001), but baseline total BA, total glycine conjugated BAs (GCBA) and total taurine conjugated BA (TCBA) were similar between both groups. The T2DM group compared to the normoglycaemic group had a higher post-prandial peak change in total BAs 4.28 (3.51-5.38) mmol/L vs. 0.88 (0.60-1.57) mmol/L (P<0.001) and peak total GCBA 2.77 (1.07-4.19) mmol/L vs. 0.94 (0.34-1.15) mmol/L (P<0.0001), but similar peak total TCBA 0.36 (0.02-0.76) mmol/L vs. 0.08 (0.04-0.22) mmol/L (P 0.91).

    Conclusion: The post-prandial bile acid response is elevated in obese patients with T2DM compared to matched normoglycaemic individuals.

    Original languageEnglish
    Pages (from-to)360-364
    Number of pages5
    JournalAnnals of Clinical Biochemistry
    Volume50
    Issue number4
    DOIs
    Publication statusPublished - Jul 2013

    Keywords

    • Bile acids
    • type 2 diabetes mellitus
    • glucagon like peptide-1
    • TGR5 receptor
    • CHOLESTEROL 7-ALPHA-HYDROXYLASE GENE
    • INSULIN SENSITIVITY
    • HUMAN HEPATOCYTES
    • GLUCOSE
    • PLASMA
    • PATHOPHYSIOLOGY
    • PHYSIOLOGY
    • INHIBIT

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