Page 37 - Human Bile Acid Metabolism: a Postprandial Perspective
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and the individual bile acids (total concentrations) showed similar patterns (NGT
vs T2D: CA, r = 0.426 and P < .001 vs r = 0.471 and P < .001; CDCA, r = 0.384
and P = .003 vs r = 0.520 and P < .001; DCA, r = 0.361 and P = .005 vs r = 0.322
and P < .017; UDCA, r = 0.188 and P = .15 vs r = 0.107 and P = .44). Postprandial 2 concentrations of FGF19 and C-peptide were inversely associated in both NGT
subjects (r = -0.266; P = .04) and T2D patients (r = -0.383; P = .003), whereas the association between FGF19 and glucose was negatively associated only in NGT subjects (r = -0.310; P = .02) vs T2D patients (r = 0.061; P = .66).
Discussion
The major findings in this study are: 1) T2D patients exhibited increased fasting and postprandial TBA concentrations after a wide range of nutritional stimuli in comparison with NGT subjects; 2) differences reflected mainly unconjugated and glycine-conjugated forms of the secondary bile acids DCA and UDCA and to a lesser extent CA, whereas postprandial CDCA concentrations were comparable among the two groups; and 3) postprandial concentrations of taurine-conjugated bile acids were also slightly higher in T2D patients (DCA). Furthermore, both fasting and postprandial FGF19 concentrations tended tobe lower in T2D patients vs NGT subjects, but due to largevariability, these differences were not statistically significant. Lastly, in both groups, a positive correlation between postprandial TBA and FGF19 concentrations was demonstrated.
The aim of the present study was to assess postprandial bile acid concentrations in T2D patients in order to shed more light on the possible mechanisms underlying the role of bile acids in metabolic regulation and T2D pathophysiology. Recent years have seen extensive research on bileacid metabolism in T2D, but no previous study has addressed postprandial bile acid concentrations of individual bile acids together with FGF19 after a wide range of different meals. The importance of this focus is highlighted by recent data showing that bile acids are not just luminal signaling molecules that activate TGR5 (leading to GLP-1 secretion) and FXR (leading to FGF19 secretion) in the intestine (3). FXR and TGR5 receptors are widely expressed and may even be found on pancreatic β-cells (6, 13–15). In fact, systemic bile acids seem to stimulate TGR5 and FXR, which positions postprandial plasma bile acids suitable for the regulation of overall glucose
Postprandial bile acid concentrations
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