Page 42 - Human Bile Acid Metabolism: a Postprandial Perspective
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Chapter 2
References
1. Kuipers F, Bloks VW, Groen AK. Beyond intestinal soap– bile acids in metabolic control. Nat Rev Endocrinol. 2014;10(8):488 – 498.
2. Duboc H, Taché Y, Hofmann AF. The bile acid TGR5 membranereceptor: from basic research to clinical application. Dig Liver Dis. 2014;46(4):302–312.
3. Sonne DP, Hansen M, Knop FK. Bile acid sequestrants in type 2 diabetes: potential effects on GLP1 secretion. Eur J Endocrinol. 2014;171(2):R47–R65.
4. Adrian TE, Gariballa S, Parekh KA, et al. Rectal taurocholate increases L cell and insulin secretion, and decreases blood glucose and food intake in obese type 2 diabetic volunteers. Diabetologia. 2012; 55(9):2343–23437.
5. Lefebvre P, Cariou B, Lien F, Kuipers F, Staels B. Role of bile acidsand bile acid receptors in metabolic regulation. Physiol Rev. 2009; 89(1):147–91.
6. Trabelsi MS, Daoudi M, Prawitt J, et al. Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine Lcells. Nat Commun. 2015;6:7629.
7. Schaap FG, Trauner M, Jansen PL. Bile acid receptors as targets for drug development. Nat Rev Gastroenterol Hepatol. 2014; 11(1):55– 67.
8. Rudling M, Camilleri M, Graffner H, Holst JJ, Rikner L. Specific inhibition of bile acid transport alters plasma lipids and GLP-1. BMC Cardiovasc Disord. 2015;15:75.
9. Kir S, Beddow SA, Samuel VT, et al. FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis. Science. 2011;331(6024):1621–1624.
10. Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with increasing levels of HbA(1c). Diabetes Care. 2003;26(3):881– 885.
11. Sonne DP, Rehfeld JF, Holst JJ, Vilsbøll T, Knop FK. Postprandial gallbladder emptying in patients with type 2 diabetes: potential implications for bile-induced secretion of glucagon-like peptide 1. EurJ Endocrinol. 2014;171(4):407– 419.
12. Bootsma AH. Rapid analysis of conjugated bile acids in plasma using electrospray tandem mass spectrometry: application for selective screening of peroxisomal disorders. J Inherit Metab Dis. 1999;22(3):307–310.
13. Düfer M, Hörth K, Wagner R, et al. Bile acids acutely stimulate insulin secretion of mouse β-cells via farnesoid X receptor activation and K(ATP) channel inhibition. Diabetes. 2012;61(6):1479 –1489.
14. Kumar DP, Rajagopal S, Mahavadi S, et al. Activation of transmembrane bile acid receptor TGR5 stimulates insulin secretion in pancreatic β cells. Biochem Biophys Res Commun. 2012;427(3): 600 – 605.
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16. Ullmer C, Alvarez Sanchez R, Sprecher U, et al. Systemic bile acidsensing by G protein-coupled bile acid receptor 1 (GPBAR1) promotes PYY and GLP-1 release. Br J Pharmacol. 2013;169(3):671– 684.
17. Brighton CA, Rievaj J, Kuhre RE, et al. Bile acids trigger GLP-1 release predominantly by accessing basolaterally located G proteincoupled bile acid receptors. Endocrinology. 2015;156(11):3961– 3970.
18. Donahue RP, Abbott RD, Reed DM, Yano K. Postchallenge glucoseconcentration and coronary heart disease in men of Japanese ancestry. Honolulu Heart Program. Diabetes. 1987;36(6):689 – 692.
19. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. The DECODE study group. European Diabetes Epidemiology Group. Diabetes Epidemiology: Collaborative Analysis Of Diagnostic Criteria in Europe. Lancet. 1999;354(9179):617– 621.
20. Duboc H, Aelion H, Rainteau D, et al. Crosstalk between the hepatologist and the cardiologist: a future place for the lithocholic acid as a coronary atheroma risk factor? Hepatology. 2012;56(6):2426.
21. Bennion LJ, Grundy SM. Effects of diabetes mellitus on cholesterolmetabolism in man. N Engl J Med. 1977;296(24):1365–1371.
22. Brufau G, Stellaard F, Prado K, et al. Improved glycemic control with colesevelam treatment in patients with type 2 diabetes is not directly associated with changes in bile acid metabolism. Hepatology. 2010;52(4):1455–1464.
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