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FGF19 was found to decrease in subjects with isolated-impaired fasting glucose (I-IFG) and type 2 diabetes mellitus (T2DM). However, the reason for the change of FGF19 in subjects with different glucometabolic status remained unclear. Here we measured six BAs including chenodeoxycholic acid (CDCA), cholic acid, deoxycholic acid, their glycine conjugates and FGF19 levels during oral glucose tolerance test (OGTT) in normal glucose tolerance (NGT), isolated-impaired glucose tolerance, I-IFG, combined glucose intolerance (CGI) and T2DM subjects. After OGTT, serum FGF19 peaked at 120\u2009min in all subjects. Glycine conjugated BAs peaked at 30\u2009min, while free BAs did not elevated significantly. Consistent with the decrease trend in FGF19 levels, fasting serum CDCA levels in subjects with I-IFG, CGI and T2DM were significantly lower than NGT subjects (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). Fasting serum CDCA was independently associated with FGF19. CDCA strongly upregulated FGF19 mRNA levels in LS174T cells in a dose- and time-dependent manner. These results suggest that the decrease of FGF19 in subjects with I-IFG was at least partially due to their decrease of CDCA acting via FXR.<\/jats:p>","DOI":"10.1038\/s41598-017-06252-6","type":"journal-article","created":{"date-parts":[[2017,7,14]],"date-time":"2017-07-14T11:46:23Z","timestamp":1500032783000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Lowered fasting chenodeoxycholic acid correlated with the decrease of fibroblast growth factor 19 in Chinese subjects with impaired fasting glucose"],"prefix":"10.1038","volume":"7","author":[{"given":"Jing","family":"Zhang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huating","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hu","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Li","family":"Fang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingjing","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Han","family":"Yan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shuqin","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qianqian","family":"Song","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yinan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aimin","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qichen","family":"Fang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yang","family":"Ye","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weiping","family":"Jia","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2017,7,20]]},"reference":[{"key":"6252_CR1","doi-asserted-by":"publisher","first-page":"31","DOI":"10.1016\/S0140-6736(11)60679-X","volume":"378","author":"G Danaei","year":"2011","unstructured":"Danaei, G. et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet \n                           378, 31\u201340, doi:10.1016\/s0140-6736(11)60679-x (2011).","journal-title":"Lancet"},{"key":"6252_CR2","doi-asserted-by":"crossref","unstructured":"Morrish, N. J., Wang, S. L., Stevens, L. K., Fuller, J. H. & Keen, H. Mortality and causes of death in the WHO Multinational Study of Vascular Disease in Diabetes. Diabetologia \n                           44 Suppl 2, S14\u201321 (2001).","DOI":"10.1007\/PL00002934"},{"key":"6252_CR3","doi-asserted-by":"publisher","first-page":"1909","DOI":"10.2337\/dc06-0438","volume":"29","author":"C Meyer","year":"2006","unstructured":"Meyer, C. et al. Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans. Diabetes Care \n                           29, 1909\u20131914, doi:10.2337\/dc06-0438 (2006).","journal-title":"Diabetes Care"},{"key":"6252_CR4","doi-asserted-by":"publisher","first-page":"1475","DOI":"10.2337\/diabetes.52.6.1475","volume":"52","author":"JB Meigs","year":"2003","unstructured":"Meigs, J. B., Muller, D. C., Nathan, D. M., Blake, D. R. & Andres, R. The natural history of progression from normal glucose tolerance to type 2 diabetes in the Baltimore Longitudinal Study of Aging. Diabetes \n                           52, 1475\u20131484 (2003).","journal-title":"Diabetes"},{"key":"6252_CR5","doi-asserted-by":"publisher","first-page":"2113","DOI":"10.2337\/dc11-0294","volume":"34","author":"C Chen","year":"2011","unstructured":"Chen, C. et al. High plasma level of fibroblast growth factor 21 is an Independent predictor of type 2 diabetes: a 5.4-year population-based prospective study in Chinese subjects. Diabetes Care \n                           34, 2113\u20132115, doi:10.2337\/dc11-0294 (2011).","journal-title":"Diabetes Care"},{"key":"6252_CR6","doi-asserted-by":"publisher","first-page":"2810","DOI":"10.2337\/dc12-1766","volume":"36","author":"Q Fang","year":"2013","unstructured":"Fang, Q. et al. Serum fibroblast growth factor 19 levels are decreased in Chinese subjects with impaired fasting glucose and inversely associated with fasting plasma glucose levels. Diabetes Care \n                           36, 2810\u20132814, doi:10.2337\/dc12-1766 (2013).","journal-title":"Diabetes Care"},{"key":"6252_CR7","doi-asserted-by":"publisher","first-page":"235","DOI":"10.1038\/nrd2792","volume":"8","author":"A Beenken","year":"2009","unstructured":"Beenken, A. & Mohammadi, M. The FGF family: biology, pathophysiology and therapy. Nat Rev Drug Discov \n                           8, 235\u2013253, doi:10.1038\/nrd2792 (2009).","journal-title":"Nat Rev Drug Discov"},{"key":"6252_CR8","doi-asserted-by":"publisher","first-page":"223","DOI":"10.1146\/annurev-physiol-021115-105339","volume":"78","author":"FM Fisher","year":"2016","unstructured":"Fisher, F. M. & Maratos-Flier, E. Understanding the Physiology of FGF21. Annu Rev Physiol \n                           78, 223\u2013241, doi:10.1146\/annurev-physiol-021115-105339 (2016).","journal-title":"Annu Rev Physiol"},{"key":"6252_CR9","doi-asserted-by":"publisher","first-page":"121","DOI":"10.1038\/ijo.2014.76","volume":"39","author":"JM Gallego-Escuredo","year":"2015","unstructured":"Gallego-Escuredo, J. M. et al. Opposite alterations in FGF21 and FGF19 levels and disturbed expression of the receptor machinery for endocrine FGFs in obese patients. Int J Obes (Lond) \n                           39, 121\u2013129, doi:10.1038\/ijo.2014.76 (2015).","journal-title":"Int J Obes (Lond)"},{"key":"6252_CR10","doi-asserted-by":"publisher","first-page":"1581","DOI":"10.1101\/gad.1083503","volume":"17","author":"JA Holt","year":"2003","unstructured":"Holt, J. A. et al. Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. Genes Dev \n                           17, 1581\u20131591, doi:10.1101\/gad.1083503 (2003).","journal-title":"Genes Dev"},{"key":"6252_CR11","doi-asserted-by":"publisher","first-page":"217","DOI":"10.1016\/j.cmet.2005.09.001","volume":"2","author":"T Inagaki","year":"2005","unstructured":"Inagaki, T. et al. Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis. Cell Metab \n                           2, 217\u2013225, doi:10.1016\/j.cmet.2005.09.001 (2005).","journal-title":"Cell Metab"},{"key":"6252_CR12","doi-asserted-by":"publisher","first-page":"312","DOI":"10.1101\/gad.184788.111","volume":"26","author":"MJ Potthoff","year":"2012","unstructured":"Potthoff, M. J., Kliewer, S. A. & Mangelsdorf, D. J. Endocrine fibroblast growth factors 15\/19 and 21: from feast to famine. Genes Dev \n                           26, 312\u2013324, doi:10.1101\/gad.184788.111 (2012).","journal-title":"Genes Dev"},{"key":"6252_CR13","doi-asserted-by":"publisher","first-page":"1741","DOI":"10.1210\/endo.143.5.8850","volume":"143","author":"E Tomlinson","year":"2002","unstructured":"Tomlinson, E. et al. Transgenic mice expressing human fibroblast growth factor-19 display increased metabolic rate and decreased adiposity. 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Science \n                           331, 1621\u20131624, doi:10.1126\/science.1198363 (2011).","journal-title":"Science"},{"key":"6252_CR16","doi-asserted-by":"publisher","first-page":"729","DOI":"10.1016\/j.cmet.2011.03.019","volume":"13","author":"MJ Potthoff","year":"2011","unstructured":"Potthoff, M. J. et al. FGF15\/19 regulates hepatic glucose metabolism by inhibiting the CREB-PGC-1alpha pathway. Cell Metab \n                           13, 729\u2013738, doi:10.1016\/j.cmet.2011.03.019 (2011).","journal-title":"Cell Metab"},{"key":"6252_CR17","doi-asserted-by":"publisher","first-page":"501","DOI":"10.1080\/00365510701854967","volume":"68","author":"D Stejskal","year":"2008","unstructured":"Stejskal, D., Karpisek, M., Hanulova, Z. & Stejskal, P. Fibroblast growth factor-19: development, analytical characterization and clinical evaluation of a new ELISA test. 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J Clin Endocrinol Metab \n                           101, 3002\u20133009, doi:10.1210\/jc.2016-1607 (2016).","journal-title":"J Clin Endocrinol Metab"},{"key":"6252_CR30","doi-asserted-by":"publisher","first-page":"655","DOI":"10.1056\/NEJM197309272891303","volume":"289","author":"JL Thistle","year":"1973","unstructured":"Thistle, J. L. & Hofmann, A. F. Efficacy and specificity of chenodeoxycholic acid therapy for dissolving gallstones. N Engl J Med \n                           289, 655\u2013659, doi:10.1056\/nejm197309272891303 (1973).","journal-title":"N Engl J Med"},{"key":"6252_CR31","doi-asserted-by":"publisher","first-page":"1649","DOI":"10.1056\/NEJM198412273112601","volume":"311","author":"VM Berginer","year":"1984","unstructured":"Berginer, V. M., Salen, G. & Shefer, S. Long-term treatment of cerebrotendinous xanthomatosis with chenodeoxycholic acid. 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