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8. Gender and gut microbiota composition determine hepatic bile acid, metabolic and inflammatory response to a single fast-food meal in healthy adults

Author

Figge, A., Sydor, S., Wenning, C., Manka, P., Assmuth, S., Vilchez-Vargas, R., Link, A., Jaehnert, A., Brodesser, S., Lucas, C., Nevzorova, Y. A., Faber, K. N., Moshage, H., Porsch-Oezcueruemez, M., Gerken, G., Cubero, F. J., Canbay, A., Bechmann, L. P., Figge, A., Sydor, S., Wenning, C., Manka, P., Assmuth, S., Vilchez-Vargas, R., Link, A., Jaehnert, A., Brodesser, S., Lucas, C., Nevzorova, Y. A., Faber, K. N., Moshage, H., Porsch-Oezcueruemez, M., Gerken, G., Cubero, F. J., Canbay, A., and Bechmann, L. P.

Abstract

Background & aims: Regular consumption of fast-food (FF) as a form of typical Western style diet is associated with obesity and the metabolic syndrome, including its hepatic manifestation nonalcoholic fatty liver disease. Currently, it remains unclear how intermittent excess FF consumption may influence liver metabolism. The study aimed to characterize the effects of a single FF binge on hepatic steatosis, inflammation, bile acid (BA), glucose and lipid metabolism. Methods: Twenty-five healthy individuals received a FF meal and were asked to continue eating either for a two-hour period or until fully saturated. Serum levels of transaminases, fasting BA, lipid profile, glucose and cytokine levels as well as transient elastography and controlled attenuation parameter (CAP; to assess hepatic steatosis) were analyzed before (day 0) and the day after FF binge (day 1). Feces was collected prior and after the FF challenge for microbiota analysis. Results: The FF meal induced a modest increase in CAP, which was accompanied by a robust increase of fasting serum BA levels. Surprisingly, levels of cholesterol and bilirubin were significantly lower after the FF meal. Differentiating individuals with a relevant delta BA ( 1 mmol/l) increase vs. individuals without (delta BA <1 mmol/l), identified several gut microbiota, as well as gender to be associated with the BA increase and the observed alterations in liver function, metabolism and inflammation. Conclusion: A single binge FF meal leads to a robust increase in serum BA levels and alterations in parameters of liver injury and metabolism, indicating a novel metabolic aspect of the gut-liver axis. (c) 2021 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Published
2021

12. Concepts and Controversies in Haemostasis and Thrombosis Associated with Liver Disease: Proceedings of the 7th International Coagulation in Liver Disease Conference

Author

Intagliata, N M, Argo, C K, Stine, J G, Lisman, T, Caldwell, S H, Violi, F, Angelico, M, Argo, C, Basili, S, Bechmann, L, Berna, l W, Büller, H, Caldwell, S, Garcia-Pagan, Jc, Giannini, E, Greenberg, C, Intagliata, N, Jenne, C, Lee, S, Luyendyk, J, Magnusson, M, Maitland, H, Mallett, S, Mendez-Sanchez, N, Munoz, S, Northup, P, Raparelli, V, Rautou, Pe, Reuben, A, Riggio, O, Senzolo, M, Shah, N, Simioni, P, Stanworth, S, Stine, J, Thornburg, B, Valla, D, Villa, E, and Violi, F.

Subjects
Hemostasis, Biomedical Research, Liver Diseases, Hemorrhage, Thrombosis, Hematology, Meeting Report, Prognosis, NO, Liver, Risk Factors, Animals, Humans, Blood Coagulation Tests
Published
2018

17. Serological diagnosis of early HCC in NASH: A German multicenter study

Author

Best, J., primary, Bechmann, L., additional, Dechêne, A., additional, Pflanz, K., additional, Bedreli, S., additional, Schotten, C., additional, Berg, T., additional, Fischer, J., additional, Vogel, A., additional, Bantel, H., additional, Weinmann, A., additional, Schattenberg, J., additional, Huber, Y., additional, Wege, H., additional, Schulze, K., additional, von Felden, J., additional, Dominik, B., additional, Thimme, R., additional, Sinner, F., additional, Schuette, K., additional, Weiss, K.H., additional, Berhane, S., additional, Johnson, P., additional, Gerken, G., additional, and Canbay, A., additional

Published
2018
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20. Thyroid Hormone Receptor (TR): a regulator in Liver Fibrogenesis

Author

Manka, PP, additional, Coombes, JD, additional, Bechmann, L, additional, Swiderska-Syn, M, additional, Reid, D, additional, Claridge, LC, additional, Younis, R, additional, Mehta, K, additional, Briones, MA, additional, Kitamura, N, additional, Mi, Z, additional, Kuo, PC, additional, Williams, R, additional, Eksteen, B, additional, Diehl, AM, additional, Gerken, G, additional, Canbay, A, additional, Flamant, F, additional, Gauthier, K, additional, and Syn, WK, additional

Published
2016
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34. Glucokinase links Krüppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease

Author

Bechmann, L. P., Gastaldelli, A., Vetter, D., Patman, G. L., Pascoe, L., Hannivoort, R. A., Lee, U. E., Fiel, I., Munoz, U., Ciociaro, D., Lee, Y. -M., Buzzigoli, E., Miele, Luca, Hui, K. Y., Bugianesi, E., Burt, A. D., Day, C. P., Mari, A., Agius, L., Walker, M., Friedman, S. L., Reeves, H. L., Miele L. (ORCID:0000-0003-3464-0068), Bechmann, L. P., Gastaldelli, A., Vetter, D., Patman, G. L., Pascoe, L., Hannivoort, R. A., Lee, U. E., Fiel, I., Munoz, U., Ciociaro, D., Lee, Y. -M., Buzzigoli, E., Miele, Luca, Hui, K. Y., Bugianesi, E., Burt, A. D., Day, C. P., Mari, A., Agius, L., Walker, M., Friedman, S. L., Reeves, H. L., and Miele L. (ORCID:0000-0003-3464-0068)

Abstract

The polymorphism, KLF6-IVS1-27A, in the Krüppel-like factor 6 (KLF6) transcription factor gene enhances its splicing into antagonistic isoforms and is associated with delayed histological progression of nonalcoholic fatty liver disease (NAFLD). To explore a potential role for KLF6 in the development of insulin resistance, central to NAFLD pathogenesis, we genotyped KLF6-IVS1-27 in healthy subjects and assayed fasting plasma glucose (FPG) and insulin sensitivities. Furthermore, we quantified messenger RNA (mRNA) expression of KLF6 and glucokinase (GCK), as an important mediator of insulin sensitivity, in human livers and in liver tissues derived from a murine Klf6 knockdown model (DeltaKlf6). Klf6 overexpression studies in a mouse hepatocyte line were utilized to mechanistically link KLF6 with Gck promoter activity. KLF6-IVS1-27Gwt (i.e., less KLF6 splicing) was associated with stepwise increases in FPG and insulin and reduced hepatic insulin sensitivity. KLF6 binds to the liver-specific Gck promoter and activates a GCK promoter-reporter, identifying GCK as a KLF6 direct transcriptional target. Accordingly, in DeltaKlf6 hepatocytes Gck expression was reduced and stable transfection of Klf6 led to up-regulation of Gck. GCK and KLF6 mRNAs correlate directly in human NAFLD tissues and immunohistochemistry studies confirm falling levels of both KLF6 and GCK in fat-laden hepatocytes. In contrast to full-length KLF6, splice variant KLF6-SV1 increases in NAFLD hepatocytes and inversely correlates with glucokinase regulatory protein, which negatively regulates GCK activity. Conclusion: KLF6 regulation of GCK contributes to the development of hepatic insulin resistance. The KLF6-IVS1-27A polymorphism, which generates more KLF6-SV1, combats this, lowering hepatic insulin resistance and blood glucose. © 2011 American Association for the Study of Liver Diseases.

Published
2012

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