Disturbed energy metabolism and lipid profile after a 4 week high oral fructose challenge: potential role of bile acids?

C Kienbacher; S Traussnigg; E Halilbasic; C Fuchs; W Dolak; P Steindl-Munda; T Stojakovic; G Fauler; T Claudel; M Trauner

doi:10.1055/s-0035-1551743

Zeitschrift für Gastroenterologie, Table of Contents

Disturbed energy metabolism and lipid profile after a 4 week high oral fructose challenge: potential role of bile acids?

C Kienbacher ¹, S Traussnigg ¹, E Halilbasic ¹, C Fuchs ², W Dolak ¹, P Steindl-Munda ¹, T Stojakovic ³, G Fauler ³, T Claudel ², M Trauner ¹

¹Medical University of Vienna, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Wien, Austria
²Medical University of Vienna, Division of Gastroenterology and Hepatology – Hans Popper Laboratory, Department of Internal Medicine III, Wien, Austria
³Medical University of Graz, Clinical Institute of Medical and Chemical Laboratory Diagnostics, Graz, Austria

Abstract

Background and Aims: Fructose overconsumption is linked to non-alcoholic fatty liver disease and impaired lipid and glucose metabolism. Since bile acids (BA) are critical regulators of lipid and energy metabolism, we aimed to explore whether dietary fructose challenge (FC; 150 g/day for 4 weeks) may impact on lipid and glucose dysbalance by changing BA metabolism.

Methods: Ten healthy volunteers were enrolled (m: f = 5: 5; age = 24.5 [21 – 37]). Blood was collected prior and after FC for routine laboratory analysis, BA and lipid profiling. Hepatic fat content was measured using magnetic-resonance-spectroscopy (MRS).

Results: FC increased BMI (p < 0.001) and fasted serum glucose (p = 0.035), indicating changes in energy metabolism. Although no changes were observed in total serum cholesterol and triglyceride levels; VLDL-cholesterol (p = 0.034), -cholesterol-ester (p = 0.025), and -ApoB (p = 0.039) were reduced after FC, reflecting lower hepatic VLDL excretion and/or faster clearance. FC did not change total serum BA concentrations that could explain lower VLDL excretion via FXR-activation. However, increased ApoAII levels (p = 0.042) may favor faster VLDL clearance. Notably, FC did not increase total intrahepatic lipids in MRS and serum liver enzymes. The secondary BAs (converted by intestinal bacteria) lithocholic-acid (p = 0.097) and ursodeoxycholic-acid (p = 0.075) tended to decrease under FC.

Conclusions: FC induced changes in energy metabolism reflected by weight gain, increased fasted glucose and changes in VLDL metabolism that may be linked to increased ApoAII. Moreover, changes in BA-composition could be due to shifts in the intestinal microbiome thus influencing BA-mediated FXR/TGR-5 signalling.