Mol Nutr Food Res.: co-auth.: F.Preitner

 2020 May 7:e1901141. doi: 10.1002/mnfr.201901141. [Epub ahead of print]

Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.



Intake of fructose-sweetened beverages and chronic stress both increase risk of cardiometabolic diseases. The aim was to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney.


We measured fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics and key metabolic genes expression at the end of feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + chronic stress (CS), 20% liquid high-fructose supplementation (HFr), or HFr+CS. HFr induced hypertriglyceridemia, up-regulated fructose-metabolism and gluconeogenic enzymes, increased IHTG and DNPalm content in IHTG and IRTG, and augmented fDNL at the end of feeding phase. These changes were diminished after the non-feeding phase. CS did not exert such effects, but when combined with HFr, it reduced IHTG and visceral adiposity, enhanced lipogenic gene expression and fDNL, and increased VLDL-DNPalm secretion.


Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of the high-fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase. This article is protected by copyright. All rights reserved.


Chronic stress; high-fructose supplementation; kidney; lipogenesis; liver

PMID: 32379936