Abstract
Human studies support the relationship between high intake of fructose-sweetened beverages and type 2 diabetes, but there is a debate on whether this effect is fructose-specific or it is merely associated to an excessive caloric intake. Here we investigate the effects of 2 months’ supplementation to female rats of equicaloric 10% w/v fructose or glucose solutions on insulin sensitivity in target tissues. Fructose supplementation caused hepatic deposition of triglycerides and changed the fatty acid profile of this fraction, with an increase in monounsaturated and a decrease in polyunsaturated species, but did not cause inflammation and oxidative stress. Fructose but not glucose-supplemented rats displayed an abnormal glucose tolerance test, and did not show increased phosphorylation of V-akt murine thymoma viral oncogene homolog-2 (Akt) in white adipose tissue and liver after insulin administration. In skeletal muscle, phosphorylation of Akt and of Akt substrate of 160 kDA (AS160) was not impaired but the expression of the glucose transporter type 4 (GLUT4) in the plasma membrane was reduced only in fructose-fed rats. In conclusion, fructose but not glucose supplementation causes fatty liver without inflammation and oxidative stress and impairs insulin signaling in the three major insulin-responsive tissues independently from the increase in energy intake.
Highlights
Binding protein (ChREBP)[10,11]
We show that supplementation with 10% w/v liquid fructose for 2 months to female rats causes liver deposition of triglycerides enriched in monounsaturated fatty acids (MUFA) with no signs of liver and vWAT inflammation and oxidative stress
Fructose-supplemented rats display an abnormal glucose tolerance test (GTT) and an impairment of insulin signaling in the three major insulin-responsive tissues: in vWAT and liver, where fructose inhibits insulin-induced Akt phosphorylation, and in skeletal muscle, where Akt is correctly activated by insulin but GLUT4 expression in the plasma membrane is reduced
Summary
Binding protein (ChREBP)[10,11]. In these studies, fructose was administered for 14 days, which is a short treatment period given that fructose consumption patterns in humans extend over many years. We studied the effects on insulin signaling in target tissues of a 2-month period of fructose supplementation, comparable to 6 human years of daily fructose consumption[12]. We investigated whether there is a dissociation between fatty liver and insulin resistance and inflammation, as reported in mice with ChREBP overexpression[13]. To distinguish between effects related to increased caloric intake and the specific effects of fructose, we performed a second set of experiments including a group supplemented with liquid glucose under equicaloric conditions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
