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Fructose, but not glucose, impairs insulin signaling in the three major insulin-sensitive tissues
Baena Muñoz, Miguel; Sangüesa Puigventós, Gemma; Dávalos, Alberto; Latasa, Maria-Jesús; Sala Vila, Aleix; Sánchez Peñarroya, Rosa M.; Roglans i Ribas, Núria; Laguna Egea, Juan Carlos; Alegret i Jordà, Marta
Universitat de Barcelona
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.
Diabetis
Resistència a la insulina
Fructosa
Experimentació animal
Diabetes
Insulin resistance
Fructose
Animal experimentation
cc-by-nc-nd (c) Baena Muñoz, Miguel et al., 2016
http://creativecommons.org/licenses/by-nc-nd/3.0/es
Artículo
info:eu-repo/semantics/publishedVersion
Nature Publishing Group
         

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