PPARβ/δ ameliorates fructose-induced insulin resistance in adipocytes by preventing Nrf2 activation

Biochimica Et Biophysica Acta
Emma BarrosoManuel Vázquez-Carrera

Abstract

We studied whether PPARβ/δ deficiency modifies the effects of high fructose intake (30% fructose in drinking water) on glucose tolerance and adipose tissue dysfunction, focusing on the CD36-dependent pathway that enhances adipose tissue inflammation and impairs insulin signaling. Fructose intake for 8 weeks significantly increased body and liver weight, and hepatic triglyceride accumulation in PPARβ/δ-deficient mice but not in wild-type mice. Feeding PPARβ/δ-deficient mice with fructose exacerbated glucose intolerance and led to macrophage infiltration, inflammation, enhanced mRNA and protein levels of CD36, and activation of the JNK pathway in white adipose tissue compared to those of water-fed PPARβ/δ-deficient mice. Cultured adipocytes exposed to fructose also exhibited increased CD36 protein levels and this increase was prevented by the PPARβ/δ activator GW501516. Interestingly, the levels of the nuclear factor E2-related factor 2 (Nrf2), a transcription factor reported to up-regulate Cd36 expression and to impair insulin signaling, were increased in fructose-exposed adipocytes whereas co-incubation with GW501516 abolished this increase. In agreement with Nrf2 playing a role in the fructose-induced CD36 protein level increa...Continue Reading

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Citations

Apr 12, 2016·BioMed Research International·Mehmet Bilgehan PektasFatma Akar
Nov 4, 2016·Nature Reviews. Endocrinology·Barbara GrossBart Staels
Apr 4, 2017·The Journal of Clinical Investigation·Vanessa DuboisBart Staels
Mar 28, 2017·Brain Plasticity·Davide GuerrieriHenriette van Praag
Jan 22, 2021·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Liliya V VasilevaMilen I Georgiev
Jul 25, 2021·International Journal of Molecular Sciences·Stefan BlunderSandrine Dubrac

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