The CCR group of Michael Schupp has published novel finding concerning a cellular glucose-sensing protein (ChREBP). The first authors Nicole Witte and Matthias Muenzner and their co-authors could show that ChREBP in adipocytes regulates the activity of a nuclear receptor that plays a pivotal role in fat cell differentiation and insulin sensitivity (PPARg). In a collaborative study with scientists from Baylor College of Medicine in Houston was then tested whether the expression of active ChREBP in adipose tissue of transgenic mice impacts metabolic parameters. Indeed, ChREBP activation in adipose tissue protected against obesity, fatty liver, and insulin resistance and may thus represent a future therapeutic intervention for treating metabolic disease.
Witte, N., M. Muenzner, J. Rietscher, M. Knauer, S. Heidenreich, A.M. Nuotio-Antar, F.A. Graef, R. Fedders, A. Tolkachov, I. Goehring I, M. Schupp, The glucose sensor ChREBP links de-novo lipogenesis to PPARγ activity and adipocyte differentiation. Endocrinology, 2015 Jul. [Epub ahead of print]
Nuotio-Antar, A.M., N. Poungvarin, M. Li, M. Schupp, M. Mohammad, S. Gerard, F. Zou, L. Chan, FABP4-Cre Mediated Expression of Constitutively Active ChREBP Protects Against Obesity, Fatty Liver, and Insulin Resistance. Endocrinology, 2015 Aug. [Epub ahead of print]
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