The group of Michael Schupp together with collaboration partners at the MDC and clinicians of the Charite and the University of Jena collected new findings on the function of the enzyme Retinol Saturase (RetSat) in the fatty acid and glucose metabolism of the liver. RetSat expression is increased in livers of obese and insulin-resistant individuals. A liver-specific depletion of RetSat in obese mice could normalize certain elevated lipid parameters. Mechanically, RetSat depletion appears to prevent the diet-induced over-activation of a cellular glucose sensor, called carbohydrate response element binding protein (ChREBP). Thus, inhibition of hepatic RetSat may represent a new therapeutic approach for metabolic liver disease.
Original work: Heidenreich S., N. Witte, P. Weber, I. Goehring, A. Tolkachov, C. von Loeffelholz, S. Döcke, M. Bauer, M. Stockmann, A.F. Pfeiffer, A. L. Birkenfeld, M. Pietzke, S. Kempa, M. Muenzner, and Schupp M., Retinol Saturase Coordinates Liver Metabolism by Regulating ChREBP Activity. Nat Commun 2017, 8(1):384
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