Inhibition of Foxo1 function is associated with improved fasting glycemia in diabetic mice

American Journal of Physiology. Endocrinology and Metabolism
Jennifer AltomonteHengjiang Dong

Abstract

Excessive hepatic glucose production is a contributing factor to fasting hyperglycemia in diabetes. Insulin suppresses hepatic glucose production by inhibiting the expression of two gluconeogenic enzymes, phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase). The forkhead transcription factor Foxo1 has been implicated as a mediator of insulin action in regulating hepatic gluconeogenesis, and a Foxo1 mutant (Foxo1-Delta256), devoid of its carboxyl domain, has been shown to interfere with Foxo1 function and inhibit gluconeogenic gene expression in cultured cells. To study the effect of Foxo1-Delta256 on glucose metabolism in animals, the Foxo1-Delta256 cDNA was delivered to the livers of mice by adenovirus-mediated gene transfer. Hepatic Foxo1-Delta256 production resulted in inhibition of gluconeogenic activity, as evidenced by reduced PEPCK and G-6-Pase expression in the liver. Mice treated with the Foxo1-Delta256 vector exhibited significantly reduced blood glucose levels. In contrast, blood glucose levels in control vector-treated animals remained unchanged, which coincided with the lack of alterations in the expression levels of PEPCK and G-6-Pase. When tested in diabetic db/db mice, hepatic productio...Continue Reading

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May 28, 2014·BioMed Research International·Yu WangDana T Graves
Jun 6, 2009·Current Diabetes Reports·Danielle N GrossMorris J Birnbaum
Oct 20, 2004·The Journal of Experimental Medicine·Francesca FallarinoPaolo Puccetti
Nov 17, 2004·The Journal of Clinical Investigation·Jennifer AltomonteHengjiang Henry Dong
Aug 15, 2006·The Journal of Clinical Investigation·Michihiro MatsumotoDomenico Accili
Aug 19, 2006·The Journal of Clinical Investigation·Jun NakaeYoshitake Hayashi
Sep 21, 2006·American Journal of Physiology. Endocrinology and Metabolism·Shen QuH Henry Dong
Apr 18, 2007·Journal of Lipid Research·Shen QuH Henry Dong
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