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Histone Deacetylase 6 ( HDAC6 ) Is an Essential Modifier of Glucocorticoid-Induced Hepatic Gluconeogenesis
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Histone Deacetylase 6 ( HDAC6 ) Is an Essential Modifier of Glucocorticoid-Induced Hepatic Gluconeogenesis
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Journal Article
Histone Deacetylase 6 ( HDAC6 ) Is an Essential Modifier of Glucocorticoid-Induced Hepatic Gluconeogenesis
2012
Overview
In the current study, we investigated the importance of histone deacetylase (HDAC)6 for glucocorticoid receptor-mediated effects on glucose metabolism and its potential as a therapeutic target for the prevention of glucocorticoid-induced diabetes. Dexamethasone-induced hepatic glucose output and glucocorticoid receptor translocation were analyzed in wild-type (wt) and HDAC6-deficient (HDAC6KO) mice. The effect of the specific HDAC6 inhibitor tubacin was analyzed in vitro. wt and HDAC6KO mice were subjected to 3 weeks' dexamethasone treatment before analysis of glucose and insulin tolerance. HDAC6KO mice showed impaired dexamethasone-induced hepatic glucocorticoid receptor translocation. Accordingly, dexamethasone-induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in vitro. Glucose output of primary hepatocytes from HDAC6KO mice was diminished. A significant improvement of dexamethasone-induced whole-body glucose intolerance as well as insulin resistance in HDAC6KO mice compared with wt littermates was observed. This study demonstrates that HDAC6 is an essential regulator of hepatic glucocorticoid-stimulated gluconeogenesis and impairment of whole-body glucose metabolism through modification of glucocorticoid receptor nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the prodiabetogenic actions of glucocorticoids.
Publisher
American Diabetes Association
Subject
/ Active Transport, Cell Nucleus
/ Animals
/ Biological and medical sciences
/ Dexamethasone - pharmacology
/ Diabetes
/ Diabetes. Impaired glucose tolerance
/ Endocrine pancreas. Apud cells (diseases)
/ Etiopathogenesis. Screening. Investigations. Target tissue resistance
/ Gluconeogenesis - drug effects
/ Glucose
/ Histone Deacetylases - physiology
/ Ligands
/ Lipopolysaccharides - pharmacology
/ Male
/ Mice
/ Pharmacology and Therapeutics
/ Phosphoenolpyruvate Carboxykinase (GTP) - physiology
/ Proteins
