Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11297
Title: Increased adiposity in DNA binding-dependent androgen receptor knockout male mice associated with decreased voluntary activity and not insulin resistance.
Authors: Rana, Kesha;Fam, Barbara C;Clarke, Michele V;Pang, Tammy P S;Zajac, Jeffrey D;MacLean, Helen E
Affiliation: Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria, Australia.
Issue Date: 28-Jun-2011
Citation: American Journal of Physiology. Endocrinology and Metabolism 2011; 301(5): E767-78
Abstract: In men, as testosterone levels decrease, fat mass increases and muscle mass decreases. Increased fat mass in men, in particular central obesity, is a major risk factor for type 2 diabetes, cardiovascular disease, and all-cause mortality. Testosterone treatment has been shown to decrease fat mass and increase fat-free mass. We hypothesize that androgens act directly via the DNA binding-dependent actions of the androgen receptor (AR) to regulate genes controlling fat mass and metabolism. The aim of this study was to determine the effect of a global DNA binding-dependent (DBD) AR knockout (DBD-ARKO) on the metabolic phenotype in male mice by measuring body mass, fat mass, food intake, voluntary physical activity, resting energy expenditure, substrate oxidation rates, serum glucose, insulin, lipid, and hormone levels, and metabolic gene expression levels and second messenger protein levels. DBD-ARKO males have increased adiposity despite a decreased total body mass compared with wild-type (WT) males. DBD-ARKO males showed reduced voluntary activity, decreased food intake, increased serum leptin and adiponectin levels, an altered lipid metabolism gene profile, and increased phosphorylated CREB levels compared with WT males. This study demonstrates that androgens acting via the DNA binding-dependent actions of the AR regulate fat mass and metabolism in males and that the increased adiposity in DBD-ARKO male mice is associated with decreased voluntary activity, hyperleptinemia and hyperadiponectinemia and not with insulin resistance, increased food intake, or decreased resting energy expenditure.
Internal ID Number: 21712531
URI: http://ahro.austin.org.au/austinjspui/handle/1/11297
DOI: 10.1152/ajpendo.00584.2010
URL: http://www.ncbi.nlm.nih.gov/pubmed/21712531
Type: Journal Article
Subjects: Adiponectin.blood
Adiposity.genetics
Animals
DNA.metabolism
DNA-Binding Proteins.metabolism
Down-Regulation
Eating.genetics.physiology
Insulin Resistance.genetics.physiology
Leptin.blood
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Motivation.genetics.physiology
Motor Activity.genetics
Protein Interaction Domains and Motifs.genetics
Receptors, Androgen.chemistry.genetics.metabolism
Up-Regulation.genetics
Appears in Collections:Journal articles

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