• Biomedical Science Letters
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• v.13 no.2
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• pp.91-97
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• 2007

Obesity is defined as increased mass of adipose tissue, conferring a higher risk of cardiovascular and metabolic disorders such as diabetes, hyperlipidemia, and coronary heart disease. To get a better understanding of the role of a male sex hormone testosterone on obesity, we thus measured the effects of testosterone on white adipose tissue (WAT) mass, adipocyte histology and hepatic lipid accumulation in male castrated (CAST) C57BL/6J mice. Compared to male CAST control mice, testosterone-treated mice had the decreased WAT mass and the increased the number of adipocytes. Especially, histological data showed that the adipocyte size was reduced in a dose-dependent manner and was most effective at dose 150 $\mu$g per mouse for testosterone. In addition, the administration of testosterone resulted in the inhibition of hepatic lipid accumulation compared with control mice. Our results suggest that testosterone regulates adipocytes development and hepatic lipid metabolism, resulting in the prevention of obesity in male CAST mice.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.17 no.12
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• pp.2995-3000
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• 2013

We investigated the effects of testosterone on the improvement of white adipose tissue explant and its molecular mechanism in adipose tissue of high fat diet-fed male castrated (CAST) mice. The CAST mice treated with testosterone had lower adipose tissue weights, the average size of adipocytes and mRNA levels of $C/EBP{\alpha}$ as well as adipocyte marker genes than the vehicle-treated CAST mice. These results suggest that testosterone prevent the expression of $C/EBP{\alpha}$ and $C/EBP{\alpha}$-mediated adipocyte marker genes, resulting in decreased adipose tissue mass and adipocyte metabolism in male CAST mice. Moreover, this study give a valuable molecular and biological knowledge on testosterone therapy in obese hypogonadal men.

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.31-31
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• 1999

Characterization of mutant mice has been utilized as an animal model for the study of human inherited diseases. In addition to the pathogenesis stduy using the mutant mice, the mice have been used for the identification of the genes causing the phenotypes. Functional cloning and positional cloning are two approaches, depending on the phenotypes of the mutant mice. Though it takes a long time positional cloning has been well used to identify the gene of which function can not be presumed from the mouse phenotype. Recently by the advance of the molecular tools and the human genome project close to 10,000 genetic markers are developed to make the procedure faster. We obtained a new mutant mouse, sims, spontaneously arose and the affected mouse has a mild tremor and seizure was observed. Homozygote in either sex is sterile since uterus growth in female and seminal vesicle in male are not induced for the growth in puberty, implying the abnormal hormonal regulation during puberty. Supporting this, there is no detectable testosterone in the serum of the mutant male and the brain of the mutant is 30% heavier than littermate. To identify the location of the mutated gene, intraspecies cross to CAST/Ei was carried out and the 37 affected mice was analyzed for the linkage. The gene was mapped on chromosome 18, 20 cM from the centromere. More than 500 F2 progenies have been analyzed for the linkage and the locus becomes narrow within 3cM between Egrl and Fgf gene.f gene.