• 대한의생명과학회지
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• 제13권2호
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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.

• 한국정보통신학회논문지
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• 제17권12호
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• pp.2995-3000
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• 2013

본 연구는 고지방식이를 섭취한 정소절제수술을 한 수컷 마우스에서 백색지방증가의 개선에 대한 testosterone의 영향과 그것에 대한 분자생물학적 조절기전을 규명하였다. Testosterone이 처리된 정소절제수술 마우스(CAST+T)는 정소절제수술 마우스 (CAST)에 비해 지방조직무게, 지방세포크기 및 $C/EBP{\alpha}$와 지방세포 표지유전자의 mRNA 발현이 감소되었다. 본 연구결과는 testosterone이 $C/EBP{\alpha}$와 $C/EBP{\alpha}$에 의해 조절되는 지방세포 표지 유전자들의 발현을 억제시킴으로써 지방세포 조절기전이 억제되고 지방조직의 무게가 감소된다는 것을 시사하고 있다. 따라서 본 연구는 성선기능저하증 남성의 비만조절에 대한 testosterone therapy의 유익한 분자생물학적 정보를 제공할 것이다.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1999년도 한국생물과학협회 학술발표대회
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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.