Atrophy of brown adipocytes in the adult mouse causes transformation into white adipocyte-like cells
Experimental & Molecular Medicine
; : 518-526, 2003.
Article
em En
| WPRIM
| ID: wpr-197470
Biblioteca responsável:
WPRO
ABSTRACT
Adipose tissue is an important endocrine regulator of glucose metabolism and energy homeostasis. Researches have focused on this tissue not only as a target for pharmacotherapy of obesity and insulin resistance but also as an endocrine tissue with leptin secretion and high insulin sensitivity. Brown adipose tissue (BAT) additionally plays a unique role in thermoregulation through the mitochondrial uncoupling protein 1 (UCP1), which uncouples oxidative phosphorylation. As a genetic tissue ablation model of BAT, we made transgenic mice expressing herpes simplex virus thymidine kinase (HSV-TK) driven by the brown adipocyte- specific UCP1 minimal regulatory element. The HSV-TK transgene was expressed specifically in BAT and more than 35% increase of apoptosis was induced by ganciclovir (GCV) treatment. Nevertheless, the expression level was not high enough to induce BAT ablation in GCV-treated adult mice. Importantly, however, we found that brown adipocytes in the periphery of interscapular BAT were transformed into white adipocyte-like unilocular cells. These cells express white adipocyte-specific leptin protein but are different in the ultrastructure of mitochondria from classical white adipocytes. Our data indicates that atrophy of BAT causes transformation into white adipocyte-like cells in the adult mouse and also suggests that further molecular understanding of adipocyte plasticity using our transgenic mouse model might be beneficial for the development of anti-obesity/anti-diabetic therapies.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Especificidade de Órgãos
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Timidina Quinase
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Peso Corporal
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Envelhecimento
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Camundongos Transgênicos
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Proteínas de Transporte
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Ganciclovir
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Diferenciação Celular
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Tecido Adiposo
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Leptina
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
Experimental & Molecular Medicine
Ano de publicação:
2003
Tipo de documento:
Article