Atrophy of brown adipocytes in the adult mouse causes transformation into white adipocyte-like cells.
- Author:
Dae Whan KIM
1
;
Beom Sue KIM
;
Hee Seok KWON
;
Chan Gil KIM
;
Han Woong LEE
;
Woong Hwan CHOI
;
Chul Geun KIM
Author Information
1. The Department of Life Science and the Research Institute for Natural Sciences, College of Natural Sciences Hanyang University, Seoul 133-791, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
adipocyte differentiation;
brown adipose tissue;
energy homeostasis;
genetic tissue ablation;
transgenic mice
- MeSH:
Adipose Tissue/*cytology/drug effects/metabolism/ultrastructure;
Aging/physiology;
Animals;
Body Weight;
Carrier Proteins/genetics/metabolism;
*Cell Differentiation/drug effects;
Ganciclovir/pharmacology;
Ion Channels;
Leptin/metabolism;
Membrane Proteins/genetics/metabolism;
Mice;
Mice, Transgenic;
Mitochondrial Proteins;
Obesity/chemically induced;
Organ Specificity;
Thymidine Kinase/genetics/metabolism
- From:Experimental & Molecular Medicine
2003;35(6):518-526
- CountryRepublic of Korea
- Language:English
-
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.
