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1 Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan
2 Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan; Japan Science and Technology Agency, PRESTO, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: ezaki{at}nih.go.jp.
Obesity is a common and serious metabolic disorder in the developed world,
which is occasionally accompanied by type II diabetes, atherosclerosis,
hypertension and hyperlipidemia. We have found that Mest (Mesoderm specific
transcript) / Peg1 (Paternally expressed gene 1) gene expression was markedly
enhanced in white adipose tissue of mice with diet-induced and genetically caused
obesity/diabetes, but not with streptozotocin-induced diabetes which does not cause
obesity. Administration of pioglitazone, a drug for type II diabetes and activator of
PPAR
, in db/db mice reduced the enhanced expression of Mest mRNA in adipose
tissue, concomitant with an increase in body weight and a decrease in the size of
adipose cells. Ectopic expression of Mest in 3T3-L1 cells caused increased gene
expression of adipose markers, such as PPAR
, C/EBP
and aP2. In transgenic
mice overexpressing Mest in adipose tissue, enhanced expression of the adipose
genes was observed. Moreover, adipocytes were markedly enlarged in the
transgenic mice. Thus, Mest appears to enlarge adipocytes and could be a novel
marker of the size of adipocytes.
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