Change in lipid components in the adipose and liver tissues of regucalcin transgenic rats with increasing age: suppression of leptin and adiponectin gene expression.
Regucalcin plays a multifunctional role as a regulatory protein in intracellular signaling pathway in many cell types. Regucalcin transgenic (TG) rats have been shown to experience hyperlipidemia with increasing age. This study was undertaken to determine whether lipid components in the adipose and liver tissues are changed in regucalcin TG rats in vivo. Female regucalcin TG rats were used at 7 or 50 weeks of age. Serum triglyceride or HDL-cholesterol concentrations were significantly increased in 7-week-old regucalcin TG rats as compared with those in 7-week-old normal rats. Serum triglyceride, total cholesterol, HDL-cholesterol, or free fatty acid concentrations were significantly increased in 50-week-old regucalcin TG rats. Meanwhile, triglyceride content in the adipose tissues was significantly increased in 50-week-old regucalcin TG rats,while the free fatty acid content was not significantly changed. Triglyceride, total cholesterol, or free fatty acid content in the liver tissues was significantly decreased in 50-week-old regucalcin TG rats. Liver glycogen content was significantly decreased in 7- or 50-week-old regucalcin TG rats. In addition, regucalcin mRNA and its protein levels were seen in the adipose tissues of normal rats. Those levels were not significantly changed in regucalcin TG rats at 50 weeks of age. Leptin mRNA expression in the adipose or liver tissues was significantly decreased in 50-week-old regucalcin TG rats. Adiponectin mRNA levels were not significantly changed in the adipose tissues of 50-week-old regucalcin TG rats, while the levels were significantly decreased in the liver tissues. This study demonstrates that the disorder of lipid metabolism in the adipose and liver tissues is induced in regucalcin TG rats with aging, and that the gene expression of leptin or adiponectin is suppressed in TG rats.
Yamaguchi
Masayoshi
M
Laboratory of Endocrinology and Molecular Metabolism, Graduate School of Nutritional Sciences, University of Shizuoka, Shizuoka 422-8526, Japan. yamaguch@u-shizuoka-ken.ac.jp
Nakagawa
Taeko
T
D052242:Adiponectin / Q000235:genetics*; D000273:Adipose Tissue / Q000378:metabolism; D000375:Aging / Q000235:genetics* / Q000378:metabolism*; D000818:Animals; D030801:Animals, Genetically Modified; D001483:Base Sequence; D002135:Calcium-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D002265:Carboxylic Ester Hydrolases; D018076:DNA, Complementary / Q000235:genetics; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006949:Hyperlipidemias / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics* / Q000378:metabolism; D020738:Leptin / Q000235:genetics*; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
D052242:Adiponectin; D002135:Calcium-Binding Proteins; D018076:DNA, Complementary; D005230:Fatty Acids, Nonesterified; D047908:Intracellular Signaling Peptides and Proteins; D020738:Leptin; D012333:RNA, Messenger; D011994:Recombinant Proteins; D014280:Triglycerides; D002265:Carboxylic Ester Hydrolases; C513325:Rgn protein, rat