期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2002
卷号：99
期号：18
页码：11848-11853
DOI：10.1073/pnas.182420899
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Adenovirus-induced hyperleptinemia causes rapid disappearance of body fat in normal rats, presumably by up-regulating fatty acid oxidation within white adipocytes. To determine the role of peroxisomal proliferation-activated receptor (PPAR) expression, which was increased during the rapid loss of fat, we infused adenovirus-leptin into PPAR-/- and PPAR+/+ mice. Despite similar degrees of hyperleptinemia and reduction in food intake, epididymal fat pad weight declined 55% in wild-type but only 6% in PPAR-/- mice; liver triacylglycerol fell 39% in the wild-type group but was unchanged in PPAR-/- mice. Carnitine palmitoyl transferase-1 mRNA rose 52% in the wild-type mice but did not increase in PPAR-/- mice. PPAR{gamma} coactivator-1 rose 3-fold in the fat and 46% in the liver of wild-type mice but was unchanged in PPAR-/- mice. Although AMP-activated protein kinase could not be implicated in the lipopenic actions of hyperleptinemia, acetyl CoA carboxylase protein was reduced in the liver of wild-type but not in PPAR-/- mice. Thus, in PPAR-/- mice, up-regulation of carnitine palmitoyl transferase-1 mRNA in fat, down-regulation of acetyl CoA carboxylase in liver, and up-regulation of PPAR{gamma} coactivator-1 mRNA in both tissues are abolished, as is the reduction in their triacylglycerol content.
