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The Imprinted Gene Neuronatin Is Regulated by Metabolic Status and Associated With Obesity
Author(s) -
Vrang Niels,
Meyre David,
Froguel Phillippe,
Jelsing Jacob,
TangChristensen Mads,
Vatin Vincent,
Mikkelsen Jens D.,
Thirstrup Kenneth,
Larsen Leif K.,
Cullberg Karina B.,
Fahrenkrug Jan,
Jacobson Per,
Sjöström Lars,
Carlsson Lena M.S.,
Liu Yongjun,
Liu Xiaogang,
Deng HongWen,
Larsen Philip J.
Publication year - 2010
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2009.361
Subject(s) - leptin , energy homeostasis , endocrinology , medicine , gene expression , gene , hypothalamus , obesity , appetite , single nucleotide polymorphism , biology , genomic imprinting , genetics , genotype , dna methylation
Using restriction fragment differential display (RFDD) technology, we have identified the imprinted gene neuronatin ( Nnat ) as a hypothalamic target under the influence of leptin. Nnat mRNA expression is decreased in several key appetite regulatory hypothalamic nuclei in rodents with impaired leptin signaling and during fasting conditions. Furthermore, peripheral administration of leptin to ob/ob mice normalizes hypothalamic Nnat expression. Comparative immunohistochemical analysis of human and rat hypothalami demonstrates that NNAT protein is present in anatomically equivalent nuclei, suggesting human physiological relevance of the gene product(s). A putative role of Nnat in human energy homeostasis is further emphasized by a consistent association between single nucleotide polymorphisms (SNPs) in the human Nnat gene and severe childhood and adult obesity.