ArticleProceedings of the National Academy of Sciences of the United States of America2007
Silencing of OB-RGRP in mouse hypothalamic arcuate nucleus increases leptin receptor signaling and prevents diet-induced obesity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
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- Molecular Therapy of Melanocortin-4-Receptor Obesity by an Autoregulatory BDNF Vector.Molecular therapy. Methods & clinical development · 2017Article
- Pan-cancer analysis of homozygous deletions in primary tumours uncovers rare tumour suppressors.Nature communications · 2017Article
- The Leptin Receptor Complex: Heavier Than Expected?Frontiers in endocrinology · 2017Review
- On the Molecular Evolution of Leptin, Leptin Receptor, and Endospanin.Frontiers in endocrinology · 2017Article
- Endospanin1 affects oppositely body weight regulation and glucose homeostasis by differentially regulating central leptin signaling.Molecular metabolism · 2017Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Obesity is a major public health problem and is often associated with type 2 diabetes mellitus, cardiovascular disease, and metabolic syndrome. Leptin is the crucial adipostatic hormone that controls food intake and body weight through the activation of specific leptin receptors (OB-R) in the hypothalamic arcuate nucleus (ARC). However, in most obese patients, high circulating levels of leptin fail to bring about weight loss. The prevention of this "leptin resistance" is a major goal for obesity research. We report here a successful prevention of diet-induced obesity (DIO) by silencing a negative regulator of OB-R function, the OB-R gene-related protein (OB-RGRP), whose transcript is genetically linked to the OB-R transcript. We provide in vitro evidence that OB-RGRP controls OB-R function by negatively regulating its cell surface expression. In the DIO mouse model, obesity was prevented by silencing OB-RGRP through stereotactic injection of a lentiviral vector encoding a shRNA directed against OB-RGRP in the ARC. This work demonstrates that OB-RGRP is a potential target for obesity treatment. Indeed, regulators of the receptor could be more appropriate targets than the receptor itself. This finding could serve as the basis for an approach to identifying potential new therapeutic targets for a variety of diseases, including obesity.
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