AI Article Synopsis
- SHLP2 is a mitochondrial peptide linked to aging and oxidative stress, but its role in energy balance and receptor remains unspecified.
- Administering SHLP2 to mice on a high-fat diet reduces obesity and enhances insulin sensitivity by activating POMC neurons in the hypothalamus, which helps control food intake and increase thermogenesis.
- The study identifies CXCR7 as the receptor for SHLP2, highlighting its potential as a therapeutic agent for metabolic disorders and providing insights into its functioning in energy regulation.
Article Abstract
Small humanin-like peptide 2 (SHLP2) is a mitochondrial-derived peptide implicated in several biological processes such as aging and oxidative stress. However, its functional role in the regulation of energy homeostasis remains unclear, and its corresponding receptor is not identified. Hereby, we demonstrate that both systemic and intracerebroventricular (ICV) administrations of SHLP2 protected the male mice from high-fat diet (HFD)-induced obesity and improved insulin sensitivity. In addition, the activation of pro-opiomelanocortin (POMC) neurons by SHLP2 in the arcuate nucleus of the hypothalamus (ARC) is involved in the suppression of food intake and the promotion of thermogenesis. Through high-throughput structural complementation screening, we discovered that SHLP2 binds to and activates chemokine receptor 7 (CXCR7). Taken together, our study not only reveals the therapeutic potential of SHLP2 in metabolic disorders but also provides important mechanistic insights into how it exerts its effects on energy homeostasis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10356901 | PMC |
| http://dx.doi.org/10.1038/s41467-023-40082-7 | DOI Listing |
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