Study summary · research use only
Mitochondria-derived peptide SHLP2 regulates energy homeostasis through the activation of hypothalamic neurons
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in male mice investigated the mitochondrial-derived peptide SHLP2 (small humanin-like peptide 2) and its role in energy homeostasis. Systemic and intracerebroventricular administration of SHLP2 protected mice from high-fat diet-induced obesity and improved insulin sensitivity. SHLP2 activated pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus, which was associated with suppressed food intake and increased thermogenesis. Using high-throughput structural complementation screening, the authors found that SHLP2 binds to and activates the chemokine receptor CXCR7, and describe this as providing mechanistic insight into how SHLP2 affects energy homeostasis, with potential relevance to metabolic disorders.
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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