ArticleMolecular metabolism2020
BRS3 in both MC4R- and SIM1-expressing neurons regulates energy homeostasis in mice.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
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- A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types.Cell reports · 2026Article
- A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types.Research square · 2025Article
- Uncovering the role of Gpr45 in obesity regulation.Molecular metabolism · 2025Article
- Repetitive transcranial magnetic stimulation elicits weight loss and improved insulin sensitivity in type 2 diabetic rats.Animal models and experimental medicine · 2025Article
- Gut-Brain Dialogues in Fruit Fly (Current drug targets · 2025Review
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- Molecular Diversity of Neuron Types in the Salamander Amygdala and Implications for Amygdalar Evolution.Brain, behavior and evolution · 2023Article
- Preoptic BRS3 neurons increase body temperature and heart rate via multiple pathways.Cell metabolism · 2021Article
- Paraventricular Calcitonin Receptor-Expressing Neurons Modulate Energy Homeostasis in Male Mice.Endocrinology · 2021Article
- Effect of Sleeve Gastrectomy on Glycometabolism via Forkhead Box O1 (FoxO1)/Lipocalin-2 (LCN2) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Activation of neuronal adenosine A1 receptors causes hypothermia through central and peripheral mechanisms.PloS one · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveBombesin-like receptor 3 (BRS3) is an orphan receptor and Brs3 knockout mice develop obesity with increased food intake and reduced resting metabolic rate and body temperature. The neuronal populations contributing to these effects were examined.
methodsWe studied energy metabolism in mice with Cre-mediated recombination causing 1) loss of BRS3 selectively in SIM1- or MC4R-expressing neurons or 2) selective re-expression of BRS3 from a null background in these neurons.
resultsThe deletion of BRS3 in MC4R neurons increased body weight/adiposity, metabolic efficiency, and food intake, and reduced insulin sensitivity. BRS3 re-expression in these neurons caused partial or no reversal of these traits. However, these observations were confounded by an obesity phenotype caused by the Mc4r-Cre allele, independent of its recombinase activity. The deletion of BRS3 in SIM1 neurons increased body weight/adiposity and food intake, but not to the levels of the global null. The re-expression of BRS3 in SIM1 neurons reduced body weight/adiposity and food intake, but not to wild type levels. The deletion of BRS3 in either MC4R- or SIM1-expressing neurons affected body temperature, with re-expression in either population reversing the null phenotype. MK-5046, a BRS3 agonist, increases light phase body temperature in wild type, but not Brs3 null, mice and BRS3 re-expression in either population restored response to MK-5046.
conclusionsBRS3 in both MC4R- and SIM1-expressing neurons contributes to regulation of body weight/adiposity, insulin sensitivity, food intake, and body temperature.
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