ArticleCell metabolism2014
Biphasic effect of melanocortin agonists on metabolic rate and body temperature.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Article
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- Preoptic BRS3 neurons increase body temperature and heart rate via multiple pathways.Cell metabolism · 2021Article
- Hypothalamic Pomc Neurons Innervate the Spinal Cord and Modulate the Excitability of Premotor Circuits.Current biology : CB · 2020Article
- Incendiary Leptin.Nutrients · 2020Review
- Activation of neuronal adenosine A1 receptors causes hypothermia through central and peripheral mechanisms.PloS one · 2020Article
- Macrophage derived TNFα promotes hepatic reprogramming to Warburg-like metabolism.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Androgens and Blood Pressure Control: Sex Differences and Mechanisms.Mayo Clinic proceedings · 2019Review
- Physiology and effects of nucleosides in mice lacking all four adenosine receptors.PLoS biology · 2019Article
- Signal Transduction and Pathogenic Modifications at the Melanocortin-4 Receptor: A Structural Perspective.Frontiers in endocrinology · 2019Article
- Brs3 neurons in the mouse dorsomedial hypothalamus regulate body temperature, energy expenditure, and heart rate, but not food intake.Nature neuroscience · 2018Article
- Melanotan II causes hypothermia in mice by activation of mast cells and stimulation of histamine 1 receptors.American journal of physiology. Endocrinology and metabolism · 2018Article
- Comparative in Vivo Investigation of Intrathecal and Intracerebroventricular Administration with Melanocortin Ligands MTII and AGRP into Mice.ACS chemical neuroscience · 2018Article
- αMSH inhibits adipose inflammation via reducing FoxOs transcription and blocking Akt/JNK pathway in mice.Oncotarget · 2017Article
- Hypothermia in mouse is caused by adenosine ANeuropharmacology · 2017Article
- The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances.Neuroendocrinology · 2017Review
- Melanocortin-3 receptors in the limbic system mediate feeding-related motivational responses during weight loss.Molecular metabolism · 2016Article
- Peripheral Adenosine A3 Receptor Activation Causes Regulated Hypothermia in Mice That Is Dependent on Central Histamine H1 Receptors.The Journal of pharmacology and experimental therapeutics · 2016Article
- Social huddling and physiological thermoregulation are related to melanism in the nocturnal barn owl.Oecologia · 2016Article
- Dopamine/Tyrosine Hydroxylase Neurons of the Hypothalamic Arcuate Nucleus Release GABA, Communicate with Dopaminergic and Other Arcuate Neurons, and Respond to Dynorphin, Met-Enkephalin, and Oxytocin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The melanocortin system regulates metabolic homeostasis and inflammation. Melanocortin agonists have contradictorily been reported to both increase and decrease metabolic rate and body temperature. We find two distinct physiologic responses occurring at similar doses. Intraperitoneal administration of the nonselective melanocortin agonist MTII causes a melanocortin-4 receptor (Mc4r)-mediated hypermetabolism/hyperthermia. This is preceded by a profound, transient hypometabolism/hypothermia that is preserved in mice lacking any one of Mc1r, Mc3r, Mc4r, or Mc5r. Three other melanocortin agonists also caused hypothermia, which is actively achieved via seeking a cool environment, vasodilation, and inhibition of brown adipose tissue thermogenesis. These results suggest that the hypometabolic/hypothermic effect of MTII is not due to a failure of thermoregulation. The hypometabolism/hypothermia was prevented by dopamine antagonists, and MTII selectively activated arcuate nucleus dopaminergic neurons, suggesting that these neurons may contribute to the hypometabolism/hypothermia. We propose that the hypometabolism/hypothermia is a regulated response, potentially beneficial during extreme physiologic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.