ArticleBiochemical and biophysical research communications2014
Profound and rapid reduction in body temperature induced by the melanocortin receptor agonists.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Sympathetic innervation of interscapular brown adipose tissue is not a predominant mediator of oxytocin-elicited reductions of body weight and adiposity in male diet-induced obese mice.Frontiers in endocrinology · 2024Article
- 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
- Red blood cell β-adrenergic receptors contribute to diet-induced energy expenditure by increasing O2 supply.JCI insight · 2017Article
- The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances.Neuroendocrinology · 2017Review
- Review
- Hypothalamic Non-AgRP, Non-POMC GABAergic Neurons Are Required for Postweaning Feeding and NPY Hyperphagia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
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Authors and funding
7 authors.
Funding
Abstract
The melanocortin receptor 4 (MC4R) plays a major role in body weight regulation and its agonist MTII has been widely used to study the role of MC4Rs in energy expenditure promotion and feeding reduction. Unexpectedly, we observed that intraperitoneal (i.p.) administration of MTII induced a rapid reduction in both body temperature and energy expenditure, which was independent of its effect on feeding and followed by a prolonged increase in energy expenditure. The rapid reduction was at least partly mediated by brain neurons since intracerebroventricular (icv) administration of alpha melanocyte-stimulating hormone, an endogenous melanocortin receptor agonist, produced a similar response. In addition, the body temperature-lowering effect of MTII was independent of the presence of MC4Rs, but in a similar fashion to the previously shown effect on body temperature by 5'AMP. Moreover, β-adrenergic receptors (β-ARs) were required for the recovery from low body temperature induced by MTII and further pharmacological studies showed that the MTII's effect on body temperature may be partially mediated by the vasopressin V1a receptors. Collectively, our results reveal a previously unappreciated role for the melanocortin pathway in rapidly lowering body temperature.
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