Melanocortin-4 Receptors Expressed by Cholinergic Neurons Regulate Energy Balance and Glucose Homeostasis
Open accessAbstract
Melanocortin-4 receptor (MC4R) mutations cause dysregulation of energy balance and hyperinsulinemia. We have used mouse models to study the physiological roles of extrahypothalamic MC4Rs. Re-expression of MC4Rs in cholinergic neurons (ChAT-Cre, loxTB MC4R mice) modestly reduced body weight gain without altering food intake and was sufficient to normalize energy expenditure and attenuate hyperglycemia and hyperinsulinemia. In contrast, restoration of MC4R expression in brainstem neurons including those in the dorsal motor nucleus of the vagus (Phox2b-Cre, loxTB MC4R mice) was sufficient to attenuate hyperinsulinemia, while the hyperglycemia and energy balance were not normalized. Additionally, hepatic insulin action and insulin-mediated suppression of hepatic glucose production were improved in ChAT-Cre, loxTB MC4R mice. These findings suggest that MC4Rs expressed by cholinergic neurons regulate energy expenditure and hepatic glucose production. Our results also provide further evidence of the dissociation in pathways mediating the effects of melanocortins on energy balance and glucose homeostasis.
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MC4R is a transmembrane G protein-coupled receptor found in greatest abundance in central nervous system neuronal populations important for autonomic regulation, including the nucleus of the solitary tract, dorsal motor nucleus of the vagus, paraventricular nucleus, lateral hypothalamus and preganglionic sympathetic neurons of the intermediolateral cell column.
“MC4R is a transmembrane G protein-coupled receptor that is found in greatest abundance in CNS neuronal populations that are important for autonomic regulation, including the NTS, dorsal motor nucleus of the vagus, PVN, lateral hypothalamus and preganglionic sympathetic neurons of the IML192,207 (FIG. 5a).”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [207]
MC4R activation in cholinergic preganglionic parasympathetic and sympathetic neurons may contribute to autonomic regulation and increased blood pressure in obese mice fed a high fat diet.
“There is evidence, however, that MC4R activation in cholinergic preganglionic parasympathetic and sympathetic neurons [35] may contribute to autonomic regulation and increased BP in obese mice fed a high fat diet, as discussed later.”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [35]
The central nervous system regions with the greatest abundance of MC4R are the hypothalamus and hindbrain preganglionic sympathetic neurons of the nucleus tractus solitarius, dorsal motor nucleus of the vagus and intermediolateral nucleus, which are important sites for autonomic regulation.
“The CNS regions with the greatest abundance of MC4R are the hypothalamus and hindbrain preganglionic sympathetic neurons of the NTS, DMV and IML [35] (Figure 3) which are important sites for autonomic regulation.”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [35]
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Self-citation
- Authors
- Rossi, J., Balthasar, N., Olson, D., Scott, M., Berglund, E., Lee, C. E., Choi, M. J., Lauzon, D., Lowell, B. B., & Elmquist, J. K.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Lowell, Bradford B.
- Elmquist, Joel K.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 13
- Issue
- 2
- Pages
- 195-204
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3033043
- OpenAlex
- W2086991865
- Cited by
- 672
- References
- 50
- Citations by year
- 2026: 37 · 2025: 53 · 2024: 52 · 2023: 39 · 2022: 67 · 2021: 41 · 2020: 40 · 2019: 42 · 2018: 45 · 2017: 48 · 2016: 48 · 2015: 43 · 2014: 47 · 2013: 29 · 2012: 27
- FWCI
- 17.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Funders
- University of Texas Southwestern Medical Center
- Wellcome Trust
- Boston Area Diabetes Endocrinology Research Center
- British Heart Foundation (FS/06/057)
- National Institutes of Health (1tl1dk081181-01)
- Boston Nutrition Obesity Research Center, Boston University
- Engineering and Physical Sciences Research Council (EP/E500110/1)
- National Institute on Drug Abuse (K99DA024719)
- National Institute of Diabetes and Digestive and Kidney Diseases (TL1-DK081181, P30DK057521, PL1DK081182, RL1DK081185, R01DK075632, R56DK071320, R01DK53301, R01DK053301, P30DK046200, K08DK071561, R01DK071320, DK071320, R37DK053301, R01DK056690, K99DK024719-02, 5TL1DK081181)
- National Institute of Dental and Craniofacial Research (UL1DE019584)
- National Center for Research Resources (UL1RR024923)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- melanocortin-4 receptor, cholinergic neurons, energy balance, glucose homeostasis, hyperinsulinemia, hyperglycemia, energy expenditure, hepatic glucose production, hepatic insulin action, dorsal motor nucleus of the vagus, brainstem neurons, weight gain, melanocortin signaling
- MeSH terms
- Animals, Choline O-Acetyltransferase, Eating, Energy Metabolism, Glucose, Homeostasis, Hyperglycemia, Hyperinsulinism, Mice, Transgenic, Neurons, Integrases, Receptor, Melanocortin, Type 4, Mice
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