ArticleProceedings of the National Academy of Sciences of the United States of America2012
Melanocortin-3 receptor regulates the normal fasting response.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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Who cites it
60 citing papers in PubMed.
- Sex-differential associations of MC3R p.F45S with human metabolic profile.Journal of neuroendocrinology · 2026Article
- Dual activation of MC3R and MC4R drives weight loss and reduces food intake in male primates with obesity.Nature communications · 2026Article
- Effect of a partial loss of function MC3R mutation on MC3R+GHSR-1A heterodimer activity and RNF11 regulation.Journal of endocrinological investigation · 2026Article
- The melanocortin receptors as targets for general obesity: contextualizing clinical failures and analyzing future perspectives.Frontiers in endocrinology · 2026Review
- Cross-species studies implicate the melanocortin 3 receptor more strongly in the control of pubertal development than energy balance.Molecular metabolism · 2026Article
- Melanocortin 3 receptor regulates hepatic autophagy and systemic adiposity.Nature communications · 2025Article
- Pro-Opiomelanocortin and Melanocortin Receptor 3 and 4 Mutations in Genetic Obesity.Biomolecules · 2025Review
- Medial hypothalamic MC3R signalling regulates energy rheostasis in adult mice.The Journal of physiology · 2025Article
- Fasting-induced activity changes in MC3R neurons of the paraventricular nucleus of the thalamus.Life science alliance · 2024Article
- Hypothalamic AgRP neurons regulate the hyperphagia of lactation.Molecular metabolism · 2024Article
- Subthreshold activation of the melanocortin system causes generalized sensitization to anorectic agents in mice.The Journal of clinical investigation · 2024Article
- Neuroanatomical dissection of the MC3R circuitry regulating energy rheostasis.bioRxiv : the preprint server for biology · 2024Article
- Melanocortin-3 receptor expression in AgRP neurons is required for normal activation of the neurons in response to energy deficiency.Cell reports · 2023Article
- Targeting the central melanocortin system for the treatment of metabolic disorders.Nature reviews. Endocrinology · 2023Review
- Monocytes re-enter the bone marrow during fasting and alter the host response to infection.Immunity · 2023Article
- Specific Functions of Melanocortin 3 Receptor (MC3R)Journal of clinical research in pediatric endocrinology · 2023Review
- Atypical pituitary hormone-target tissue axis.Frontiers of medicine · 2023Review
- Glucagon receptor signaling at white adipose tissue does not regulate lipolysis.American journal of physiology. Endocrinology and metabolism · 2022Article
- Competing paradigms of obesity pathogenesis: energy balance versus carbohydrate-insulin models.European journal of clinical nutrition · 2022Review
- Melanocortin-5 Receptor: Pharmacology and Its Regulation of Energy Metabolism.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The melanocortin-3 receptor-deficient (MC3-R(-/-)) mouse exhibits mild obesity without hyperphagia or hypometabolism. MC3-R deletion is reported to increase adiposity, reduce lean mass and white adipose tissue inflammation, and increase sensitivity to salt-induced hypertension. We show here that the MC3-R(-/-) mouse exhibits defective fasting-induced white adipose tissue lipolysis, fasting-induced liver triglyceride accumulation, fasting-induced refeeding, and fasting-induced regulation of the adipostatic and hypothalamic-adrenal-pituitary axes. Close examination of the hypothalamic-pituitary-adrenal axis showed that MC3-R(-/-) mice exhibit elevated nadir corticosterone as well as a blunted fasting-induced activation of the axis. The previously described phenotypes of this animal and the reduced bone density reported here parallel those of Cushing syndrome. Thus, MC3-R is required for communicating nutritional status to both central and peripheral tissues involved in nutrient partitioning, and this defect explains much of the metabolic phenotype in the model.
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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.