ArticleProceedings of the National Academy of Sciences of the United States of America2013
Melanocortin-4 receptor mutations paradoxically reduce preference for palatable foods.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- The Melanocortin System: A Promising Target for the Development of New Antidepressant Drugs.International journal of molecular sciences · 2023Review
- Genetic Val66Met BDNF Variant Increases Hyperphagia on Fat-rich Diets in Mice.Endocrinology · 2023Article
- Deletion of the Feeding-Induced Hepatokine TSK Ameliorates the Melanocortin Obesity Syndrome.Diabetes · 2021Article
- VIPergic neurons of the infralimbic and prelimbic cortices control palatable food intake through separate cognitive pathways.JCI insight · 2019Article
- Genetic variants help define the role of the MC4R C-terminus in signaling and cell surface stability.Scientific reports · 2018Article
- The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances.Neuroendocrinology · 2017Review
- Divergent effects of central melanocortin signalling on fat and sucrose preference in humans.Nature communications · 2016Article
- Moderate voluntary exercise attenuates the metabolic syndrome in melanocortin-4 receptor-deficient rats showing central dopaminergic dysregulation.Molecular metabolism · 2015Article
- Association between MC4R rs17782313 polymorphism and overeating behaviors.International journal of obesity (2005) · 2015Article
- Mitigating or exacerbating effects of maternal-fetal programming of female mice through the food choice environment.Endocrinology · 2015Article
- Inhibitory Effect of the Melanocortin Receptor Agonist Melanotan-II (MTII) on Feeding Depends on Dietary Fat Content and not Obesity in Rats on Free-Choice Diets.Frontiers in behavioral neuroscience · 2015Article
- The melanocortin-4 receptor is expressed in enteroendocrine L cells and regulates the release of peptide YY and glucagon-like peptide 1 in vivo.Cell metabolism · 2014Article
- Elimination of Kalrn expression in POMC cells reduces anxiety-like behavior and contextual fear learning.Hormones and behavior · 2014Article
- Association between melanocortin-4 receptor mutations and eating behaviors in obese patients: a case--control study.International journal of obesity (2005) · 2014Article
- The expression of MC4Rs in D1R neurons regulates food intake and locomotor sensitization to cocaine.Genes, brain, and behavior · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Haploinsufficiency of the melanocortin-4 receptor (MC4R) results in melanocortin obesity syndrome, the most common monogenic cause of severe early onset obesity in humans. The syndrome, which produces measurable hyperphagia, has focused attention on the role of MC4R in feeding behavior and macronutrient intake. Studies show that inhibition of MC4R signaling can acutely increase the consumption of high-fat foods. The current study examines the chronic feeding preferences of mice with deletion of one or both alleles of the MC4R to model the human syndrome. Using two-choice diet paradigms with high-fat or high-carbohydrate foods alongside normal chow, we show, paradoxically, that deletion of one allele has no effect, whereas deletion of both alleles of the MC4R actually decreases preference for palatable high-fat and high-sucrose foods, compared with wild-type mice. Nonetheless, we observed hyperphagic behavior from increased consumption of the low-fat standard chow when either heterozygous or homozygous mutant animals were presented with dietary variety. Thus, decreased MC4R signaling in melanocortin obesity syndrome consistently yields hyperphagia irrespective of the foods provided, but the hyperphagia appears driven by variety and/or novelty, rather than by a preference for high-fat or high-carbohydrate foodstuffs.
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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.