ArticleThe Journal of biological chemistry2011
Lack of cAMP-response element-binding protein 1 in the hypothalamus causes obesity.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- MicroRNA-7 regulates melanocortin circuits involved in mammalian energy homeostasis.Nature communications · 2022Article
- Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice.Ecotoxicology and environmental safety · 2022Article
- Inference for high-dimensional linear mixed-effects models: A quasi-likelihood approach.Journal of the American Statistical Association · 2022Article
- Article
- Gene expression atlas of energy balance brain regions.JCI insight · 2021Article
- The central melanocortin system and human obesity.Journal of molecular cell biology · 2020Review
- Cross-disorder genetic analyses implicate dopaminergic signaling as a biological link between Attention-Deficit/Hyperactivity Disorder and obesity measures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- The melanocortin pathway and control of appetite-progress and therapeutic implications.The Journal of endocrinology · 2019Review
- Computational analyses of obesity associated loci generated by genome-wide association studies.PloS one · 2018Article
- Article
- Exchange factors directly activated by cAMP mediate melanocortin 4 receptor-induced gene expression.Scientific reports · 2016Article
- Expression of a dominant negative PKA mutation in the kidney elicits a diabetes insipidus phenotype.American journal of physiology. Renal physiology · 2015Article
- CREB/TRH pathway in the central nervous system regulates energy expenditure in response to deprivation of an essential amino acid.International journal of obesity (2005) · 2015Article
- An essential role for the K+-dependent Na+/Ca2+-exchanger, NCKX4, in melanocortin-4-receptor-dependent satiety.The Journal of biological chemistry · 2014Article
- Ventromedial hypothalamus-specific Ptpn1 deletion exacerbates diet-induced obesity in female mice.The Journal of clinical investigation · 2014Article
- Family members CREB and CREM control thyrotropin-releasing hormone (TRH) expression in the hypothalamus.Molecular and cellular endocrinology · 2013Article
- Gsα deficiency in the paraventricular nucleus of the hypothalamus partially contributes to obesity associated with Gsα mutations.Endocrinology · 2012Article
- Effects of A-CREB, a dominant negative inhibitor of CREB, on the expression of c-fos and other immediate early genes in the rat SON during hyperosmotic stimulation in vivo.Brain research · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The melanocortin system in the hypothalamus controls food intake and energy expenditure. Its disruption causes severe obesity in mice and humans. cAMP-response element-binding protein 1 (CREB1) has been postulated to play an important role downstream of the melanocortin-4 receptor (MC4R), but this hypothesis has never been confirmed in vivo. To test this, we generated mice that lack CREB1 in SIM1-expressing neurons, of the paraventricular nucleus (PVN), which are known to be MC4R-positive. Interestingly, CREB1(ΔSIM1) mice developed obesity as a result of decreased energy expenditure and impairment in maintaining their core body temperature and not because of hyperphagia, defining a new role for CREB1 in the PVN. In addition, the lack of CREB1 in the PVN caused a reduction in vasopressin expression but did not affect adrenal or thyroid function. Surprisingly, MC4R function tested pharmacologically was normal in CREB1(ΔSIM1) mice, suggesting that CREB1 is not required for intact MC4R signaling. Thus CREB1 may affect other pathways that are implicated in the regulation of body weight.
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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.