ArticleDiabetes2016
Neuronal Deletion of Ghrelin Receptor Almost Completely Prevents Diet-Induced Obesity.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 71 citations in OpenAlex.
- Autophagy in hypothalamic POMC and AgRP neurons: mechanisms and therapeutic implications for obesity.International journal of obesity (2005) · 2026Review
- GHSR suppression in neurons protects against aging-associated metabolic and cognitive impairments.GeroScience · 2026Article
- Myeloid GHSR Deficiency Protects Against Endotoxemia via Macrophage Mitochondrial Reprogramming.Biomedicines · 2026Article
- Article
- Review
- Serotonin neurons integrate GABA and dopamine inputs to regulate meal initiation.Metabolism: clinical and experimental · 2025Article
- Ghrelin Promotes Lipid Uptake into White Adipose Tissue via Endothelial Growth Hormone Secretagogue-Receptor in Mice.Nutrients · 2024Article
- Exploring the Antifibrotic Mechanisms of Ghrelin: Modulating TGF-β Signalling in Organ Fibrosis.Expert reviews in molecular medicine · 2024Review
- The effects of ghrelin and LEAP-2 in energy homeostasis are modulated by thermoneutrality, high-fat diet and aging.Journal of endocrinological investigation · 2024Article
- Genetic or pharmacological GHSR blockade has sexually dimorphic effects in rodents on a high-fat diet.Communications biology · 2024Article
- Neuronal ablation of GHSR mitigates diet-induced depression and memory impairment via AMPK-autophagy signaling-mediated inflammation.Frontiers in immunology · 2024Article
- Crosstalk between Gut Sensory Ghrelin Signaling and Adipose Tissue Sympathetic Outflow Regulates Metabolic Homeostasis.bioRxiv : the preprint server for biology · 2023Article
- Feeding-induced hepatokines and crosstalk with multi-organ: A novel therapeutic target for Type 2 diabetes.Frontiers in endocrinology · 2023Review
- The expression and function of growth hormone secretagogue receptor in immune cells: A current perspective.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Effects of Δ9-Tetrahydrocannibinol (THC) on Obesity at Different Stages of Life: A Literature Review.International journal of environmental research and public health · 2022Review
- Neuronal GHS-R Differentially Modulates Feeding Patterns under Normal and Obesogenic Conditions.Biomolecules · 2022Article
- Hypothalamic Estrogen Signaling and Adipose Tissue Metabolism in Energy Homeostasis.Frontiers in endocrinology · 2022Review
- From "Hunger Hormone" to "It's Complicated": Ghrelin Beyond Feeding Control.Physiology (Bethesda, Md.) · 2022Review
- [Quantitative analysis of differential proteins in liver tissues of patients with non-alcoholic steatohepatitis using iTRAQ technology].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- GHS-R suppression in adipose tissues protects against obesity and insulin resistance by regulating adipose angiogenesis and fibrosis.International journal of obesity (2005) · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Ghrelin signaling has major effects on energy and glucose homeostasis, but it is unknown whether ghrelin's functions are centrally and/or peripherally mediated. The ghrelin receptor, growth hormone secretagogue receptor (GHS-R), is highly expressed in the brain and detectable in some peripheral tissues. To understand the roles of neuronal GHS-R, we generated a mouse line where Ghsr gene is deleted in all neurons using synapsin 1 (Syn1)-Cre driver. Our data showed that neuronal Ghsr deletion abolishes ghrelin-induced spontaneous food intake but has no effect on total energy intake. Remarkably, neuronal Ghsr deletion almost completely prevented diet-induced obesity (DIO) and significantly improved insulin sensitivity. The neuronal Ghsr-deleted mice also showed improved metabolic flexibility, indicative of better adaption to different fuels. In addition, gene expression analysis suggested that hypothalamus and/or midbrain might be the sites that mediate the effects of GHS-R in thermogenesis and physical activity, respectively. Collectively, our results indicate that neuronal GHS-R is a crucial regulator of energy metabolism and a key mediator of DIO. Neuronal Ghsr deletion protects against DIO by regulating energy expenditure, not by energy intake. These novel findings suggest that suppressing central ghrelin signaling may serve as a unique antiobesity strategy.
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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.