ArticleThe Journal of clinical investigation2002
Hypothalamic Y2 receptors regulate bone formation.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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Who cites it
155 citing papers in PubMed, 393 citations in OpenAlex.
- Neuroendocrine and neural control of bone mass in health and disease.The Journal of clinical investigation · 2026Review
- Neural regulation of bone: from central neural circuits to peripheral innervation of the skeletal stem cell niche.Bone research · 2026Review
- Advances in the regulation of bone metabolism by central nuclei: a new perspective on the brain-bone axis.Frontiers in neuroscience · 2026Review
- Cellular and Molecular Neuro-Bone Cell Interactions Drive Alveolar Bone Remodeling During Orthodontic Mechanical Loading.International journal of biological sciences · 2026Review
- Neuropeptide Y signaling in osteoarthritis pain: neuroimmune mechanisms, joint remodeling, and translational opportunities.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- Functional and evolutionary characteristics of human genes encoding cell surface receptors involved in the regulation of appetite.Journal of integrative bioinformatics · 2025Article
- Characterization of [ACS pharmacology & translational science · 2025Article
- A Procedural Overview of the Involvement of Small Molecules in the Nervous System in the Regulation of Bone Healing.International journal of nanomedicine · 2025Review
- Neuropeptides as regulators of bone metabolism: from molecular mechanisms to traditional Chinese medicine intervention strategies.Frontiers in pharmacology · 2025Review
- Unraveling the Intricacies of OPG/RANKL/RANK Biology and Its Implications in Neurological Disorders-A Comprehensive Literature Review.Molecular neurobiology · 2024Review
- Neuropeptide Y Y2 Receptors in Sensory Neurons Tonically Suppress Nociception and Itch but Facilitate Postsurgical and Neuropathic Pain Hypersensitivity.Anesthesiology · 2024Article
- The role of immune cells settled in the bone marrow on adult hematopoietic stem cells.Cellular and molecular life sciences : CMLS · 2024Review
- The brain-bone axis: unraveling the complex interplay between the central nervous system and skeletal metabolism.European journal of medical research · 2024Review
- Revealing brain cell-stratified causality through dissecting causal variants according to their cell-type-specific effects on gene expression.Nature communications · 2024Article
- The role of adipokines in osteoporosis management: a mini review.Frontiers in endocrinology · 2024Review
- Interoceptive regulation of skeletal tissue homeostasis and repair.Bone research · 2023Review
- Causal associations of brain structure with bone mineral density: a large-scale genetic correlation study.Bone research · 2023Article
- Low bone mineral density is found in low weight female youth with avoidant/restrictive food intake disorder and associated with higher PYY levels.Journal of eating disorders · 2023Article
- Application of the neuropeptide NPVF to enhance angiogenesis and osteogenesis in bone regeneration.Communications biology · 2023Article
95 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropeptide Y (NPY) is a downstream modulator of leptin action, possibly at the level of the arcuate nucleus where NPY neurons are known to express both leptin receptors and Y2 receptors. In addition to the well-described role of NPY and leptin in energy balance and obesity, intracerebroventricular administration of NPY or leptin also causes bone loss. Here we show that Y2 receptor-deficient mice have a twofold increase in trabecular bone volume as well as greater trabecular number and thickness compared with control mice. We also demonstrate that central Y2 receptors are crucial for this process, since selective deletion of hypothalamic Y2 receptors in mature conditional Y2 knockout mice results in an identical increase in trabecular bone volume within 5 weeks. This hypothalamus-specific Y2 receptor deletion stimulates osteoblast activity and increases the rate of bone mineralization and formation, with no effect on osteoblast or osteoclast surface measurements. The lack of any changes in plasma total calcium, leptinemia, or hypothalamo-pituitary-corticotropic, -thyrotropic, -somatotropic, or -gonadotropic output suggests that Y2 receptors do not modulate bone formation by humoral mechanisms, and that alteration of autonomic function through hypothalamic Y2 receptors may play a key role in a major central regulatory circuit of bone formation.
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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.