ArticleScientific reports2018
Y1 receptor deficiency in β-cells leads to increased adiposity and impaired glucose metabolism.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Neuropeptide Y Receptor Binding Profiles of Endogenous Ligands in the Presence and Absence of Sodium: A Panoramic View.ACS pharmacology & translational science · 2026Article
- Targeting the NPY/NPY1R signaling axis in mutant p53-dependent pancreatic cancer impairs metastasis.Science advances · 2025Article
- Article
- Recent advances in neuropeptide-related omics and gene editing: Spotlight on NPY and somatostatin and their roles in growth and food intake of fish.Frontiers in endocrinology · 2022Review
- PYY, a Therapeutic Option for Type 2 Diabetes?Clinical medicine insights. Endocrinology and diabetes · 2020Review
- Nonclassical Islet Peptides: Pancreatic and Extrapancreatic Actions.Clinical medicine insights. Endocrinology and diabetes · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Insulin secretion from pancreatic β-cells is critical for maintaining glucose homeostasis and deregulation of circulating insulin levels is associated with the development of metabolic diseases. While many factors have been implicated in the stimulation of insulin secretion, the mechanisms that subsequently reduce insulin secretion remain largely unexplored. Here we demonstrate that mice with β-cell specific ablation of the Y1 receptor exhibit significantly upregulated serum insulin levels associated with increased body weight and adiposity. Interestingly, when challenged with a high fat diet these β-cell specific Y1-deficient mice also develop hyperglycaemia and impaired glucose tolerance. This is most likely due to enhanced hepatic lipid synthesis, resulting in an increase of lipid accumulation in the liver. Together, our study demonstrates that Y1 receptor signaling negatively regulates insulin release, and pharmacological inhibition of Y1 receptor signalling for the treatment of non-insulin dependent diabetes should be taken into careful consideration.
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Registered trials
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