ArticleMolecular metabolism2017
Endospanin1 affects oppositely body weight regulation and glucose homeostasis by differentially regulating central leptin signaling.
Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Recycling of Vps68 depends on retromer and Mvp1/SNX8.Biology open · 2026Article
- Whole-body deletion of Endospanin 1 protects from obesity-associated deleterious metabolic alterations.JCI insight · 2024Article
- Novel Noninvasive Approaches to the Treatment of Obesity: From Pharmacotherapy to Gene Therapy.Endocrine reviews · 2022Review
- Leptin brain entry via a tanycytic LepR-EGFR shuttle controls lipid metabolism and pancreas function.Nature metabolism · 2021Article
- From leptin to lasers: the past and present of mouse models of obesity.Expert opinion on drug discovery · 2021Article
- Leptin in Leanness and Obesity: JACC State-of-the-Art Review.Journal of the American College of Cardiology · 2021Review
- Effect of Leptin on Chronic Inflammatory Disorders: Insights to Therapeutic Target to Prevent Further Cardiovascular Complication.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Orphan GPR61, GPR62 and GPR135 receptors and the melatonin MTScientific reports · 2017Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hypothalamic arcuate nucleus (ARC) is a major integration center for energy and glucose homeostasis that responds to leptin. Resistance to leptin in the ARC is an important component of the development of obesity and type 2 diabetes. Recently, we showed that Endospanin1 (Endo1) is a negative regulator of the leptin receptor (OBR) that interacts with OBR and retains the receptor inside the cell, leading to a decreased activation of the anorectic STAT3 pathway. Endo1 is up-regulated in the ARC of high fat diet (HFD)-fed mice, and its silencing in the ARC of lean and obese mice prevents and reverses the development of obesity.
objectiveHerein we investigated whether decreased Endo1 expression in the hypothalamic ARC, associated with reduced obesity, could also ameliorate glucose homeostasis accordingly.
methodsWe studied glucose homeostasis in lean or obese mice silenced for Endo1 in the ARC via stereotactic injection of shRNA-expressing lentiviral vectors.
resultsWe observed that despite being leaner, Endo1-silenced mice showed impaired glucose homeostasis on HFD. Mechanistically, we show that Endo1 interacts with p85, the regulatory subunit of PI3K, and mediates leptin-induced PI3K activation.
conclusionsOur results thus define Endo1 as an important hypothalamic integrator of leptin signaling, and its silencing differentially regulates the OBR-dependent functions.
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