ArticleMolecular metabolism2024
Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome.
Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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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
5 citing papers in PubMed, 5 citations in OpenAlex.
- Endothelial FUNDC1 regulates metabolic reprogramming and the obesity-diabetes transition through the SIRT3/GATA2/endothelin-1 axis.Nature communications · 2026Article
- Adipocyte-specific ETPhysiological reports · 2025Article
- The Role of Endothelin-1, Kidney Function and Diabetes in Patients With Coronary Artery Disease Underwent Percutaneous Coronary Intervention.Journal of diabetes · 2025Article
- Adipocyte endothelin B receptor activation inhibits adiponectin production and causes insulin resistance in obese mice.Acta physiologica (Oxford, England) · 2024Article
- Comprehensive bioinformatics analysis identifies metabolic and immune-related diagnostic biomarkers shared between diabetes and COPD using multi-omics and machine learning.Frontiers in endocrinology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEndothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome.
methodsWild type (etb
resultsCompared to etb
conclusionsETB deficiency confers protection from metabolic syndrome by counteracting glucose intolerance, dyslipidemia, and WAT accumulation due to enhanced energy expenditure, effects at least in part dependent on enhanced production of thyroid hormone/FGF21. ETB antagonism may therefore be a novel therapeutic approach in metabolic syndrome.
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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 Socratic graph.