ArticleCanadian journal of physiology and pharmacology2020
Loss of endothelin type B receptor function improves insulin sensitivity in rats.
Article in Canadian journal of physiology and pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Dual endothelin receptor antagonism increases resting energy expenditure in people with increased adiposity.American journal of physiology. Endocrinology and metabolism · 2022Trial
- Metabolic Syndrome, Kidney-Related Adiposity, and Kidney Microcirculation: Unraveling the Damage.Biomedicines · 2024Review
- Adipocyte endothelin B receptor activation inhibits adiponectin production and causes insulin resistance in obese mice.Acta physiologica (Oxford, England) · 2024Article
- Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome.Molecular metabolism · 2024Article
- Antecubital venous endothelial ETB receptor protein expression is preserved with aging in men.American journal of physiology. Heart and circulatory physiology · 2024Article
- Endothelin receptor antagonism improves glucose tolerance and adipose tissue inflammation in an experimental model of systemic lupus erythematosus.American journal of physiology. Endocrinology and metabolism · 2023Article
- Endothelin receptor antagonism improves glucose handling, dyslipidemia, and adipose tissue inflammation in obese mice.Clinical science (London, England : 1979) · 2021Article
- Salt-Sensitivity of Blood Pressure and Insulin Resistance.Frontiers in physiology · 2021Review
- Endothelin-1 in the pathophysiology of obesity and insulin resistance.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
High salt intake (HS) is associated with obesity and insulin resistance. ET-1, a peptide released in response to HS, inhibits the actions of insulin on cultured adipocytes through ET-1 type B (ETB) receptors; however, the in vivo implications of ETB receptor activation on lipid metabolism and insulin resistance is unknown. We hypothesized that activation of ETB receptors in response to HS intake promotes dyslipidemia and insulin resistance. In normal salt (NS) fed rats, no significant difference in body mass or epididymal fat mass was observed between control and ETB deficient rats. After 2 weeks of HS, ETB-deficient rats had significantly lower body mass and epididymal fat mass compared to controls. Nonfasting plasma glucose was not different between genotypes; however, plasma insulin concentration was significantly lower in ETB-deficient rats compared to controls, suggesting improved insulin sensitivity. In addition, ETB-deficient rats had higher circulating free fatty acids in both NS and HS groups, with no difference in plasma triglycerides between genotypes. In a separate experiment, ETB-deficient rats had significantly lower fasting blood glucose and improved glucose and insulin tolerance compared to controls. These data suggest that ET-1 promotes adipose deposition and insulin resistance via the ETB receptor.
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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.