ArticleJournal of endocrinological investigation2013
Spironolactone prevents dietary-induced metabolic syndrome by inhibiting PI3-K/Akt and p38MAPK signaling pathways.
Article in Journal of endocrinological investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Qingda granule prevents obesity-induced hypertension and cardiac dysfunction by inhibiting adverse Akt signaling activation.Heliyon · 2022Article
- Single-nucleus RNA-Seq reveals singular gene signatures of human ductal cells during adaptation to insulin resistance.JCI insight · 2022Article
- Skin and metabolic syndrome: A review of the possible associations.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021Review
- Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure.European heart journal · 2020Article
- Molecular, Cellular, and Clinical Evidence That Sodium-Glucose Cotransporter 2 Inhibitors Act as Neurohormonal Antagonists When Used for the Treatment of Chronic Heart Failure.Journal of the American Heart Association · 2020Review
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAim of the study is to evaluate the impact of spironolactone (SPL) on indexes of metabolic syndrome (MS) and further investigate the mechanisms underlying its protective effects.
methodsA rat model of MS was established by administering a fat- and salt-enriched diet (FS diet). The occurrence of MS was examined by measurement of blood pressure (BP), aldosterone (ALD) content, blood lipid (BL), glucose and insulin levels. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Pancreatic gland tissue injury was assessed by β-cell apoptosis. Mineralocorticoid receptor (MR) activity, phosphatidylinositol 3- kinase/Akt (PI3-K/Akt), and phosphorylation of p38MAPK (Pp38MAPK) in pancreatic gland tissue were evaluated by western blot analysis.
resultsSPL prevented hypertension, and dyslipidemia during MS induced by the intake of FS diet, but had no effect on K+ and Na+ disturbances. Furthermore, SPL significantly attenuated ALD and MR expression levels after FS diet. Finally, SPL inhibited phosphorylation protein kinase B (p- PKB) activation in the pancreatic gland tissue, a downstream target of PI3-K, and phosphorylation of p38MAPK pathway, critical for cellular apoptosis.
conclusionsThis study demonstrates that SPL exerts a protective effect on hypertension and dyslipidemia. This protective effect may depend, at least in part, on MAPK and PI3-K pathways.
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