ArticleMetabolism: clinical and experimental2013
Direct renin inhibition modulates insulin resistance in caveolin-1-deficient mice.
Article in Metabolism: clinical and experimental, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Caveolin-1 deficiency improved glucose metabolism via modulation of β-cell autophagy in high-fat diet-fed mice.The Journal of biological chemistry · 2026Article
- Article
- Caveolin Gene, a Possible Risk Factor for Metabolic Syndrome in Humans: A Systematic Review and Meta-Analysis.International journal of preventive medicine · 2025Review
- Effects of Mineralocorticoid Receptor Blockade and Statins on Kidney Injury Marker 1 (KIM-1) in Female Rats Receiving L-NAME and Angiotensin II.International journal of molecular sciences · 2023Article
- Article
- Are caveolin-1 minor alleles more likely to be risk alleles in insulin resistance mechanisms in metabolic diseases?BMC research notes · 2021Article
- Caveolin-1 (CAV-1) up regulation in metabolic syndrome: all roads leading to the same end.Molecular biology reports · 2020Article
- mTORC1 Deficiency Modifies Volume Homeostatic Responses to Dietary Sodium in a Sex-Specific Manner.Endocrinology · 2020Article
- Histone demethylase LSD1 deficiency and biological sex: impact on blood pressure and aldosterone production.The Journal of endocrinology · 2019Article
- Dietary Fatty Acid Saturation Modulates Sphingosine-1-Phosphate-Mediated Vascular Function.Journal of diabetes research · 2019Article
- A Common Variation in the Caveolin 1 Gene Is Associated with High Serum Triglycerides and Metabolic Syndrome in an Admixed Latin American Population.Metabolic syndrome and related disorders · 2018Article
- Caloric restriction improves glucose homeostasis, yet increases cardiometabolic risk in caveolin-1-deficient mice.Metabolism: clinical and experimental · 2018Article
- Combined Salt and Caloric Restrictions: Potential Adverse Outcomes.Journal of the American Heart Association · 2017Article
- Nonnuclear Estrogen Receptor Activation Improves Hepatic Steatosis in Female Mice.Endocrinology · 2016Article
- Caveolin 1 Modulates Aldosterone-Mediated Pathways of Glucose and Lipid Homeostasis.Journal of the American Heart Association · 2016Article
- A prevalent caveolin-1 gene variant is associated with the metabolic syndrome in Caucasians and Hispanics.Metabolism: clinical and experimental · 2015Article
- Variants in striatin gene are associated with salt-sensitive blood pressure in mice and humans.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Role of caveolin 1 in AT1a receptor-mediated uptake of angiotensin II in the proximal tubule of the kidney.American journal of physiology. Renal physiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveTo test the hypothesis that aliskiren improves the metabolic phenotype in a genetic mouse model of the metabolic syndrome (the caveolin-1 (cav-1) knock out (KO) mouse). MATERIALS/
methodsEleven-week-old cav-1 KO and genetically matched wild-type (WT) mice were randomized to three treatment groups: placebo (n=8/group), amlodipine (6 mg/kg/day, n=18/ group), and aliskiren (50 mg/kg/day, n=18/ group). After three weeks of treatment, all treatment groups were assessed for several measures of insulin resistance (fasting insulin and glucose, HOMA-IR, and the response to an intraperitoneal glucose tolerance test (ipGTT)) as well as for triglyceride levels and the blood pressure response to treatment.
resultsTreatment with aliskiren did not affect the ipGTT response but significantly lowered the HOMA-IR and insulin levels in cav-1 KO mice. However, treatment with amlodipine significantly degraded the ipGTT response, as well as the HOMA-IR and insulin levels in the cav-1 KO mice. Aliskiren also significantly lowered triglyceride levels in the cav-1 KO but not in the WT mice. Moreover, aliskiren treatment had a significantly greater effect on blood pressure readings in the cav-1 KO vs. WT mice, and was marginally more effective than amlodipine.
conclusionsOur results support the hypothesis that aliskiren reduces insulin resistance as indicated by improved HOMA-IR in cav-1 KO mice whereas amlodipine treatment resulted in changes consistent with increased insulin resistance. In addition, aliskiren was substantially more effective in lowering blood pressure in the cav-1 KO mouse model than in WT mice and marginally more effective than amlodipine.
Indexed as
Identifiers
What OpenQuestion holds
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.