ArticleAmerican journal of physiology. Endocrinology and metabolism2015
High-fat diet amplifies renal renin angiotensin system expression, blood pressure elevation, and renal dysfunction caused by Ceacam1 null deletion.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- ACE2 downregulation contributes to adverse cardiovascular and reproductive outcomes in female mice on high-fat diet.American journal of physiology. Heart and circulatory physiology · 2026Article
- Review
- Influence of Butyrate on Impaired Gene Expression in Colon from Patients with High Blood Pressure.International journal of molecular sciences · 2023Article
- Dahl Salt-Resistant Rat Is Protected against Hypertension during Diet-Induced Obesity.Nutrients · 2022Article
- Maternal High-Fat Diet and Offspring Hypertension.International journal of molecular sciences · 2022Review
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- Article
- Novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway.Scientific reports · 2021Article
- Treatment With Lisinopril Prevents the Early Progression of Glomerular Injury in Obese Dahl Salt-Sensitive Rats Independent of Lowering Arterial Pressure.Frontiers in physiology · 2021Article
- Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020Review
- High-fat diet exacerbates SIV pathogenesis and accelerates disease progression.The Journal of clinical investigation · 2019Article
- Obesity, kidney dysfunction and hypertension: mechanistic links.Nature reviews. Nephrology · 2019Review
- Interferon gamma induces inflammatory responses through the interaction of CEACAM1 and PI3K in airway epithelial cells.Journal of translational medicine · 2019Article
- The (pro)renin receptor: an emerging player in hypertension and metabolic syndrome.Kidney international · 2019Review
- Educational review: measurement of GFR in special populations.Pediatric nephrology (Berlin, Germany) · 2018Review
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAMl), a substrate of the insulin receptor tyrosine kinase, regulates insulin action by promoting insulin clearance. Global null mutation of Ceacam1 gene (Cc1(-/-)) results in features of the metabolic syndrome, including insulin resistance, hyperinsulinemia, visceral adiposity, elevated blood pressure, and albuminuria. It also causes activation of the renal renin-angiotensin system (RAS). In the current study, we tested the hypothesis that high-fat diet enhances the expression of RAS components. Three-month-old wild-type (Cc1(+/+)) and Cc1(-/-) mice were fed either a regular or a high-fat diet for 8 wk. At baseline under regular feeding conditions, Cc1(-/-) mice exhibited higher blood pressure, urine albumin-to-creatinine ratio (UACR), and renal expression of angiotensinogen, renin/prorenin, angiotensin-converting enzyme, (pro)renin receptor, angiotensin subtype AT1 receptor, angiotensin II, and elevated PI3K phosphorylation, as detected by p85α (Tyr(508)) immunostaining, inflammatory response, and the expression of collagen I and collagen III. In Cc1(+/+) mice, high-fat diet increased blood pressure, UACR, the expression of angiotensin-converting enzyme and angiotensin II, PI3K phosphorylation, inflammatory response, and the expression of collagen I and collagen III. In Cc1(-/-) mice, high-fat intake further amplified these parameters. Immunohistochemical staining showed increased p-PI3K p85α (Tyr(508)) expression in renal glomeruli, proximal, distal, and collecting tubules of Cc1(-/-) mice fed a high-fat diet. Together, this demonstrates that high-fat diet amplifies the permissive effect of Ceacam1 deletion on renal expression of all RAS components, PI3K phosphorylation, inflammation, and fibrosis.
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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.