ArticleScientific reports2017
Kidney Androgen-Regulated Protein (KAP) Transgenic Mice Are Protected Against High-Fat Diet Induced Metabolic Syndrome.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Transcriptome Analysis of BAFF/BAFF-R System in Murine Nephrotoxic Serum Nephritis.International journal of molecular sciences · 2024Article
- Prediction of cellular targets in diabetic kidney diseases with single-cell transcriptomic analysis of db/db mouse kidneys.Journal of cell communication and signaling · 2023Article
- Altered molecular signatures during kidney development after intrauterine growth restriction of different origins.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Genetic polymorphisms associated with reactive oxygen species and blood pressure regulation.The pharmacogenomics journal · 2019Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic Syndrome (MS) is reaching epidemic proportions with significant social and economical burden worldwide. Since the molecular basis of MS remains poorly defined, we investigated the impact of KAP, a kidney specific androgen-regulated gene, in the development of high fat-diet (hfd)-induced MS. Tg mice overexpressing KAP specifically in proximal tubule cells of the kidney exhibited reduced body weight and lower liver and adipose tissue weight compared to control littermates when fed a hfd. KAP Tg mice showed diminished adipocyte hypertrophy and reduced hepatic steatosis, significantly correlating with expression of relevant molecular markers and lower lipid content in liver. KAP transgenic were protected from hfd-induced insulin resistance, increased blood pressure and exhibited lower IL-6 serum levels and diminished expression of inflammatory markers in the adipose. Moreover, KAP was localized in the secretory pathway of proximal tubule cells and it is released to the extracellular media, preventing IL-6 induction and STAT-3 activation upon TNFα stimulation. We conclude that KAP, which might act as a hormone-like product in extra-renal tissues, protects Tg mice against hfd-induced MS by preventing inflammatory related events that are mediated, in part, through the IL-6 pathway.
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