ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008
Glucocorticoid receptor haploinsufficiency causes hypertension and attenuates hypothalamic-pituitary-adrenal axis and blood pressure adaptions to high-fat diet.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 65 citations in OpenAlex.
- NR3C1 is required for normal somatotrope differentiation and Foxo1 expression in pituitary.Endocrinology · 2026Article
- Glucocorticoid Receptor Gene (Genes · 2023Article
- Role of glucocorticoid receptor mutations in hypertension and adrenal gland hyperplasia.Pflugers Archiv : European journal of physiology · 2022Review
- Crosstalk of hepatocyte nuclear factor 4a and glucocorticoid receptor in the regulation of lipid metabolism in mice fed a high-fat-high-sugar diet.Lipids in health and disease · 2022Article
- Salt-Sensitive Hypertension in GRInternational journal of molecular sciences · 2021Article
- Article
- Excess sucrose intake during pregnancy programs fetal brain glucocorticoid receptor expression in female but not male C57Bl/6J mice.Obesity science & practice · 2021Article
- Moderate Aerobic Exercise Training Prevents the Augmented Hepatic Glucocorticoid Response Induced by High-Fat Diet in Mice.International journal of molecular sciences · 2020Article
- Glucocorticoid receptor activation stimulates the sodium-chloride cotransporter and influences the diurnal rhythm of its phosphorylation.American journal of physiology. Renal physiology · 2019Article
- Renal and Blood Pressure Response to a High-Salt Diet in Mice With Reduced Global Expression of the Glucocorticoid Receptor.Frontiers in physiology · 2018Article
- Glucocorticoid receptor alters isovolumetric contraction and restrains cardiac fibrosis.The Journal of endocrinology · 2017Article
- Lung epithelial tip progenitors integrate glucocorticoid- and STAT3-mediated signals to control progeny fate.Development (Cambridge, England) · 2016Article
- The Potential of ACTH in the Genesis of Primary Aldosteronism.Frontiers in endocrinology · 2016Article
- NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.Nature genetics · 2015Article
- The multifaceted mineralocorticoid receptor.Comprehensive Physiology · 2014Review
- Role of the hypothalamic-pituitary-adrenal axis in developmental programming of health and disease.Frontiers in neuroendocrinology · 2013Review
- Transcriptional signatures of regulatory and toxic responses to benzo-[a]-pyrene exposure.BMC genomics · 2011Article
- Effect of exercise and high-fat diet on plasma adiponectin and nesfatin levels in mice.Experimental and therapeutic medicine · 2011Article
- Article
- Transcriptional and physiological responses to chronic ACTH treatment by the mouse kidney.Physiological genomics · 2010Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
Glucocorticoid hormones are critical to respond and adapt to stress. Genetic variations in the glucocorticoid receptor (GR) gene alter hypothalamic-pituitary-adrenal (HPA) axis activity and associate with hypertension and susceptibility to metabolic disease. Here we test the hypothesis that reduced GR density alters blood pressure and glucose and lipid homeostasis and limits adaption to obesogenic diet. Heterozygous GR(betageo/+) mice were generated from embryonic stem (ES) cells with a gene trap integration of a beta-galactosidase-neomycin phosphotransferase (betageo) cassette into the GR gene creating a transcriptionally inactive GR fusion protein. Although GR(betageo/+) mice have 50% less functional GR, they have normal lipid and glucose homeostasis due to compensatory HPA axis activation but are hypertensive due to activation of the renin-angiotensin-aldosterone system (RAAS). When challenged with a high-fat diet, weight gain, adiposity, and glucose intolerance were similarly increased in control and GR(betageo/+) mice, suggesting preserved control of intermediary metabolism and energy balance. However, whereas a high-fat diet caused HPA activation and increased blood pressure in control mice, these adaptions were attenuated or abolished in GR(betageo/+) mice. Thus, reduced GR density balanced by HPA activation leaves glucocorticoid functions unaffected but mineralocorticoid functions increased, causing hypertension. Importantly, reduced GR limits HPA and blood pressure adaptions to obesogenic diet.
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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.