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Genetic Epidemiology Network of Salt Sensitivity (GenSalt)

ABSTRACT:

The GenSalt study is aimed at identifying novel genes which interact with the effect of dietary sodium and potassium intake or cold pressor on blood pressure.

PROVIDER: phs000784 | dbGaP |

SECONDARY ACCESSION(S): PRJNA258430PRJNA258429

REPOSITORIES: dbGaP

ACCESS DATA

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Dataset's files

Source:

			Action	DRS
	GapExchange_phs000784.v1.p1.xml	Xml
	dbGaPEx2.1.5.xsd	Other
	Study_Report.phs000784.GenSalt.v1.p1.MULTI.pdf	Pdf
	manifest_phs000784.GenSalt.v1.p1.c1.GRU.pdf	Pdf
	datadict_v2.xsl	Other

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NHLBI TOPMed: Genetic Epidemiology Network of Salt Sensitivity (GenSalt)

Project description:<p>The GenSalt study aims to identify genes which interact with dietary sodium and potassium intake to influence blood pressure in Han Chinese participants from rural north China. Whole genome sequencing will be conducted among 1,860 participants of the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) Study. We will work in collaboration with participating TOPMed studies to identify novel common, low-frequency and rare variants associated with an array of cardiometabolic phenotypes. In addition, we will explore the relation of low-frequency and rare variants with salt-sensitivity among GenSalt study participants.</p>

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Project description:The “aldosterone paradox” is a poorly understood physiological mechanism in which increases in the hormone aldosterone either serve to stabilize blood pressure by increasing sodium-chloride (NaCl) reabsorption or to excrete potassium (K+). Under low NaCl intake, abundance and activity of the thiazide-sensitive NaCl cotransporter NCC, expressed in the distal convoluted tubule (DCT), is high, whereas it is low during high K+ intake - leading to increased delivery of NaCl to downstream segments and increased electrogenic K+ secretion. Despite a critical role in blood pressure and K+ homeostasis, little is known about the molecular alterations in the DCT during the aldosterone paradox, and how they control NCC levels. The objective of this study was to define the proteome of the DCT and how it is modified by increased circulating aldosterone levels subsequent to long-term low dietary NaCl or high K+ intake.

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Effects of potassium supplementation and depletion in the development of salt-sensitive hypertension in male and female rats

Project description:The inverse effects that dietary sodium and potassium have on blood pressure have been known for some time. High sodium consumption is detrimental, while potassium supplementation is known to be beneficial, and the ratio of sodium/potassium consumption is also very important to consider when determining how these electrolytes affect salt-induced hypertension; however, the mechanisms behind the beneficial effects of potassium are still not yet entirely established. Inwardly rectifying potassium (Kir) channels have been shown to play a major role in potassium transport and homeostasis in the kidney and might contribute to these effects. Here we aimed to examine how different variations in the sodium/potassium ratio affect the development of salt-sensitive hypertension and how channels and transporters in the kidney are altered to accommodate these changes. We hypothesize that these diets will affect the development of salt-sensitive hypertension, and that Kir channels will play a major role in the renal adaptations to varying intakes of potassium

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Expression data in liver from germ-free and conventional mice fed lard or fish oil for 11 weeks

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Expression data from germ-free and conventional mice fed lard or fish oil for 11 weeks

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Project description:The sodium chloride cotransporters (NCC) and the epithelial sodium channel (ENaC) have been reported to be the main effectors of aldosterone in Na+ and Cl- reabsorption in the distal nephron and dietary K+ downregulates NCC. The Cl-/HCO3- exchanger pendrin has been revealed as a key role in maintaining extracellular fluid and electrolyte homeostasis by regulating Cl- reabsorption in the aldosterone-sensitive distal nephron working in tandem with ENaC and perhaps NCC. Pendrin-mediated Cl-/HCO3- exchange is stimulated in models of metabolic alkalosis (e.g. aldosterone administration or dietary NaHCO3 intake), and plasma K+ level is thought to negatively influence pendrin. In this study we used high-throughput proteomics and bioinformatics approaches to analyze urinary exosome contents isolated from patients undergoing fludrocortisone suppression test (FST, as a means of confirming or excluding primary aldosteronism [PA]) to examine the actions of administration of aldosterone analogs, NaCl and KCl orally on transmembrane proteins existing in urinary exosomes.

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Expression data in liver from germ-free and conventional mice fed lard or fish oil for 11 weeks

Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in the liver Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Liver samples were harvested at the end of the experiment and analyzed by microarray.

2016-02-29 | E-GEOD-73195 | biostudies-arrayexpress

Expression data from germ-free and conventional mice fed lard or fish oil for 11 weeks

Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT) Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Epididymal WAT samples were harvested at the end of the experiment and analyzed by microarray.

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