Genetic, Epigenetic and Dietary Salt effects on Microbiota and Hypertension
Genetic, Epigenetic and Dietary Salt effects on Microbiota and Hypertension
批准号:
9921475
负责人:
BINA JOE
金额:
$66.65万
依托单位国家:
美国
项目类别:
财政年份:
2018
资助国家:
美国
项目状态:
已结题
起止时间:
2018-07-10 至 2022-04-30
关键词:
AddressAreaBacteriaBiochemicalBiological AvailabilityBlood PressureClinical ManagementCommunitiesCustomDahl Hypertensive RatsDataDevelopmentDietEnvironmentEnvironmental Risk FactorEpigenetic ProcessExhibitsFFAR3 geneFamilyFoundationsGenderGenerationsGenesGeneticGenomeGenomicsHumanHydrogen SulfideHypertensionHypotensionInbred SHR RatsIndividualInheritedInstitutesIntestinal permeabilityInvestigationLaboratoriesLinkMediatingMetabolicMetagenomicsMethodsMicroRNAsModelingMusPoliciesRat StrainsRattusReceptor GeneRegulationReportingResearchScienceSignal TransductionSiteSodium ChlorideSorting - Cell MovementSulfur Metabolism PathwayTechnologyTestingTissuesTransplantationUnited States National Institutes of HealthUntranslated RNAVeillonellaceaeVolatile Fatty AcidsWorkamino acid metabolismblood pressure reductionblood pressure regulationcarbohydrate metabolismdietary saltdifferential expressiondysbiosisepigenomeexpectationexperimental studyflexibilitygenetic variantgut microbiomegut microbiotahigh salt diethypertension controlimmunological statusinsightmetabolomicsmetatranscriptomicsmicrobialmicrobiomemicrobiome researchmicrobiotanoveloral microbial communityreceptorresponsesalt bacteriasalt intakesalt sensitivesalt sensitive hypertension
中文摘要
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英文摘要
7. Project Summary/Abstract
Genetics, epigenetics and environmental factors, dietary salt being the largest one, contributing to the
development of salt-sensitive hypertension is well known and intensely researched. Added to these factors, new
evidence from our laboratory and others indicates that gut microbiota constitute an important additional factor
influencing the extent of blood pressure of an individual. The host genome being `rigid', whereas the microbiome
being relatively flexible (because it is relatively easier to alter compositions of gut microbiota) makes it an
attractive proposition to contemplate microbiota-driven strategies for the clinical management of hypertension.
However, fundamental questions on how the genome, epigenome or dietary salt modify microbiota remain to be
determined. To address this point, the current proposal takes advantage of preliminary data generated with
studies on the genome and epigenome of the most popular salt-sensitive hypertensive rat model, the Dahl Salt-
sensitive (S) rat and, proposes to study how the host genetic and epigenetic factors interact with both gut and
oral microbiota to facilitate salt-sensitive BP regulation. To our knowledge, this will be the first methodical
investigation into the host genome-microbiome interactions in salt-sensitive hypertension. Our work will be
expected to provide fundamental insights into important, yet undiscovered new mechanisms governing the
genesis of hypertension involving the microbiota as a new player.
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