Impact of the gut microbiome and diet on change in insulin homeostasis and cardiometabolic risk
肠道微生物组和饮食对胰岛素稳态变化和心脏代谢风险的影响
基本信息
- 批准号:9924526
- 负责人:
- 金额:$ 58.34万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-04-01 至 2022-03-31
- 项目状态:已结题
- 来源:
- 关键词:AdultAffectAfrican AmericanAntibioticsAntiinflammatory EffectBacteriaBeveragesBiological AssayBlood CirculationButyratesC-PeptideClinic VisitsCollectionCommunitiesComplexDataDeteriorationDevelopmentDiabetes MellitusDiagnosticDietDietary ComponentDietary FiberDietary PracticesElementsEndocrinologyEquilibriumEthnic groupEvaluationExcisionFailureFastingFecesFishesFoodFrequenciesFunctional disorderGastrointestinal tract structureGlucoseHarvestHomeostasisHourHumanImpairmentIndividualInsulinInsulin ResistanceIntakeKnowledgeLeadMeasurementMeasuresMeatMediatingMetabolicMetabolismMetagenomicsMicrobiologyMissionModelingModificationNational Institute of Diabetes and Digestive and Kidney DiseasesNon-Insulin-Dependent Diabetes MellitusNot Hispanic or LatinoNutritionalNutsOralOrganismParticipantPhenotypePopulationPotatoPrediabetes syndromePreventionPreventive treatmentProbioticsProcessed MeatsProspective StudiesProspective cohort studyProtocols documentationPublic HealthQuestionnairesRaceRecombinant DNAResearchResearch PersonnelRibosomal DNARiskRisk FactorsRoleSamplingSeedsStandardizationTestingTimeTissuesVariantVisitVolatile Fatty Acidsbaseblood glucose regulationcardiometabolic riskcohortdiabetes riskdiabetogenicexperiencefruits and vegetablesglucose tolerancegood dietgut bacteriagut microbiomegut microbiotaindividual variationinnovationinsightinsulin secretioninsulin sensitivityintestinal barriermetagenomic sequencingmicrobialmicrobiomemicrobiotamicroorganismnon-diabeticnovelnutritionobesity riskoral glucose tolerancerecruitstool samplesugartrait
项目摘要
PROJECT SUMMARY
Failure to increase insulin secretion and reduce insulin clearance to overcome tissue insulin resistance leads to
the development of type 2 diabetes (T2D). Components of the insulin axis (insulin sensitivity, insulin secretion,
insulin clearance) are critical to the genesis of T2D, yet the factors that account for their dysfunction and their
interactions with other factors are not understood. The nutritional components of diet pass through the
intestinal barrier in a complex interaction with the gut microbiota (the microbiome) to impact glucose
homeostasis. Our hypothesis is that change in three insulin axis traits is associated with gut microbial
composition and function, and this association is modified by dietary components (e.g., whole grains, red meat)
including systemic short chain fatty acids produced by the gut microbiota. This study will assess the insulin
axis, the gut microbiota and diet in a cohort of 500 non-diabetic adults (half African American, half non-
Hispanic White) over 2.5 years (sampled at three time points). Specific Aim 1 will administer, at each clinic
visit, a 75-g oral glucose challenge with 0, 30, 60, 120 min measurements (of insulin, glucose, and C-peptide)
to determine insulin sensitivity, secretion, and clearance; habitual diet will be determined by use of a validated
Food Frequency Questionnaire. Specific Aim 2 will characterize the gut microbiome for each participant by
performing 16S rDNA sequencing and low-pass metagenomic sequencing on stool samples collected at all
three visits. Together, these data will test the hypothesis that increased insulin resistance, impaired insulin
secretion, and decreased insulin clearance (all diabetogenic changes) developing over time are associated
with a reduced (at baseline) or declining (over time) abundance of short chain fatty acid-producing bacteria in
the gut, in part attributable to unhealthy dietary patterns. Specific Aim 3 will utilize samples collected at the
three time points to probe the functional profile of the gut microbiome by conducting deep metagenomic
sequencing and assessment of circulating short chain fatty acid levels in a subset of 180 individuals with
extreme changes (increase and decrease) versus those with no change in insulin axis traits, thereby identifying
microbial functions that underlie change versus stability in insulin axis traits. This study has high impact,
yielding knowledge that can lead to novel microbiome-based diagnostics, prevention, and/or treatment
measures (e.g., specific diets; antibiotic or probiotic treatment) to reduce the public health burden of T2D.
项目摘要
不能增加胰岛素分泌和降低胰岛素清除率以克服组织胰岛素抵抗导致
2型糖尿病(T2 D)的发展。胰岛素轴的组成部分(胰岛素敏感性,胰岛素分泌,
胰岛素清除率)对T2 D的发生至关重要,但导致其功能障碍及其
与其他因素的相互作用尚不清楚。饮食中的营养成分通过
肠道屏障与肠道微生物群(微生物组)复杂相互作用,影响葡萄糖
体内平衡我们的假设是三个胰岛素轴特征的变化与肠道微生物相关
组成和功能,并且这种关联通过膳食组分(例如,全谷物,红肉)
包括由肠道微生物群产生的系统性短链脂肪酸。这项研究将评估胰岛素
轴,肠道微生物群和饮食在一个队列的500名非糖尿病成年人(一半非洲裔美国人,一半非
西班牙裔白色)超过2.5年(在三个时间点采样)。具体目标1将在每个诊所实施
访视,75 g口服葡萄糖激发,0、30、60、120 min测量(胰岛素、葡萄糖和C肽)
确定胰岛素敏感性、分泌和清除;将使用经验证的
食物频率问卷。具体目标2将通过以下方式表征每位参与者的肠道微生物组:
对收集的粪便样品进行16 S rDNA测序和低通宏基因组测序,
三次访问。总之,这些数据将检验增加胰岛素抵抗,受损胰岛素
随着时间的推移,胰岛素分泌和胰岛素清除率降低(所有致糖尿病变化)与
随着减少的(在基线)或下降的(随着时间的推移)丰度的短链脂肪酸生产细菌,
肠道,部分原因是不健康的饮食模式。具体目标3将利用在
三个时间点,通过进行深层宏基因组研究来探测肠道微生物组的功能谱
对180名患有高脂血症的个体的循环短链脂肪酸水平进行测序和评估,
极端变化(增加和减少)与胰岛素轴性状无变化的人相比,从而确定
微生物功能的变化与胰岛素轴性状的稳定性。这项研究影响很大,
产生可以导致新的基于微生物组的诊断、预防和/或治疗的知识
测量(例如,特定饮食;抗生素或益生菌治疗),以减少T2 D的公共卫生负担。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Mark Goodarzi其他文献
Mark Goodarzi的其他文献
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{{ truncateString('Mark Goodarzi', 18)}}的其他基金
Southern California Clinical Center of the Type 1 Diabetes in Acute Pancreatitis Consortium
南加州 1 型糖尿病急性胰腺炎联盟临床中心
- 批准号:
10670168 - 财政年份:2020
- 资助金额:
$ 58.34万 - 项目类别:
Southern California Clinical Center of the Type 1 Diabetes in Acute Pancreatitis Consortium
南加州 1 型糖尿病急性胰腺炎联盟临床中心
- 批准号:
10461111 - 财政年份:2020
- 资助金额:
$ 58.34万 - 项目类别:
Southern California Clinical Center of the Type 1 Diabetes in Acute Pancreatitis Consortium
南加州 1 型糖尿病急性胰腺炎联盟临床中心
- 批准号:
10264920 - 财政年份:2020
- 资助金额:
$ 58.34万 - 项目类别:
Greater Los Angeles Clinical Center of the Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer
慢性胰腺炎、糖尿病和胰腺癌研究联盟大洛杉矶临床中心
- 批准号:
10657640 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Greater Los Angeles Clinical Center of the Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer
慢性胰腺炎、糖尿病和胰腺癌研究联盟大洛杉矶临床中心
- 批准号:
10263513 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Greater Los Angeles Clinical Center of the Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer
慢性胰腺炎、糖尿病和胰腺癌研究联盟大洛杉矶临床中心
- 批准号:
10447160 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Pathophysiology, Epidemiology, and Prevention of Pancreatogenic Diabetes
胰源性糖尿病的病理生理学、流行病学和预防
- 批准号:
9150584 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Pathophysiology, Epidemiology, and Prevention of Pancreatogenic Diabetes - Administrative Supplement
胰源性糖尿病的病理生理学、流行病学和预防 - 行政补充
- 批准号:
9987256 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Pathophysiology, Epidemiology, and Prevention of Pancreatogenic Diabetes
胰源性糖尿病的病理生理学、流行病学和预防
- 批准号:
9352327 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
Greater Los Angeles Clinical Center of the Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer
慢性胰腺炎、糖尿病和胰腺癌研究联盟大洛杉矶临床中心
- 批准号:
10252045 - 财政年份:2015
- 资助金额:
$ 58.34万 - 项目类别:
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