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临床试验/NCT03973996
NCT03973996已完成不适用

Gut-level Antiinflammatory Activities of Green Tea in Metabolic Syndrome

Ohio State University2 个研究点 分布在 1 个国家目标入组 46 人开始时间: 2019年7月1日最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
入组人数
46
试验地点
2
主要终点
Serum Endotoxin

研究概览

简要总结

This study evaluates dietary green tea extract to improve gut health and inflammation in persons with metabolic syndrome and healthy adults. Participants will complete two phases of intervention in random order in which they will consume green tea extract or placebo for one month and then switch to the opposite treatment for an additional month.

详细描述

Tea is the most abundantly consumed prepared beverage in the world. Green tea, containing catechins, exerts antiinflammatory activities. However, a fundamental gap exists concerning its intestinal-level targets that can prevent metabolic syndrome (MetS) development and progression. Studies in obese rodents indicate that green tea inhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) activation by limiting gut-derived endotoxin translocation to the portal circulation and decreasing hepatic Toll-like receptor-4 (TLR4) pro-inflammatory signaling. The objective of this clinical investigation is to establish evidence-based recommendations for green tea, based on improvements in endotoxemia and restored gut barrier function, that promote optimal health. The hypothesis is that green tea catechins function to limit metabolic endotoxemia by ameliorating gut dysbiosis-mediated inflammation that otherwise provokes intestinal permeability. This will be tested by conducting a double-blind, placebo-controlled, randomized-order, crossover trial in MetS and healthy persons to examine the efficacy of green tea on metabolic endotoxemia. Each treatment will be one-month in duration and separated by a washout period. The anticipated outcomes are expected to be of significance, because they will advance a dietary strategy to help avert MetS complications attributed to metabolic endotoxemia by establishing antiinflammatory prebiotic and antimicrobial bioactivities of catechins that promote intestinal health.

研究设计

研究类型
Interventional
分配方式
Randomized
干预模型
Crossover
主要目的
Prevention
盲法
Double (Participant, Investigator)

入排标准

年龄范围
18 Years 至 65 Years(Adult, Older Adult)
性别
All
接受健康志愿者

入选标准

  • 未提供

排除标准

  • 未提供

结局指标

主要结局

Serum Endotoxin

时间窗: Day 28

Data are biomarker fasting concentrations.

次要结局

  • Plasma Lipopolysaccharide-binding Protein(Day 28)
  • Plasma 3,4-γ-valerolactone(Day 28)
  • Plasma 3,4,5-γ-Valerolactone(Day 28)
  • Plasma Soluble Cluster of Differentiation-14(Day 28)
  • Urinary Lactulose/Mannitol Ratio(Day 28)
  • Urinary Sucralose/Erythritol Ratio(Day 28)
  • Plasma Interleukin-6(Day 28)
  • Fecal Calprotectin(Day 25-27 (pooled samples) of the 28-day intervention)
  • Fecal Myeloperoxidase(Day 25-27 (pooled samples) of the 28-day intervention)
  • Plasma Epigallocatechin Gallate(Day 28)
  • Plasma Epicatechin(Day 28)
  • Plasma Epicatechin Gallate(Day 28)
  • Plasma Triglyceride(Day 28)
  • Plasma Total Cholesterol(Day 28)
  • Serum Alanine Transaminase(Day 28)
  • Serum Aspartate Transaminase(Day 28)
  • Blood Hematocrit(Day 28)
  • Plasma Tumor Necrosis Factor-alpha(Day 28)
  • Fecal Butyrate(Days 25-27 (pooled samples) of the 28-day intervention)
  • Fecal Acetate(Days 25-27 (pooled samples) of the 28-day intervention)
  • Plasma Glucose(Day 28)
  • Plasma Insulin(Day 28)
  • Fecal Valeric Acid(Day 25-27 (pooled samples) from the 28-day intervention)
  • Fecal Hexanoic Acid(Day 25-27 (pooled samples) from the 28-day intervention)
  • Fecal Isobutyric Acid(Day 25-27 (pooled samples) from the 28-day intervention)
  • Fecal 2-Methylbutyric(Day 25-27 (pooled samples) of the 28-day intervention)
  • Fecal Isovaleric Acid(Day 25-27 (pooled samples) of the 28-day intervention)
  • Plasma Ascorbic Acid(Day 28)
  • Plasma Uric Acid(Day 28)

研究者

申办方类型
Other
责任方
Principal Investigator
主要研究者

Richard Bruno

Principal Investigator

Ohio State University

研究点 (2)

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