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NCT Number: NCT05235464

High Protein Diet and Atherosclerosis

Atherosclerosis is the underlying cause of the majority of cardiovascular diseases, including myocardial infarction and strokes, and results in tremendous morbidity and mortality. A Western-type diet is a major risk factor for atherosclerosis because of the high saturated fat, cholesterol, and refined carbohydrate contents. Dietary strategies to reduce cardiovascular disease burden therefore focus on restriction of saturated fat, cholesterol, and refined carbohydrates whereas "lean" protein intake is recommended and has become popular. However, results from studies conducted in animal models suggest high dietary protein intake is also atherogenic. The investigators' extensive preliminary data in animal models show that dietary protein increases atherosclerotic plaque formation and size and promotes necrotic core formation, a characteristic of rupture-prone plaques. The goal of the current proposal is to provide deeper insights into the relationship between protein intake and the pathogenesis of atherosclerosis by studying the mechanisms involved in protein-mediated atherogenesis and formation of necrotic plaques. The overarching hypothesis is that high protein intake drives atherosclerosis via leucine-mediated mTORC1 signaling in macrophages, which inhibits macrophage mitophagy and aggrephagy and stimulates macrophage proliferation. Furthermore, the investigators hypothesize that proteins from animal sources are more atherogenic than proteins from plant sources, because animal proteins contain more leucine than plant proteins. The investigators will test these hypotheses by using a sophisticated array of experimental strategies, including assays in primary macrophages and human monocyte-derived macrophages and genetically engineered mouse models. In addition, they will begin to translate the results obtained in vitro and in animals to people, and explore approaches to pharmacologically target the pro-atherogenic pathways as novel cardiovascular therapeutics. This proposal represents a paradigm shift in how a Western-type diet affects vascular health which has important implications since many adults in Western societies consume excess protein and dietary protein is heavily marketed for its presumed beneficial health effects.

Recruiting

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Key information

Age range

45 year–75 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

University of Missouri School of Medicine

Columbia, Missouri, 65212, United States

Location status: Recruiting

Location contact

Vasavi Shabrish

CONTACT

[email protected]

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • >=45 and <=75 years of age
  • body mass index >=25.0 and <40.0 kg/m2

Exclusion criteria

  • <45 and >75 years of age
  • body mass index <25.0 or >39.9 kg/m2
  • plasma triglyceride <125 mg/dl
  • history of or current significant organ system dysfunction
  • allergies or intolerances to meal ingredients
  • use of medications or dietary supplements that could confound the study outcomes
  • engaged in regular structured exercise >150 min per week
  • alcohol use disorder
  • premenopausal women
  • persons who smoke
  • prisoners
  • inability to grant voluntary informed consent

Treatment and study plan

Standard meal

Other

Standard meal

High animal protein meal

Other

Meal with high animal protein content

High plant protein meal

Other

Meal with high plant protein content

High plant protein meal with additional leucine

Other

Meal with high plant protein content and additional leucine

Primary outcomes

  1. Monocyte proatherogenic pathway activation

    Time frame: baseline before meal intake to 3 hours after the meal

    Change in proatherogenic pathway activation

Other outcomes

  1. Plasma amino acids concentrations

    Time frame: baseline before meal intake to 3 hours after the meal

    Change in plasma amino acid concentrations

  2. Plasma glucose concentration

    Time frame: baseline before meal intake to 3 hours after the meal

    Change in plasma glucose concentration

  3. Plasma glucoregulatory hormone concentrations

    Time frame: baseline before meal intake to 3 hours after the meal

    Change in plasma concentrations of glucoregulatory hormones

  4. Endothelial function

    Time frame: baseline (before meal intake) and postprandially (after the meal)

    Endothelial function assessed as reactive hyperemia index

Study contacts

Contact information is provided by the study sponsor or research team.

Bettina Mittendorfer, PhD

CONTACT

[email protected]

6186103465

Sponsors and collaborators

Lead sponsor

University of Missouri-Columbia

Other

Registry information

Official study title

Dissecting the Impact of Dietary Protein on Macrophage mTOR Signaling and Atherosclerosis

Acronym: HPA

Important dates

Study start
2023
Primary completion
2027
Study completion
2028
First posted
Feb 11, 2022
Registry last updated
May 11, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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