Vasoprotective Activities of Low-Fat Milk in Individuals With Metabolic Syndrome
The purpose of this study is to define whether the acute consumption of low-fat milk protects against postprandial vascular endothelial dysfunction by reducing oxidative stress responses that limit nitric oxide bioavailability to the vascular endothelium. The investigators hypothesis is that the consumption of low-fat milk will improve postprandial vascular endothelial function in an oxidative stress-dependent manner that allows greater nitric oxide (NO) bioavailability. The objectives of this study are to 1) examine improvements in postprandial vascular endothelial function in response to low-fat milk ingestion, 2) define low-fat milk-mediated improvements in circulating biomarkers of redox status, and 3) define the mechanism by which low-fat milk improves NO bioavailability. Collectively, the successful completion of these studies is expected to define NO mediated activities of low-fat milk that protect against vascular endothelial dysfunction in individuals at high risk for developing CVD.
Other: Low-Fat Milk
Other: Rice Milk
|Study Design:||Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Investigator, Outcomes Assessor)
Primary Purpose: Basic Science
|Official Title:||Vasoprotective Activities of Low-Fat Milk in Individuals With Metabolic Syndrome|
- endothelial function [ Time Frame: 3 hours ] [ Designated as safety issue: No ]Brachial artery flow-mediated dilation will be assessed at 30 min intervals during a 3 hour postprandial period
- Biomarkers of oxidative stress and nitric oxide metabolism [ Time Frame: 3 hours ] [ Designated as safety issue: No ]At 30 min intervals throughout a 3 hour postprandial period, biomarkers of oxidative stress (glutathione, malondialdehyde, nitrotyrosine, and antioxidants) as well as nitric oxide metabolism (arginine, asymmetric dimethylarginine, and nitric oxide metabolites) will be evaluated.
|Study Start Date:||August 2011|
|Study Completion Date:||October 2013|
|Primary Completion Date:||August 2012 (Final data collection date for primary outcome measure)|
Experimental: Low-Fat Dairy
Participants will ingest 2 cups of low-fat milk on 1 occasion prior to measure postprandial changes in vascular function
Other: Low-Fat Milk
Participants will ingest 2 cups of low-fat milk on 1 occasion.
Active Comparator: Rice Milk
Participants will ingest 2 cups of rice milk on 1 ocassion prior to measuring postprandial vascular function
Other: Rice Milk
Participants will ingest 2 cups of rice milk on 1 occasion.
Cardiovascular disease (CVD) is the leading cause of death in the United States, accounting for ~830,000 deaths annually. Oxidative stress and inflammatory responses are fundamental mechanisms leading to vascular endothelial dysfunction because of their role in reducing nitric oxide (NO) bioavailability. Greater intakes of dairy foods have been associated with a lower incidence of CVD-related morbidity. Although the mechanisms by which dairy protects against CVD remain unclear, epidemiological and experimental evidence suggest that the concerted actions of bioactive milk-derived peptides and micronutrients may protect against hypertension and future CVD risk by improving vascular endothelial function. Therefore, the objective of this study is to define the mechanisms by which the acute consumption of low-fat milk protects against postprandial vascular endothelial dysfunction by reducing oxidative stress responses that limit NO bioavailability to the vascular endothelium. In this study, participants having the metabolic syndrome will ingest low-fat milk or rice milk on a single occasion. Then, vascular function and biomarkers of oxidative stress and NO metabolism will be monitored at 30 min intervals throughout a 180 min postprandial period. Collectively, these studies will help identify how postprandial vascular function is regulated in individuals at high-risk for CVD, and whether low-fat dairy consumption can be used as a strategy to better improve vascular function.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01411293
|United States, Connecticut|
|University of Connecticut|
|Storrs, Connecticut, United States, 06269|
|Principal Investigator:||Richard S Bruno, PhD, RD||University of Connecticut|