Fat Metabolism in OSA and COPD

Completed

Conditions studied: Obstructive Sleep Apnea, Chronic Obstructive Pulmonary Disease, Obesity

In brief

Obstructive sleep apnea (OSA) is the most common type of sleep apnea and is caused by an obstruction of the upper airways. The obstruction results in periods of intermittent hypoxia and re-oxygenation, which lead to increased oxidative stress, increased inflammation, endothelial dysfunction, and insulin resistance. Chronic obstructive pulmonary disease (COPD) is a lung disease that leads to poor airflow. This disease leads to systemic hypoxia, reduced oxidative capacity, and increased inflammation. The direct cause of OSA and COPD is unclear, but OSA and COPD may be linked to other comorbid conditions such as obesity and type II diabetes. Upon onset of OSA and COPD, metabolic disturbances associated with obesity and type II diabetes can be exacerbated. Obesity is a condition characterized by an increase in visceral fat, elevated plasma levels of free fatty acids, inflammation, and insulin resistance. Although the effects of body fat distribution have not been studied in these patients, an increase in both subcutaneous and abdominal fat mass in non-OSA older women was shown to increase morbidity and mortality. Fat/adipose tissue is an active tissue capable of secreting proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, reactive oxygen species and adipokines. Particularly, abdominal fat is a prominent source of pro-inflammatory cytokines, which contributes to a low grade, chronic inflammatory state in these patients. Additionally, an increased inflammatory state is associated with reduced lean body mass, and together with elevated circulating free fatty acids may increase the occurrence of lipotoxicity and insulin resistance. Thus, increased fat deposition is associated with a poor prognosis in OSA and COPD patients and therefore it is of clinical and scientific importance to understand the changes in fat metabolism and digestion as a result of OSA and COPD. It is therefore our hypothesis that fat synthesis and insulin resistance is increased and whole body protein synthesis is decreased in OSA and COPD patients, leading to a poor prognosis.

Key facts

Study ID

NCT02157844

Run by

Texas A&M University

People needed

62

Starts

2014-04-01

Expected to finish

2017-12-01

Last updated by the study team

2022-02-04

Who can join

Age: 30 and older. Sex: any. Healthy volunteers: accepted.

You may not qualify if…

• Established diagnosis of malignancy
• Untreated metabolic diseases including hepatic or renal disorder
• Presence of acute illness or metabolically unstable chronic illness
• Presence of fever within the last 3 days
• Any other condition according to the PI or study physician that would interfere with proper conduct of the study / safety of the patient
• Use of long-term oral corticosteroids or short course of oral corticosteroids in the preceding month before enrollment
• Use of protein or amino acid containing nutritional supplements within 5 days of first study day 5 days of first study day
• Failure to give informed consent or Investigator's uncertainty about the willingness or ability of the subject to comply with the protocol requirements
• History of hypo- or hyper-coagulation disorders, including use of a Coumadin derivative, history of deep venous thrombosis (DVT), or pulmonary embolism (PE) at any point in lifetime
• Currently taking anti-thrombotics and cannot stop for 7 days (i.e. medical indication)
• Recent myocardial infarction ( < 1 year ago)
• Current alcohol or drug abuse
• (Possible) pregnancy

Where it is running

• Texas A&M University — College Station, Texas, United States

Full record on ClinicalTrials.gov

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