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A Pilot Study About the Dysfunction of Adipose Tissue in Male, Sleep Apneic Patients in Relation to Psychological Symptoms. | LitMetric

AI Article Synopsis

  • - Obstructive sleep apnea (OSA) is linked to visceral obesity and often presents with depression and anxiety symptoms, but the direct impact on fat tissue dysfunction is uncertain.
  • - A study evaluated 10 men with severe OSA and matched controls, examining various health metrics and taking fat biopsies to assess inflammation and other changes in adipose tissue.
  • - Results showed a positive correlation between anxiety symptoms and macrophage accumulation in fat, along with significant relationships between fat fibrosis and body measurements, indicating complex interactions between OSA, obesity, and mental health.

Article Abstract

Obstructive sleep apnea (OSA) and its cardiometabolic alterations are closely associated with visceral obesity. Patients with OSA frequently present with symptoms of depression and anxiety. Although these subjective symptoms of OSA are the result of complex biological dysregulation, it remains unclear if they have a direct effect on the dysfunction of adipose tissue. In a pilot, prospective, randomized study, we evaluated 10 recently diagnosed male patients with severe OSA by full polysomnography (PSG) and 4 male non-apneic subjects matched for age and body mass index (BMI) with abdomen adipose tissue biopsies. Subjects with diabetes/prediabetes and cardiovascular and psychiatric diseases and who are current smokers were excluded. All patients underwent anthropometric measurements and completed the following questionnaires: Epworth Sleepiness Scale (ESS), Fatigue Severity Scale (FSS), and Hospital Anxiety and Depression Scale (HADS-A and HADS-D). Fasting venous blood samples were collected on the day after PSG, between 8:00 and 9:00 a.m., after an overnight fast. Fat biopsies were performed at the same time periods and adipose tissue samples of 300 mg were obtained from abdominal fat. Fat cell size, extent of fibrosis, vascularity, leukocyte common antigen inflammatory infiltration, and tissue macrophage accumulation were microscopically evaluated. The mean age of the group was 47.4 ± 13.8 years, with mean BMI of 35.8 ± 4.8 kg/m and mean apnea-hypopnea index of 79.4 ± 46.1 events per hour of sleep (severe OSA). HADS-A and HADS-D scores were 5.8 ± 2.3 (3.0-8.0) and 4.7 ± 2.3 (2.0-8.0), respectively. HADS-A score correlated positively with macrophage accumulation in fat biopsy (r = 0.82, p = 0.047), whereas ESS, FSS, and HADS-D did not. Severity of fibrosis correlated largely with waist circumference (r = -0.66, p = 0.038) and neck circumference (r = -0.790, p = 0.006). Respiratory events correlated negatively with the extent of vascularization of adipose tissue (r = -0.614, p = 0.05). In the preliminary results of our pilot study, we assessed that the symptoms of anxiety mainly contribute to macrophage accumulation, whereas the increased number of respiratory events reduces the extent of vascularization in visceral fat in OSA. Based on this observation, further larger studies are required to verify if anxious OSA patients are more vulnerable to the metabolic manifestations of the syndrome.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6673696PMC
http://dx.doi.org/10.3389/fpsyt.2019.00527DOI Listing

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