Visceral Adiposity, Pro-Inflammatory Signaling and Vasculopathy in Metabolically Unhealthy Non-Obesity Phenotype

oleh: Meng-Ting Tsou, Chun-Ho Yun, Jiun-Lu Lin, Kuo-Tzu Sung, Jui-Peng Tsai, Wen-Hung Huang, Chia-Yuan Liu, Charles Jia-Yin Hou, I.-Hsien Tsai, Cheng-Huang Su, Chung-Lieh Hung, Ta-Chuan Hung

Format: Article
Diterbitkan: MDPI AG 2020-12-01

Deskripsi

The debate regarding the actual cardiovascular burden in metabolically healthy obese or metabolically unhealthy non-obesity individuals is ongoing. Accumulating data have suggested a unique pathophysiological role of pro-inflammatory cytokines in mediating metabolic and cardiovascular disorders by dysregulated visceral adiposity. To compare the burden of visceral adiposity, the inflammatory marker high-sensitivity C-reactive protein (hs-CRP) and the prevalent atherosclerotic burden in metabolically healthy obese (MHO) or metabolically unhealthy (MU) populations, were compared to those of metabolically healthy non-obesity subjects (MHNO). Coronary artery calcification score (CACS) and visceral fat, including pericardial fat (PCF)/thoracic peri-aortic fat (TAT), were quantified in 2846 asymptomatic subjects using a CT dataset. A cross-sectional analysis comparing CACS, inflammatory marker hs-CRP, and visceral fat burden among four obesity phenotypes (MHNO, metabolically unhealthy non-obesity (MUNO), MHO, and metabolically unhealthy obese (MUO)) was performed. Both MUNO and MUO demonstrated significantly higher hs-CRP and greater CACS than MHNO/MHO (adjusted coefficient: 25.46, 95% confidence interval (CI): 5.29–45.63; 43.55, 95% CI: 23.38–63.73 for MUNO and MUO (MHNO as reference); both <i>p</i> < 0.05). Visceral fat (PCF/TAT) was an independent determinant of MU and was similarly higher in the MUNO/MHO groups than in the MHNO group, with the MUO group having the largest amount. PCF/TAT, obesity, and MU remained significantly associated with higher CACS even after adjustment, with larger PCF/TAT modified effects for MU and diabetes in CACS (both p<sub>interaction</sub> < 0.05). MU tightly linked to excessive visceral adiposity was a strong and independent risk factor for coronary atherosclerosis even in lean individuals, which could be partially explained by its coalignment with pathological pro-inflammatory signaling.