Abstract
Background: Visceral abdominal tissue (VAT) is a unique pathogenic fat depot that is associated with cardiometabolic risk above and beyond overall body mass index (BMI). Higher lipid content of adipose tissue is associated with lower tissue attenuation (i.e. more negative) in computed tomography (CT) and is expressed as Hounsfield units (HU). Given this framework, we hypothesized that lower CT attenuation of adipose tissue is associated with more adverse metabolic risk. Methods: Framingham Heart Study participants (n=3198, mean age 51 years, 47% women) who participated in a computed tomography sub-study with volumetrically assessed VAT and documented HU were studied. Cardiovascular risk factors were measured using standard definitions. The association between HU and metabolic risk factors was assessed using sex-specific multivariable-adjusted regression models. Results: Mean visceral HU was −93.9 (Range −105.7 to −79.0). Mean HU were overall lower in men (−95.2) than women (−92.4). Lower HU correlated with higher BMI levels in women (age adjusted r = −0.51, p<0.001) and men (age adjusted r = −0.42, p<0.001). Risk factors levels were more adverse with decreasing HU levels. For example, the age-adjusted prevalence of metabolic syndrome ranged from 50% in the lowest negative tertile of visceral HU to 5.5% in the least negative tertile in women (p for trend across tertiles <0.001) with similar trends observed in men (p<0.001). In women, per 1 standard deviation (SD) decrease in visceral HU, the odds ratio (OR) for metabolic syndrome was 3.6 (95% CI 3.1 to 4.3, p<0.001), which persisted after adjustment for BMI (OR 2.5, p<0.001) and VAT (OR 1.5, p<0.001). Also in women, 1-SD decrease in visceral HU was associated with increased odds of hypertension (OR 1.8, 95% CI 1.6 to 2.1, p<0.001), impaired fasting glucose (OR 2.1, 95% CI 1.8 to 2.4, p<0.001) and insulin resistance (OR 3.3, 95% CI 2.8 to 4.0, p<0.001). These associations remained significant after adjustment for BMI (OR 1.4 to 2.3, all p<0.001). After adjustment for VAT, impaired fasting glucose (OR 1.5, p<0.001) and insulin resistance (OR 1.4, p=0.003) remained associated but hypertension did not (OR 1.2, p=0.19). Finally, per 1-SD decrease in visceral HU, HDL levels were 5.2 mg/dL lower (p <0.001) and log triglycerides were 0.20 mg/dL higher (p<0.001), both of which persisted after VAT adjustment. Similar findings were observed in men. Conclusion: Lower CT attenuation of visceral fat, a marker of higher lipid content of adipose tissue, is associated with increased adverse metabolic risk above and beyond total VAT volume. These findings highlight that both quantity and quality of fat depots may provide additional information regarding cardiometabolic risk.
Published Version
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