Key result
HIV infection in men was strongly associated with higher triglycerides (+76%, 95% CI: 53 to 103) and lower HDL-C, with greater visceral and less leg subcutaneous adipose tissue driving this risk.
Why the study?
How do regional adipose tissue depots and HIV infection associate with fasting lipid levels in men?
Observational (n=882)
How do regional adipose tissue depots and HIV infection associate with fasting lipid levels in men?
In HIV-infected men, reduced leg subcutaneous adipose tissue and increased visceral adipose tissue are associated with a proatherogenic dyslipidemia profile characterized by high triglycerides and low HDL-C.
Adipose distribution may refine dyslipidemia risk assessment in HIV men; extends cross-sectional links but leaves causality and interventions open.
BACKGROUND: HIV infection and antiretroviral therapy are associated with dyslipidemia, but the association between regional adipose tissue depots and lipid levels is not defined. METHODS: The association of magnetic resonance imaging-measured visceral adipose tissue (VAT) and regional subcutaneous adipose tissue (SAT) volume with fasting lipid parameters was analyzed by multivariable linear regression in 737 HIV-infected and 145 control men from the study of Fat Redistribution and Metabolic Change in HIV Infection. RESULTS: HIV-infected men had higher median triglycerides (170 mg/dL vs. 107 mg/dL; P < 0.0001), lower high-density lipoprotein cholesterol (HDL-C; 38 mg/dL vs. 46 mg/dL; P < 0.0001), and lower low-density lipoprotein cholesterol (LDL-C; 105 mg/dL vs. 125 mg/dL; P < 0.0001) than controls. After adjustment, greater VAT was associated with higher triglycerides and lower HDL-C in HIV-infected and control men, whereas greater leg SAT was associated with lower triglycerides in HIV-infected men with a similar trend in controls. More upper trunk SAT was associated with higher LDL-C and lower HDL-C in controls, whereas more lower trunk SAT was associated with higher triglycerides in controls. After adjustment, HIV infection remained strongly associated (P < 0.0001) with higher triglycerides (+76%, 95% confidence interval [CI]: 53 to 103), lower LDL-C (-19%, 95% CI: -25 to -12), and lower HDL-C (-18%, 95% CI: -22 to -12). CONCLUSIONS: HIV-infected men are more likely than controls to have higher triglycerides and lower HDL-C, which promote atherosclerosis, but also lower LDL-C. Less leg SAT and more VAT are important factors associated with high triglycerides and low HDL-C in HIV-infected men. The reduced leg SAT in HIV-infected men with lipoatrophy places them at increased risk for proatherogenic dyslipidemia.
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Wohl et al. (2008) conducted an observational in HIV infection and dyslipidemia (n=882). HIV infection and regional adipose tissue vs. Healthy controls was evaluated on Fasting triglycerides (mg/dL) (+76%, 95% CI 53 to 103, p=< 0.0001). HIV infection in men was strongly associated with higher triglycerides (+76%, 95% CI: 53 to 103) and lower HDL-C, with greater visceral and less leg subcutaneous adipose tissue driving this risk.
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