BACKGROUND: Hepatic steatosis is increasing worldwide. Whether HIV and its associated metabolic perturbations exacerbate steatosis is unclear. Sex differences in adipose tissue distribution may also affect steatosis risk. We examined the contribution of HIV and sex to steatosis. METHODS: Using MRI and spectroscopy, visceral adipose tissue (VAT) and liver fat fraction (LFF) were measured in 121 HIV-infected and 107 uninfected men and women without viral hepatitis. Differences in LFF by HIV status and sex were evaluated using multivariable linear regression, adjusting for demographic, lifestyle, VAT, homeostasis model assessment-estimated insulin resistance, and HIV-related factors. RESULTS: HIV-infected women had lower LFF than uninfected women (demographic-adjusted mean: 1.9 vs. 3.1%; P = 0.028); LFF was similar in HIV-infected and uninfected men (4.6 vs. 4.1%; P = 0.78). HIV-infected and uninfected women had less VAT than men (median: 139 and 161 vs. 201 cm and 188 cm, respectively). After adjustment, HIV-infected women had 34% [95% confidence interval (CI): -54%, -5.5%] lower LFF than uninfected women, whereas there was little difference in men (-5.5%; 95% CI: -26%, 21%). Among HIV-infected persons, greater VAT and homeostasis model assessment-estimated insulin resistance were associated with greater LFF. HIV-related factors (CD4 cell count, HIV RNA level, or antiretroviral therapy use) had little association with LFF. Although HIV-infected men had 81% (95% CI: 32%, 148%) greater LFF than HIV-infected women, the association was attenuated after multivariable adjustment (25%; 95% CI: -9.1%, 73%). CONCLUSION: Contrary to expectation, HIV infection is not associated with greater steatosis compared with uninfected adults. It is possible that less fat is stored in the liver to maintain subcutaneous fat (which is reduced in HIV) and the effect is magnified in HIV-infected women, who also have less VAT.
BACKGROUND:Hepatic steatosis is increasing worldwide. Whether HIV and its associated metabolic perturbations exacerbate steatosis is unclear. Sex differences in adipose tissue distribution may also affect steatosis risk. We examined the contribution of HIV and sex to steatosis. METHODS: Using MRI and spectroscopy, visceral adipose tissue (VAT) and liver fat fraction (LFF) were measured in 121 HIV-infected and 107 uninfected men and women without viral hepatitis. Differences in LFF by HIV status and sex were evaluated using multivariable linear regression, adjusting for demographic, lifestyle, VAT, homeostasis model assessment-estimated insulin resistance, and HIV-related factors. RESULTS:HIV-infectedwomen had lower LFF than uninfected women (demographic-adjusted mean: 1.9 vs. 3.1%; P = 0.028); LFF was similar in HIV-infected and uninfected men (4.6 vs. 4.1%; P = 0.78). HIV-infected and uninfected women had less VAT than men (median: 139 and 161 vs. 201 cm and 188 cm, respectively). After adjustment, HIV-infectedwomen had 34% [95% confidence interval (CI): -54%, -5.5%] lower LFF than uninfected women, whereas there was little difference in men (-5.5%; 95% CI: -26%, 21%). Among HIV-infectedpersons, greater VAT and homeostasis model assessment-estimated insulin resistance were associated with greater LFF. HIV-related factors (CD4 cell count, HIV RNA level, or antiretroviral therapy use) had little association with LFF. Although HIV-infectedmen had 81% (95% CI: 32%, 148%) greater LFF than HIV-infectedwomen, the association was attenuated after multivariable adjustment (25%; 95% CI: -9.1%, 73%). CONCLUSION: Contrary to expectation, HIV infection is not associated with greater steatosis compared with uninfected adults. It is possible that less fat is stored in the liver to maintain subcutaneous fat (which is reduced in HIV) and the effect is magnified in HIV-infectedwomen, who also have less VAT.
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