Clinical Significance of Lipoprotein Lipase (LPL) in People Living with HIV: A Comprehensive Assessment Including Lipidemia, Body Composition, Insulin Secretion, and Insulin Resistance

<b>Background/Objectives</b>: Dyslipidemia is one of the major problems of long-term management in people living with human immunodeficiency virus (HIV) (PLH) as a risk factor for cardiovascular diseases. Lipoprotein lipase (LPL) is anchored on the surface of the capillary endothelial cells and plays a pivotal role in triglyceride metabolism by catabolizing dietary chylomicrons and very low-density lipoprotein synthesized in the liver. However, the details of the mechanisms in the era of integrase strand transfer inhibitor-based antiretroviral therapy have not yet been clarified. <b>Methods</b>: This study was a cross-sectional, single-center, non-interventional study evaluating the underlying factors associated with dyslipidemia, insulin resistance or secretion, and changes in the body composition of PLH. <b>Results</b>: Among PLH (<i>n</i> = 48), lower LPL (<60.8 ng/mL) and older age independently predicted antilipemic drug (ALD) necessity. A comparison of ALD-naïve PLH (<i>n</i> = 33) and age- and sex-matched non-HIV controls (<i>n</i> = 33) showed that PLH were significantly associated with lower high-density lipoprotein cholesterol (HDL-C) and higher HOMA-β. LPL was also the independent predictor of HDL-C < 40 mg/dL in PLH (adjusted odds ratio = 0.901, <i>p</i> = 0.044). Furthermore, LPL < 65.3 ng/mL predicted HDL-C < 40 mg/dL with 100% sensitivity and 60.9% specificity. Low levels of HIV-RNA were detected in the high HOMA-β group. <b>Conclusions</b>: In Japanese individuals, compared to non-HIV controls, PLH has low HDL-C and LPL. The measurement of LPL may confer the risk assessment and decision-making with relevance to ALD in PLH. Additionally, the effectiveness of HIV antiviral therapy and glucose tolerance may interact with each other.