Reciprocal Fluctuations in Lipoprotein Lipase, Glycosylphosphatidylinositol-Anchored High-Density Lipoprotein-Binding Protein 1, and Hepatic Triglyceride Lipase Levels in the Peripheral Bloodstream Are Correlated with Insulin Resistance

Background/Objectives: This study aimed to identify the regulatory system of lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein (HDL)-binding protein 1 (GPIHBP1), and hepatic triglyceride lipase (HTGL) in the peripheral bloodstream. Methods: In total, 207 individuals (100 males and 107 females) who were diagnosed with normal glucose tolerance or prediabetes during their comprehensive health checkup were investigated. Results: Circulating LPL levels were positively correlated with the GPIHBP1 and HDL-cholesterol (HDL-C) levels, and negatively correlated with body mass index (BMI), waist circumference (WC), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) scores, triglyceride–glucose index, and triglyceride, fasting insulin, ferritin, and C-reactive protein (CRP) levels. The GPIHBP1 level was positively correlated with LPL and HTGL levels, and negatively correlated with estimated glomerular filtration rate (eGFR). The HTGL level was positively correlated with BMI, WC, HOMA-IR score, and GPIHBP1, low-density lipoprotein cholesterol (LDL-C), fasting insulin, and ferritin levels. Meanwhile, it was negatively correlated with HDL-C levels. The multiple regression analysis revealed that the circulating LPL level was independently affected by BMI, red blood cell (RBC) count, GPIHBP1, fasting plasma glucose (FPG), fasting insulin, HDL-C, CRP, and ferritin levels. The GPIHBP1 level was independently affected by age, eGFR, FPG, LPL, and HTGL levels and RBC count. The HTGL level was independently affected by WC, GPIHBP1 and LDL-C levels. Conclusions: LPL and HTGL levels reflect insulin resistance. In particular, individuals with a greater insulin resistance present with a lower LPL level and a higher HTGL level. An increased GPIHBP1 level might compensate for decreased LPL levels due to insulin resistance.