Department of Endocrinology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Eur J Clin Invest. 2018 Sep;48(9):e12988. doi: 10.1111/eci.12988. Epub 2018 Jul 13.
Nonalcoholic fatty liver disease (NAFLD) is a highly prevalent condition which contributes to atherogenic apolipoprotein B dyslipoproteinemias. Lecithin:cholesterol acyltransferase (LCAT) and phospholipid transfer protein (PLTP) are both synthesized by the liver and are important in lipid metabolism. Here, we interrogated the impact of NAFLD on plasma LCAT and PLTP activities.
Plasma LCAT activity (exogenous substrate assay) and PLTP activity (phospholipid vesicles-HDL assay) were determined in 348 subjects (279 men; 81 subjects with type 2 diabetes (T2DM); 123 with metabolic syndrome (MetS)). A Fatty Liver Index (FLI) ≥60 was used as a proxy of NAFLD. Insulin resistance was determined by homoeostasis model assessment (HOMA-IR).
A total of 147 participants had an FLI ≥60 coinciding with T2DM and MetS (P < 0.001 for each). Plasma LCAT activity and PLTP activity were on average 12% and 5% higher, respectively, in subjects with an FLI ≥ 60 (P < 0.001 for each). In age- and sex-adjusted partial linear regression analysis, LCAT activity and PLTP activity were positively related to various obesity measures and HOMA-IR (P < 0.001 for each). In multivariable linear regression analyses adjusted for age and sex, LCAT activity was associated with an FLI ≥ 60 independent of T2DM and MetS, the waist/hip ratio, or HOMA-IR (β = 0.307 to 0.366, P < 0001 for all models). PLTP activity was also associated with an FLI ≥ 60 independent of these variables (β = 0.151 to 0223, P = 0.013 to 0.001).
NAFLD, as inferred from an FLI≥60, confers higher plasma LCAT and to a lesser extent PLTP activity, even when taking account of T2DM, MetS, central obesity and insulin resistance.
非酒精性脂肪性肝病（NAFLD）是一种高发疾病，可导致致动脉粥样硬化载脂蛋白 B 血脂异常。卵磷脂胆固醇酰基转移酶（LCAT）和磷脂转移蛋白（PLTP）均由肝脏合成，在脂质代谢中发挥重要作用。本研究旨在探讨 NAFLD 对血浆 LCAT 和 PLTP 活性的影响。
在 348 名受试者（279 名男性；81 名 2 型糖尿病（T2DM）患者；123 名代谢综合征（MetS）患者）中测定血浆 LCAT 活性（外源性底物测定法）和 PLTP 活性（磷脂囊泡-HDL 测定法）。使用 Fatty Liver Index（FLI）≥60 作为 NAFLD 的替代指标。胰岛素抵抗用稳态模型评估（HOMA-IR）来测定。
共有 147 名参与者的 FLI≥60，同时伴有 T2DM 和 MetS（P<0.001）。FLI≥60 的受试者的血浆 LCAT 活性和 PLTP 活性平均分别升高 12%和 5%（均 P<0.001）。在年龄和性别校正的部分线性回归分析中，LCAT 活性和 PLTP 活性与各种肥胖指标和 HOMA-IR 呈正相关（均 P<0.001）。在调整年龄和性别的多变量线性回归分析中，LCAT 活性与 FLI≥60 独立相关，与 T2DM 和 MetS、腰围/臀围比或 HOMA-IR 无关（β=0.307 至 0.366，所有模型 P<0.001）。PLTP 活性与 FLI≥60 也独立相关，与这些变量无关（β=0.151 至 0.223，P=0.013 至 0.001）。
即使考虑到 T2DM、MetS、中心性肥胖和胰岛素抵抗，FLI≥60 推断的 NAFLD 可导致较高的血浆 LCAT 和较小程度的 PLTP 活性。
