Effects of omega-3 fatty acids on intravascular lipolysis of very-low-density lipoproteins in humans.
Effects of omega-3 fatty acids on intravascular lipolysis of very-low-density lipoproteins in humans.
复制标题
omega-3 脂肪酸对人体极低密度脂蛋白血管内脂肪分解的影响。
DOI：
10.1016/0026-0495(95)90020-9
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Almario,R
中科院分区：
文献类型：
--
作者：
Kasim-Karakas,SE;Herrmann,R;Almario,R
Very-low-density lipoproteins (VLDLs) are the major carriers of fasting plasma triglyceride (TG). TG-enriched VLDLs become cholesterol (C)-enriched low-density lipoproteins (LDLs) through hydrolysis facilitated by lipoprotein lipase (LPL). Omega-3 fatty acid (n-3 FA) supplementation may increase LDL-C while decreasing plasma TG in hypertriglyceridemic patients. It has been proposed that n-3 FAs increase LDL-C by promoting production of TG-poor VLDL and accelerating conversion of VLDL to LDL. To study the effects of n-3 FA supplementation on in vivo lipolysis of VLDL directly, we treated 11 hypertriglyceridemic subjects with n-3 FA (3.3 g/d). Each participant was studied three times: at baseline, after a 1-month period of run-in olive oil placebo, and after 1 more month of n-3 FA supplementation. Lipolysis was induced by intravenous infusion of heparin for 2 hours. Plasma samples were obtained every 30 minutes for determination of lipids and apoproteins (apos), separation of individual lipoproteins by fast protein liquid chromatography (FPLC), and measurement of LPL and hepatic TG lipase (HTGL) levels. n-3 FA supplementation decreased fasting plasma TG (2.51 ± 0.23 v 3.97 ± 0.46 mmol/L), VLDL-TG (1.08 ± 0.18 v 2.35 ± 0.35 mmol/L), and VLDL-C (0.39 ± 0.05 v 0.72 ± 0.13 mmol/L) while increasing LDL-C (3.59 ± 0.21 v 3.00 ± 0.23 mmol/L) and plasma apo B (3.31 ± 0.19 v 2.90 ± 0.17 mmol/L). The absolute rate of TG lipolysis correlated with fasting TG (r = .74, P < .005) and was lower after n-3 FA supplementation (0.11 ± 0.01 mmol/mL/min) as compared with placebo (0.19 ± 0.01, P < .01), whereas percent decreases from baseline TG levels were similar at entry onto the study (57.4% ± 2.5%), after placebo (58.8% ± 2.7%), and after n-3 FA (52% ± 3.6%). During lipolysis, LDL-C increased in correlation with the decrease in VLDL-C (r = -.41, P < .03), consistent with the product-precursor relationship. Postheparin LPL activity at 2 hours correlated inversely with fasting TG (r = −.53, P < .05), but not with either the decreases in VLDL-TG and VLDL-C or the increase in LDL-C. These data demonstrate that n-3 FA supplementation does not accelerate lipolysis of VLDL and even decreases the VLDL-C pool, which is the precursor of LDL-C. Therefore, the increase seen in fasting LDL-C is probably mediated through mechanisms other than acceleration of VLDL lipolysis.
