Lipoprotein lipase polymorphisms and responses to long-term overfeeding.
Lipoprotein lipase polymorphisms and responses to long-term overfeeding.
复制标题
脂蛋白脂肪酶多态性和对长期过度喂养的反应。
DOI：
10.1046/j.1365-2796.2002.00981.x
复制
发表时间：
2002
影响因子：
11.1
通讯作者：
Bouchard,C
中科院分区：
文献类型：
--
作者：
Ukkola,O;Tremblay,A;Bouchard,C
摘要：Ukkola O，Tremblay A，Bouchard C（路易斯安那州立大学，巴吞鲁日，LA，美国;欧卢大学，欧卢，芬兰;和拉瓦尔大学，Ste‐Foy，魁北克，加拿大）。脂蛋白脂酶多态性和对长期过度喂养的反应。J Intern Med 2002;251：429- 436. Objective. The role of the lipoprotein lipase（LPL）gene Hind III，S447 X，Bam HI and Pvu II polymorphisms on body composition and lipid and lipoprotein changes in response to long‐term overfeeding was studied.Subjects. 12对男性单卵双胞胎吃了4.2 MJ day− 1能量盈余，每周6天，在100天的时间内。Results.Overfeeding induced a decrease in high‐density lipoprotein 2 cholesterol（HDL 2 ‐C）and HDL 2 ‐C to HDL 3 ‐C ratio in the H2 H2（n= 12）subjects of the LPL Hind III polymorphism. 相比之下，H1 H1/H1 H2（n= 12）受试者的HDL 2-C和HDL 2-C与HDL 3-C比值均升高（H2 H2和H1 H1/H1 H2之间的百分比变化差异分别为P= 0.009和0.007）。 此外，H2 H2基因型与过度喂养前后极低密度脂蛋白甘油三酯（VLDL-TG）（P<0.03）和VLDL-C（P<0.05）水平较高以及过度喂养后HDL-TG水平较高（P<0.003）相关。 肝素后脂蛋白脂酶（PH‐LPL）活性在H1 H1/H1 H2受试者中倾向于升高，在H2 H2受试者中倾向于降低。在过度喂养后4个月和5年，H2 H2受试者的总HDL-C低于基因型H1 H1/H1 H2的受试者（分别为P= 0.04和0.10）。 在S447 X的S447 S（n= 4）基因型和Hind III多态性的H2 H2基因型的受试者中，血浆脂质差异相似。 身体组成的变化，过度喂养之间没有不同的Hind III基因型。LPL Pvu II和Hind III多态性与体重增加弱相关（P= 0.015-0.039），但在热量过剩后与脂肪组织LPL活性强相关（P<0.01）。结论：我们得出结论，LPL基因Hind III多态性的H2 H2受试者在暴露于长期正能量平衡时，抗致雌激素性脂蛋白浓度降低。 这可能部分是由于H2 H2受试者中富含TG颗粒的催化剂减少所致。LPL Pvu II和Bam HI多态性与体重增加和脂肪组织LPL活性相关。因此，LPL基因座的遗传变异可能是导致血浆脂质和脂蛋白对慢性正能量平衡反应的个体间差异的因素之一。必须记住，本研究的样本量较小。尽管如此，它提供了关于基因和途径的有用信息，应该进一步探索。
Abstract.Ukkola O, Tremblay A, Bouchard C (Louisiana State University, Baton Rouge, LA, USA; University of Oulu, Oulu, Finland; and Laval University, Ste‐Foy, Quebec, Canada). Lipoprotein lipase polymorphisms and responses to long‐term overfeeding.J Intern Med2002;251:429–436.Objectives.The role of the lipoprotein lipase (LPL) gene Hind III, S447X, Bam HI and Pvu II polymorphisms on body composition and lipid and lipoprotein changes in response to long‐term overfeeding was studied.Subjects.Twelve pairs of male monozygotic twins ate a 4.2 MJ day−1energy surplus, 6 days a week, during a period of 100 days.Results.Overfeeding induced a decrease in high‐density lipoprotein 2 cholesterol (HDL2‐C) and HDL2‐C to HDL3‐C ratio in the H2H2 (n= 12) subjects of the LPL Hind III polymorphism. In contrast, the H1H1/H1H2 (n= 12) subjects experienced increases both in the HDL2‐C and HDL2‐C to HDL3‐C ratio (P= 0.009 and 0.007, respectively, for differences in percentage changes between H2H2 and H1H1/H1H2). In addition, the H2H2 genotype was associated with higher levels of very‐low‐density lipoprotein triglyceride (VLDL‐TG) (P< 0.03) and VLDL‐C (P< 0.05) before and after overfeeding and higher HDL‐TG levels (P< 0.003) after overfeeding. Postheparin lipoprotein lipase (PH‐LPL) activity tended to increase in H1H1/H1H2 and decrease in H2H2 subjects. The H2H2 subjects had lower total HDL‐C than those with the genotype H1H1/H1H2 4 months and 5 years after overfeeding (P= 0.04 and 0.10, respectively). The plasma lipid differences were similar amongst subjects with the S447S (n= 4) genotype of the S447X and H2H2 genotype of the Hind III polymorphisms. Body composition changes in response to overfeeding were not different between the Hind III genotypes. LPL Pvu II and Hind III polymorphisms were associated weakly with body weight gain (P= 0.015–0.039) but strongly with adipose tissue LPL activity (P< 0.01) after the caloric surplus.Conclusions.We conclude that the H2H2 subjects of the LPL gene Hind III polymorphism experience a decrease in the concentration of antiaterogenic lipoproteins when they are exposed to long‐term positive energy balance. This may have been partly caused by a diminished catabolism of TG‐rich particles in H2H2 subjects. LPL Pvu II and Bam HI polymorphisms were associated with body weight gain and adipose tissue LPL activity. Genetic variation at the LPL locus could thus be one of the factors responsible for the inter‐individual differences observed in plasma lipid and lipoprotein responses to chronic positive energy balance. It must be kept in mind that the sample size for this study was small. Nonetheless, it provides useful information on the genes and pathways that should be further explored.