[1]占小锋 张长磊 李刚.β肾上腺素受体阻滞剂对甘油三酯代谢的影响及其作用机制的阐述[J].心血管病学进展,2019,(9):1298-1300.[doi:10.16806/j.cnki.issn.1004-3934.2019.09.029]
 ZHAN Xiaofeng,ZHANG Changlei,LI Gang.Effect of -adrenergic Receptor Blockers on Triglyceride Metabolism and Mechanism[J].Advances in Cardiovascular Diseases,2019,(9):1298-1300.[doi:10.16806/j.cnki.issn.1004-3934.2019.09.029]
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β肾上腺素受体阻滞剂对甘油三酯代谢的影响及其作用机制的阐述()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2019年9期
页码:
1298-1300
栏目:
综述
出版日期:
2019-12-25

文章信息/Info

Title:
Effect of -adrenergic Receptor Blockers on Triglyceride Metabolism and Mechanism
作者:
占小锋12 张长磊23 李刚12
(1.华北理工大学研究生院,河北 唐山 063000 ;2.河北省人民医院老年心血管科,河北 石家庄 050051;3.河北医科大学研究生院,河北 石家庄 050051)
Author(s):
ZHAN Xiaofeng2ZHANG Changlei23LI Gang12
(1.Graduate school of North China University of Science and Technology,Tangshan 063000,Hebei,China;2.Geriatric Cardiology of Hebei General Hospital, Shijiazhuang 050051,Hebei,China; 3.Graduate School of Hebei Medical University,Shijiazhuang 050051,Hebei,China)
关键词:
β肾上腺素能受体阻滞剂甘油三酯胰岛素抵抗脂蛋白脂肪酶基因突变
Keywords:
Beta adrenalin receptor blockersTriglycerideInsulinresistanceLipoprotein lipaseGene mutations
DOI:
10.16806/j.cnki.issn.1004-3934.2019.09.029
摘要:
β肾上腺素能受体阻滞剂是心血管领域应用较广泛的药物之一。其常见的不良反应有窦性心率过缓、传导阻滞、撤药综合征及代谢紊乱等。此类药物导致脂代谢[主要探讨甘油三酯(TG)]紊乱的机制较为复杂。β肾上腺素能受体阻滞剂导致TG水平升高的机制如下:(1)通过诱发胰岛素抵抗进而影响TG代谢。(2)直接抑制脂蛋白脂肪酶活性影响TG代谢。(3)与脂蛋白脂肪酶相关基因突变共同影响TG水平。
Abstract:
Beta adrenalin receptor blockers(β-blockers)are one of the widely used drugs in cardiovascular medicine. The common adverse reactions include sinus bradycardia, Cardiac conduction block,rebound reaction and metabolicdisorders Etc.The mechanism of lipid (triglyceride)metabolism disorder?by such drugs is complex.The mechanism of beta adrenergic receptor blockers increase triglyceride levels is as follows:(1)Upset triglyceride metabolism by affecting insulinresistance.(2)Directly control lipoprotein lipase activity and break triglyceride metabolism.(3)Llipoprotein lipase related with gene mutations jointly affect triglyceride metabolism.

参考文献/References:


[1]冷晓宁,贾静,张伟华.β肾上腺素受体阻滞剂的研究进展[J].心血管病学进展,2011,32(4):569-572.

[2]Ahmad AA, Yasir AB,Ahmad HA,et al.Comparison of the effects of metoprolol and bisoprolol on lipid and glucose profiles in cardiovascular patients[J].Current Drug Safety, 2019,14(1):27-30.

[3]刘立伟,陈国良,刘红.口服美托洛尔引起血脂紊乱和β2肾上腺素受体基因多态性关系的研究[J].中国新药杂志,2010,19(18):1661-1665.

[4]黎镇赐.β-受体阻滞剂常见不良反应及处理对策[J].中华高血压杂志,2012,5:419-420.

[5]Angelo MC,Giuseppe A,Matteo C,et al.Antihypertensive treatment with beta-blockers in the metabolic syndrome: a review[J].Curr Diabetes Rev, 2010,6(4),215-221.

[6]Ali GO,Serpil E,Ugur B,et al.Effects of carvedilol compared to nebivolol on insulin resistance and lipid profile in patients with essential hypertension[J].J Cardiovasc Pharmacol Ther,2017,22(1): 65-70.

[7]Bharati SM,Singh N.Effect of losartan and atenolol on insulin sensitivity in nondiabetic hypertensive patients[J].J Pharmacol Pharmacother,2016,7(2):80-86.

[8]Sparks JD,Sparks CE,Adeli K.Selective hepatic insulin resistance, VLDL overproduction, and hypertriglyceridemia[J].Arterioscler Thromb Vasc Biol,2012,32(9):2104-2112.

[9] Cheng Z.FoxO1:mute for a tuned metabolism?[J].Trends Endocrinol Metab,2015,26(8):402-403.

[10]Ting Z,Dae HK,Xiang WX,et al.FoxO1 plays an important role in regulating beta-cell compensation for insulin resistance in male mice[J].Endocrinology,2016,157(3):1055-1070.

[11]Shen QU,Ting Z,Henry D.Effect of hepatic insulin expression on lipid metabolism in diabetic mice[J].J Diabetes,2016,8(3):314-323.

[12] Kobayashi J,Mabuchi H.Lipoprotein lipase and atherosclerosis[J]. Ann Clin Biochem,2015,52(6):632-637.

[13]Casanovas A,Parramon N,Llobera M,et al.Retroperitoneal white adipose tissue lipoprotein lipase activity is rapidly down-regulated in response to acute stress[J].J Lipid Res,2007,48(4):863-868.

[14]Bouvy LM,Heinaniemi M,John E,et al.Combinatorial regulation of lipoprotein lipase by microRNAs during mouse adipogenesis[J].RNA Biol,2014,11(1):76-91.

[15]Larsson M, Vorrsj? E, Talmud P,et al.Apolipoprotein C-I and C-III inhibit lipoprotein lipase activity by displacement of the enzyme from lipid droplets[J].J Biol Chem,2013,288(47):33997-34008.

[16]Surendran RP,Visser ME,Heemelaar S,et al.Mutations in LPL, APOC2, APOA5, GPIHBP1 and LMF1 in patients with severe hypertriglyceridaemia[J].J Intern Med,2012,272(2):185-196.

[17]De CO,Fernando C,Maria JP,et al.Rare genetic variants with large effect on triglycerides in subjects with a clinical diagnosis of familial versus non-familial hypertriglyceridemia[J].J Clin Lipidol,2016,10(4):790-797.

[18]Kolovou GD,Kolovou V,Panagiotakos DB,et al.Study of common variants of the apolipoprotein E and lipoprotein lipase genes in patients with coronary heart disease and variable body mass index[J].Hormones (Athens),2015,14(3):376-382.

[19]Chi X, Britt EC, Shows HW,et al.ANGPTL8 promotes the ability of ANGPTL3 to bind and inhibit lipoprotein lipase[J].Mol Metab,2017,6(10):1137-1149.

[20]Chen Y,Wang X, Shen Z,et al.Effect of the beta-3 adrenergic receptor Trp64Arg and uncoupling protein 1-3826 A>G genotypes on lipid and apolipoprotein levels in overweight/obese and non-obese Chinese subjects[J].Lipids Health Dis,2015,14:34.

[21]Liu J,Zhang B,Li M,et al.Study on relationship between Trp64Arg polymorphism of β3-adrenergic receptor gene and obesity and blood lipids[J].Zhonghua Yi Xue Za Zhi,2015,95(20):1558-1562.

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更新日期/Last Update: 2020-02-06