• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

营养素、遗传因素及其在非酒精性脂肪性肝病和心血管疾病中的相互作用。

Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease.

机构信息

Department of Pathophysiology and Transplantation, University of Milan, 20122 Milan, Italy.

Ca' Granda IRCCS Foundation, Policlinico Hospital of Milan, 20122 Milan, Italy.

出版信息

Int J Mol Sci. 2020 Nov 19;21(22):8761. doi: 10.3390/ijms21228761.

DOI:10.3390/ijms21228761
PMID:33228237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7699550/
Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries and expose patients to increased risk of hepatic and cardiovascular (CV) morbidity and mortality. Both environmental factors and genetic predisposition contribute to the risk. An inappropriate diet, rich in refined carbohydrates, especially fructose, and saturated fats, and poor in fibers, polyunsaturated fats, and vitamins is one of the main key factors, as well as the polymorphism of patatin-like phospholipase domain containing 3 (PNPLA3 gene) for NAFLD and the apolipoproteins and the peroxisome proliferator-activated receptor (PPAR) family for the cardiovascular damage. Beyond genetic influence, also epigenetics modifications are responsible for various clinical manifestations of both hepatic and CV disease. Interestingly, data are accumulating on the interplay between diet and genetic and epigenetic modifications, modulating pathogenetic pathways in NAFLD and CV disease. We report the main evidence from literature on the influence of both macro and micronutrients in NAFLD and CV damage and the role of genetics either alone or combined with diet in increasing the risk of developing both diseases. Understanding the interaction between metabolic alterations, genetics and diet are essential to treat the diseases and tailoring nutritional therapy to control NAFLD and CV risk.

摘要

非酒精性脂肪性肝病(NAFLD)是西方国家最常见的慢性肝病,使患者面临增加的肝和心血管(CV)发病率和死亡率风险。环境因素和遗传易感性都促成了这种风险。饮食不当,富含精制碳水化合物,尤其是果糖和饱和脂肪,而纤维、多不饱和脂肪和维生素含量低,是主要的关键因素之一,此外,载脂蛋白和过氧化物酶体增殖物激活受体(PPAR)家族的多态性与 NAFLD 以及心血管损害有关。除了遗传影响外,表观遗传修饰也与肝脏和心血管疾病的各种临床表现有关。有趣的是,关于饮食与遗传和表观遗传修饰相互作用,调节 NAFLD 和 CV 疾病发病机制途径的资料正在不断积累。我们报告了文献中关于宏量营养素和微量营养素对 NAFLD 和 CV 损害的影响的主要证据,以及遗传因素单独或与饮食联合增加这两种疾病发病风险的作用。了解代谢改变、遗传学和饮食之间的相互作用对于治疗这些疾病以及定制营养治疗以控制 NAFLD 和 CV 风险至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e34f/7699550/b51f7bcde001/ijms-21-08761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e34f/7699550/b51f7bcde001/ijms-21-08761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e34f/7699550/b51f7bcde001/ijms-21-08761-g001.jpg

相似文献

1
Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease.营养素、遗传因素及其在非酒精性脂肪性肝病和心血管疾病中的相互作用。
Int J Mol Sci. 2020 Nov 19;21(22):8761. doi: 10.3390/ijms21228761.
2
Role of nutrition, gene polymorphism, and gut microbiota in non-alcoholic fatty liver disease.营养、基因多态性和肠道微生物群在非酒精性脂肪性肝病中的作用。
Discov Med. 2017 Sep;24(131):95-106.
3
Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD).非酒精性脂肪性肝病 (NAFLD) 中维生素 A 代谢紊乱。
Nutrients. 2017 Dec 29;10(1):29. doi: 10.3390/nu10010029.
4
Non-alcoholic fatty liver disease, metabolic syndrome and patatin-like phospholipase domain-containing protein3 gene variants.非酒精性脂肪性肝病、代谢综合征与含patatin样磷脂酶结构域蛋白3基因变异体
Eur J Intern Med. 2014 Jul;25(6):566-70. doi: 10.1016/j.ejim.2014.05.012. Epub 2014 Jun 16.
5
The genetic backgrounds in nonalcoholic fatty liver disease.非酒精性脂肪性肝病中的遗传背景。
Clin J Gastroenterol. 2018 Apr;11(2):97-102. doi: 10.1007/s12328-018-0841-9. Epub 2018 Feb 28.
6
Targeted-bisulfite sequence analysis of the methylation of CpG islands in genes encoding PNPLA3, SAMM50, and PARVB of patients with non-alcoholic fatty liver disease.非酒精性脂肪性肝病患者基因编码区 CpG 岛的 PNPLA3、SAMM50 和 PARVB 的靶向亚硫酸氢盐测序分析。
J Hepatol. 2015 Aug;63(2):494-502. doi: 10.1016/j.jhep.2015.02.049. Epub 2015 Mar 14.
7
Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables.促进非酒精性脂肪性肝病的遗传学研究:通过多态性和临床变量联合风险评分。
World J Gastroenterol. 2018 Nov 21;24(43):4835-4845. doi: 10.3748/wjg.v24.i43.4835.
8
Validation of PNPLA3 polymorphisms as risk factor for NAFLD and liver fibrosis in an admixed population.验证 PNPLA3 多态性作为混合人群非酒精性脂肪性肝病和肝纤维化的危险因素。
Ann Hepatol. 2019 May-Jun;18(3):466-471. doi: 10.1016/j.aohep.2018.10.004. Epub 2019 Apr 18.
9
Effect of the patatin-like phospholipase domain containing 3 gene (PNPLA3) I148M polymorphism on the risk and severity of nonalcoholic fatty liver disease and metabolic syndromes: A meta-analysis of paediatric and adolescent individuals.含帕他丁样磷脂酶结构域蛋白3基因(PNPLA3)I148M多态性对非酒精性脂肪性肝病及代谢综合征风险和严重程度的影响:一项针对儿童和青少年个体的荟萃分析
Pediatr Obes. 2020 Jun;15(6):e12615. doi: 10.1111/ijpo.12615. Epub 2020 Feb 5.
10
PNPLA3 Expression Is Related to Liver Steatosis in Morbidly Obese Women with Non-Alcoholic Fatty Liver Disease.PNPLA3表达与患有非酒精性脂肪性肝病的病态肥胖女性的肝脏脂肪变性有关。
Int J Mol Sci. 2016 Apr 27;17(5):630. doi: 10.3390/ijms17050630.

引用本文的文献

1
The Triglyceride/HDL Ratio as a Non-Invasive Marker for Early-Stage NAFLD: A Retrospective Cross-Sectional Study of 2588 Patients.甘油三酯/高密度脂蛋白比值作为非酒精性脂肪性肝病早期阶段的无创标志物:一项对2588例患者的回顾性横断面研究。
Diagnostics (Basel). 2025 Aug 14;15(16):2045. doi: 10.3390/diagnostics15162045.
2
Assessment of dietary, genetic and metabolic factors in South Indian adolescents with metabolic dysfunction-associated steatotic liver disease: a case-control study protocol.南印度患有代谢功能障碍相关脂肪性肝病的青少年的饮食、遗传和代谢因素评估:一项病例对照研究方案
BMJ Paediatr Open. 2025 Mar 24;9(1):e003138. doi: 10.1136/bmjpo-2024-003138.
3

本文引用的文献

1
Nutrition Management in Older Adults with Diabetes: A Review on the Importance of Shifting Prevention Strategies from Metabolic Syndrome to Frailty.老年人糖尿病的营养管理:从代谢综合征到虚弱转变预防策略的重要性综述。
Nutrients. 2020 Nov 1;12(11):3367. doi: 10.3390/nu12113367.
2
Curcumin protects cardiomyopathy damage through inhibiting the production of reactive oxygen species in type 2 diabetic mice.姜黄素通过抑制 2 型糖尿病小鼠活性氧的产生保护心肌病损伤。
Biochem Biophys Res Commun. 2020 Sep 10;530(1):15-21. doi: 10.1016/j.bbrc.2020.05.053. Epub 2020 Jul 28.
3
The impact of type of dietary protein, animal versus vegetable, in modifying cardiometabolic risk factors: A position paper from the International Lipid Expert Panel (ILEP).
The role and function of lncRNA in ageing-associated liver diseases.
长链非编码RNA在衰老相关肝脏疾病中的作用与功能。
RNA Biol. 2025 Dec;22(1):1-8. doi: 10.1080/15476286.2024.2440678. Epub 2024 Dec 19.
4
Personalizing Nutrition Strategies: Bridging Research and Public Health.个性化营养策略:连接研究与公共卫生
J Pers Med. 2024 Mar 13;14(3):305. doi: 10.3390/jpm14030305.
5
The Intersection of Genetic Factors, Aberrant Nutrient Metabolism and Oxidative Stress in the Progression of Cardiometabolic Disease.遗传因素、异常营养代谢与氧化应激在心脏代谢疾病进展中的交集
Antioxidants (Basel). 2024 Jan 10;13(1):87. doi: 10.3390/antiox13010087.
6
Associations between types and sources of dietary carbohydrates and liver fat: a UK Biobank study.膳食碳水化合物的类型和来源与肝脂肪之间的关联:英国生物库研究。
BMC Med. 2023 Nov 16;21(1):444. doi: 10.1186/s12916-023-03135-8.
7
Involvement of the vagus nerve and hepatic gene expression in serum adiponectin concentrations in mice.迷走神经和肝脏基因表达对小鼠血清脂联素浓度的影响。
J Physiol Biochem. 2024 Feb;80(1):99-112. doi: 10.1007/s13105-023-00987-9. Epub 2023 Oct 14.
8
Epidemiologic, Genetic, Pathogenic, Metabolic, Epigenetic Aspects Involved in NASH-HCC: Current Therapeutic Strategies.非酒精性脂肪性肝炎-肝细胞癌涉及的流行病学、遗传学、致病性、代谢、表观遗传学方面:当前治疗策略
Cancers (Basel). 2022 Dec 20;15(1):23. doi: 10.3390/cancers15010023.
9
PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?PPARα在非酒精性脂肪性肝病的表观遗传驱动位置:表观遗传药物的新治疗机会?
Biomedicines. 2022 Nov 25;10(12):3041. doi: 10.3390/biomedicines10123041.
10
Ornithine Aspartate and Vitamin-E Combination Has Beneficial Effects on Cardiovascular Risk Factors in an Animal Model of Nonalcoholic Fatty Liver Disease in Rats.精氨酸天门冬氨酸与维生素 E 联合应用对非酒精性脂肪性肝病大鼠心血管危险因素的影响
Biomolecules. 2022 Nov 28;12(12):1773. doi: 10.3390/biom12121773.
不同类型膳食蛋白质(动物蛋白与植物蛋白)对心血管代谢危险因素的影响:国际脂质专家小组(ILEP)的立场文件。
Clin Nutr. 2021 Jan;40(1):255-276. doi: 10.1016/j.clnu.2020.05.017. Epub 2020 May 26.
4
Mitochondrial Dysfunction is a Key Pathway that Links Saturated Fat Intake to the Development and Progression of NAFLD.线粒体功能障碍是将饱和脂肪摄入与 NAFLD 的发生和发展联系起来的关键途径。
Mol Nutr Food Res. 2021 Jan;65(1):e1900942. doi: 10.1002/mnfr.201900942. Epub 2020 Jul 13.
5
A systemic review on the antioxidant and anti-inflammatory effects of resveratrol, curcumin, and dietary nitric oxide supplementation on human cardiovascular health.关于白藜芦醇、姜黄素和膳食一氧化氮补充剂对人类心血管健康的抗氧化和抗炎作用的系统评价。
Nutr Res. 2020 Jun;78:11-26. doi: 10.1016/j.nutres.2020.03.002. Epub 2020 Mar 10.
6
The associations of plant-based protein intake with all-cause and cardiovascular mortality in patients on peritoneal dialysis.植物性蛋白质摄入与腹膜透析患者全因和心血管死亡率的关联。
Nutr Metab Cardiovasc Dis. 2020 Jun 9;30(6):967-976. doi: 10.1016/j.numecd.2020.03.003. Epub 2020 Mar 12.
7
Dietary cellulose prevents gut inflammation by modulating lipid metabolism and gut microbiota.膳食纤维通过调节脂代谢和肠道微生物群预防肠道炎症。
Gut Microbes. 2020 Jul 3;11(4):944-961. doi: 10.1080/19490976.2020.1730149. Epub 2020 Mar 5.
8
Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.高胰岛素血症下调 Mboat7 诱导肝细胞脂肪堆积。
EBioMedicine. 2020 Feb;52:102658. doi: 10.1016/j.ebiom.2020.102658. Epub 2020 Feb 12.
9
MAFLD: A Consensus-Driven Proposed Nomenclature for Metabolic Associated Fatty Liver Disease.MAFLD:代谢相关脂肪性肝病的共识驱动命名建议。
Gastroenterology. 2020 May;158(7):1999-2014.e1. doi: 10.1053/j.gastro.2019.11.312. Epub 2020 Feb 8.
10
mir-101-3p Downregulation Promotes Fibrogenesis by Facilitating Hepatic Stellate Cell Transdifferentiation During Insulin Resistance.miR-101-3p 下调通过促进肝星状细胞转分化促进胰岛素抵抗中的肝纤维化。
Nutrients. 2019 Oct 29;11(11):2597. doi: 10.3390/nu11112597.