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Advances in Genetics of Regeneration in Metabesity.代谢肥胖症再生遗传学研究进展。
Genes (Basel). 2019 May 20;10(5):383. doi: 10.3390/genes10050383.
2
Recent developments on the role of epigenetics in obesity and metabolic disease.近年来,表观遗传学在肥胖和代谢性疾病中的作用的研究进展。
Clin Epigenetics. 2015 Jul 11;7:66. doi: 10.1186/s13148-015-0101-5. eCollection 2015.
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Dissecting the Brain/Islet Axis in Metabesity.解析代谢肥胖中的脑/胰岛轴
Genes (Basel). 2019 May 8;10(5):350. doi: 10.3390/genes10050350.
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Metabesity: expert panel recommendation for taking up the challenge by a multidisciplinary approach.代谢性肥胖:多学科方法应对挑战的专家小组建议
J Pak Med Assoc. 2020 Aug;70(8):1418-1424. doi: 10.5455/JPMA.56654.
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Epigenetics and nutrition-related epidemics of metabolic diseases: Current perspectives and challenges.表观遗传学与营养相关的代谢性疾病流行:当前观点与挑战
Food Chem Toxicol. 2016 Oct;96:191-204. doi: 10.1016/j.fct.2016.08.006. Epub 2016 Aug 5.
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本文引用的文献

1
Dissecting the Brain/Islet Axis in Metabesity.解析代谢肥胖中的脑/胰岛轴
Genes (Basel). 2019 May 8;10(5):350. doi: 10.3390/genes10050350.
2
Complement Component C3 Is Highly Expressed in Human Pancreatic Islets and Prevents β Cell Death via ATG16L1 Interaction and Autophagy Regulation.补体成分 C3 在人胰腺胰岛中高度表达,并通过 ATG16L1 相互作用和自噬调控防止β细胞死亡。
Cell Metab. 2019 Jan 8;29(1):202-210.e6. doi: 10.1016/j.cmet.2018.09.009. Epub 2018 Oct 4.
3
Epigenetic Control of Pancreatic Regeneration in Diabetes.糖尿病中胰腺再生的表观遗传调控
Genes (Basel). 2018 Sep 7;9(9):448. doi: 10.3390/genes9090448.
4
Complement Factor C3 Methylation and mRNA Expression Is Associated to BMI and Insulin Resistance in Obesity.补体因子C3甲基化及mRNA表达与肥胖中的体重指数和胰岛素抵抗相关。
Genes (Basel). 2018 Aug 13;9(8):410. doi: 10.3390/genes9080410.
5
Genetic Targeting of GRP78 in the VMH Improves Obesity Independently of Food Intake.视前内侧下丘脑(VMH)中葡萄糖调节蛋白78(GRP78)的基因靶向独立于食物摄入量改善肥胖。
Genes (Basel). 2018 Jul 17;9(7):357. doi: 10.3390/genes9070357.
6
The type 2 diabetes-associated HMG20A gene is mandatory for islet beta cell functional maturity.2 型糖尿病相关的 HMG20A 基因是胰岛β细胞功能成熟所必需的。
Cell Death Dis. 2018 Feb 15;9(3):279. doi: 10.1038/s41419-018-0272-z.
7
PCSK1 Mutations and Human Endocrinopathies: From Obesity to Gastrointestinal Disorders.PCSK1 突变与人类内分泌疾病:从肥胖到胃肠道疾病。
Endocr Rev. 2016 Aug;37(4):347-71. doi: 10.1210/er.2015-1117. Epub 2016 May 17.
8
The therapeutic potential of chemical chaperones in protein folding diseases.化学伴侣在蛋白质折叠疾病中的治疗潜力。
Prion. 2014 Mar-Apr;8(2):197-202. doi: 10.4161/pri.28938. Epub 2014 May 12.
9
Recruitment of MLL by HMG-domain protein iBRAF promotes neural differentiation.HMG结构域蛋白iBRAF对MLL的招募促进神经分化。
Nat Cell Biol. 2005 Nov;7(11):1113-7. doi: 10.1038/ncb1312.

代谢肥胖症再生遗传学研究进展。

Advances in Genetics of Regeneration in Metabesity.

机构信息

Andalusian Center of Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucia-University of Pablo de Olavide-University of Seville-CSIC, 41092 Seville, Spain.

Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain.

出版信息

Genes (Basel). 2019 May 20;10(5):383. doi: 10.3390/genes10050383.

DOI:10.3390/genes10050383
PMID:31137597
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6563018/
Abstract

'Metabesity' is a recent term comprising a wide range of diseases with underlying metabolic disarrangements at its root, and whose aetiology lies in complex relationships among genes and the obesogenic environment to which individuals are currently exposed in most countries. Of note, epigenetic changes are increasingly being reported to play an outstanding role in carrying deleterious information that, together with susceptibility genes, boost the development of metabesity in subsequent generations. In this context, it is noteworthy to mention that the transition from the pre-industrial era to the current high-technology society and global economy, even after suffering two world wars, has been very fast. By contrast, evolution-driven processes, such as biological ones, are slow. In fact, there is a general consensus that at the metabolic level, adipogenic processes and thrifty pathways prevail over those promoting energy expenditure in a way that currently leads to metabolic diseases by excessive energy storage. In such an imbalanced social-biological scenario, genes that were beneficial in the past have shifted to becoming detrimental, i.e., favouring metabesity, which is quickly growing to reach pandemic proportions.

摘要

“代谢肥胖症”是一个最近出现的术语,它包含了广泛的疾病,其根本原因是代谢紊乱,其病因在于基因与肥胖环境之间的复杂关系,而在大多数国家,个体目前都处于肥胖环境中。值得注意的是,越来越多的表观遗传变化被报道在传递有害信息方面发挥着突出作用,这些信息与易感基因一起,促进了代谢肥胖症在后代中的发展。在这种情况下,值得一提的是,从工业前时代到当前的高科技社会和全球经济的转变,即使经历了两次世界大战,也非常迅速。相比之下,进化驱动的过程,如生物学过程,是缓慢的。事实上,人们普遍认为,在代谢水平上,脂肪生成过程和节俭途径胜过促进能量消耗的途径,从而导致目前通过过度能量储存导致代谢疾病。在这种不平衡的社会生物学环境中,过去有益的基因已经转变为有害的基因,即有利于代谢肥胖症,代谢肥胖症迅速发展到流行程度。