{"title":"DNA Methylation in the Hypothalamic Feeding Center and Obesity.","authors":"Chiharu Yoshikawa, Winda Ariyani, Daisuke Kohno","doi":"10.7570/jomes23073","DOIUrl":null,"url":null,"abstract":"<p><p>Obesity rates have been increasing worldwide for decades, mainly due to environmental factors, such as diet, nutrition, and exercise. However, the molecular mechanisms through which environmental factors induce obesity remain unclear. Several mechanisms underlie the body's response to environmental factors, and one of the main mechanisms involves epigenetic modifications, such as DNA methylation. The pattern of DNA methylation is influenced by environmental factors, and altered DNA methylation patterns can affect gene expression profiles and phenotypes. DNA methylation may mediate the development of obesity caused by environmental factors. Similar to the factors governing obesity, DNA methylation is influenced by nutrients and metabolites. Notably, DNA methylation is associated with body size and weight programming. The DNA methylation levels of proopiomelanocortin (<i>Pomc</i>) and neuropeptide Y (<i>Npy</i>) in the hypothalamic feeding center, a key region controlling systemic energy balance, are affected by diet. Conditional knockout mouse studies of epigenetic enzymes have shown that DNA methylation in the hypothalamic feeding center plays an indispensable role in energy homeostasis. In this review, we discuss the role of DNA methylation in the hypothalamic feeding center as a potential mechanism underlying the development of obesity induced by environmental factors.</p>","PeriodicalId":45386,"journal":{"name":"Journal of Obesity & Metabolic Syndrome","volume":" ","pages":"303-311"},"PeriodicalIF":4.7000,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10786209/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Obesity & Metabolic Syndrome","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7570/jomes23073","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/21 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
Obesity rates have been increasing worldwide for decades, mainly due to environmental factors, such as diet, nutrition, and exercise. However, the molecular mechanisms through which environmental factors induce obesity remain unclear. Several mechanisms underlie the body's response to environmental factors, and one of the main mechanisms involves epigenetic modifications, such as DNA methylation. The pattern of DNA methylation is influenced by environmental factors, and altered DNA methylation patterns can affect gene expression profiles and phenotypes. DNA methylation may mediate the development of obesity caused by environmental factors. Similar to the factors governing obesity, DNA methylation is influenced by nutrients and metabolites. Notably, DNA methylation is associated with body size and weight programming. The DNA methylation levels of proopiomelanocortin (Pomc) and neuropeptide Y (Npy) in the hypothalamic feeding center, a key region controlling systemic energy balance, are affected by diet. Conditional knockout mouse studies of epigenetic enzymes have shown that DNA methylation in the hypothalamic feeding center plays an indispensable role in energy homeostasis. In this review, we discuss the role of DNA methylation in the hypothalamic feeding center as a potential mechanism underlying the development of obesity induced by environmental factors.
几十年来,全球肥胖率一直在上升,这主要是由于饮食、营养和运动等环境因素造成的。然而,环境因素诱发肥胖的分子机制仍不清楚。人体对环境因素的反应有多种机制,其中一种主要机制涉及 DNA 甲基化等表观遗传修饰。DNA 甲基化模式受环境因素的影响,DNA 甲基化模式的改变会影响基因表达谱和表型。DNA 甲基化可能是环境因素导致肥胖的介导因素。与肥胖的影响因素类似,DNA 甲基化也受到营养物质和代谢物的影响。值得注意的是,DNA 甲基化与体型和体重规划有关。下丘脑摄食中枢是控制全身能量平衡的关键区域,而下丘脑摄食中枢中的原绒毛膜促皮质素(Pomc)和神经肽Y(Npy)的DNA甲基化水平受饮食影响。对表观遗传酶的条件基因敲除小鼠研究表明,下丘脑摄食中枢的 DNA 甲基化在能量平衡中发挥着不可或缺的作用。在这篇综述中,我们将讨论下丘脑摄食中枢 DNA 甲基化作为环境因素诱发肥胖的潜在机制的作用。
期刊介绍:
The journal was launched in 1992 and diverse studies on obesity have been published under the title of Journal of Korean Society for the Study of Obesity until 2004. Since 2017, volume 26, the title is now the Journal of Obesity & Metabolic Syndrome (pISSN 2508-6235, eISSN 2508-7576). The journal is published quarterly on March 30th, June 30th, September 30th and December 30th. The official title of the journal is now "Journal of Obesity & Metabolic Syndrome" and the abbreviated title is "J Obes Metab Syndr". Index words from medical subject headings (MeSH) list of Index Medicus are included in each article to facilitate article search. Some or all of the articles of this journal are included in the index of PubMed, PubMed Central, Scopus, Embase, DOAJ, Ebsco, KCI, KoreaMed, KoMCI, Science Central, Crossref Metadata Search, Google Scholar, and Emerging Sources Citation Index (ESCI).