禁食和食后DNA甲基化特征在脂肪组织中,来自具有代谢变化的无症状个体
Fabiola Escalante-Araiza1,2, Angélica Martínez-Hernández1, Humberto García-Ortiz1
1Immunogenomics and Metabolic Diseases Laboratory, Instituto Nacional de Medicina Genómica, Secretaría de Salud, Mexico City 14610, Mexico.
International journal of molecular sciences
|December 11, 2025
概括
餐后发生皮下脂肪组织 (SAT) DNA甲基化的表观遗传变化,特别是在2型糖尿病 (T2D) 中. 这些取决于食的SAT变化可能先于血糖问题,有助于预防T2D.
科学领域:
- 代谢学和表观遗传学
- 人体生理学 人体生理学
- 内分泌学 在内分泌学.
背景情况:
- 像2型糖尿病 (T2D) 这样的心脏代谢疾病与肥胖和胰岛素抵抗有关.
- 饭后状态对于新陈代谢调节至关重要.
- 表观遗传机制,特别是对胰岛素敏感组织的DNA甲基化,是相关的,但它们在不同的prandial状态期间在皮下脂肪组织 (SAT) 中的作用尚不清楚.
研究的目的:
- 在空腹和食后状态期间在SAT中调查全基因组DNA甲基化动态.
- 将这些表观遗传变化与正常葡萄糖耐受性,糖尿病前期和T2D的个体进行比较.
- 确定T2D风险和预防的潜在早期表观遗传生物标志物.
主要方法:
- 对29名以前没有服用过药物的人 (对照组8人,糖尿病前组9人,T2D组12人) 的空腹和食后SAT活检进行分析.
- 标准化混合饮食试验,以诱导食后状态.
- 使用Illumina MethylationEPIC阵列进行全基因组DNA甲基化量化.
- 使用芯片分析甲基化管道 (ChAMP) 的生物信息分析.
主要成果:
- 在食后状态中,差异性DNA甲基化更为明显,特别是在T2D组.
- 确定了4599个差异甲基化CpG位点 (DMC),在T2D中趋向于高甲基化.
- 在糖尿病前期和T2D组之间共享了130个DMC (在99个基因中) 和110个差异甲基化区域 (DMR),这表明早期的表观遗传变化.
- 丰富的途径包括胰岛素耐药性,AMPK信号传递和免疫反应.
结论:
- 在SAT中Prandial依赖的表观遗传变化发生在早期,甚至在明显的失糖症之前.
- 这些发现突显了SAT DNA甲基化在代谢调节和T2D病变发生过程中的作用.
- 鉴定的表观遗传变化可能为个性化T2D预防策略提供新的目标.
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