在2型糖尿病和肥胖症中,N-乙转移酶1和2的功能和表达在淋巴细胞中发生改变
Víctor Alejandro Paz-Rodríguez1, Diana Judith Herrera-Vargas1, Eneida Turiján-Espinoza2
1Research Center for Health Sciences and Biomedicine, Autonomous University of San Luis Potosi (UASLP), Mexico.
Biochemistry and biophysics reports
|May 13, 2024
概括
在2型糖尿病 (T2D) 患者中,N-乙转移酶 (NAT) 的表达和活性发生变化. NAT2与血糖控制有关,而NAT1与脂质水平有关,这表明它们在T2D和与肥胖有关的脂质不良症中的作用.
科学领域:
- 生物化学 生物化学
- 代谢性疾病是一种代谢性疾病.
- 药物基因组学 药物基因组学
背景情况:
- 细胞酶N-乙转移酶1和2 (NATs) 乙化异生菌.
- NATs是通过Sirtuins (deacetylases) 进行表观遗传调节的.
- NAT中的遗传变异 (SNP) 可能会影响它们的功能.
研究的目的:
- 评估NAT1,NAT2和SIRT1表达以及NATs在2型糖尿病 (T2D) 患者中的活性.
- 为了研究NATs,sirtuins和代谢参数之间的关联.
- 探索NAT2基因变异在T2D中的作用.
主要方法:
- 用于酶表达 (NAT1,NAT2,SIRT1) 的流细胞计.
- 细胞培养和HPLC用于NATs酶活性.
- 在NAT2.2.中为六个单核酸多态 (SNPs) 进行基因定型.
- 对T2D患者 (n=29) 和健康对照组 (n=25) 的比较.
主要成果:
- 二型糖尿病患者的NAT酶表达增加,NAT2活性降低.
- NAT1水平与身体脂肪百分比和BMI负相关.
- 塞尔图因抑制/激素调节NAT2活性;NAT2快速乙化单体类型在T2D患者中更为频繁.
- 在CD3+细胞中的NAT2表达在快速乙化剂中更高.
- 与胆固醇和甘油三相关的NAT1水平;与HbA1c和葡萄糖水平相关的NAT2活性.
结论:
- NAT2在T2D代谢过程中发挥作用,由与葡萄糖和HbA1c的关联以及改变的SIRT-NAT轴证明.
- NAT1可能会导致超重/肥胖个体的脂质不良症.
- NAT2基因变异可能是T2D的危险因素.
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