NAD+激酶
尿酸
高尿酸血症
锡尔图因
烟酰胺腺嘌呤二核苷酸
胰岛素抵抗
氧化应激
果糖
内科学
炎症
西妥因1
内分泌学
化学
生物化学
生物
医学
胰岛素
下调和上调
酶
基因
作者
Bernardo Rodríguez‐Iturbe,Richard J. Johnson,Miguel A. Lanaspa,Takahiko Nakagawa,Fernando E. García‐Arroyo,Laura Gabriela Sánchez‐Lozada
出处
期刊:American Journal of Physiology-regulatory Integrative and Comparative Physiology
[American Physiological Society]
日期:2022-03-10
卷期号:322 (5): R347-R359
被引量:6
标识
DOI:10.1152/ajpregu.00238.2021
摘要
Fructose metabolism and hyperuricemia have been shown to drive insulin resistance, metabolic syndrome, hepatic steatosis, hypertension, inflammation, and innate immune reactivity in experimental studies. We suggest that these adverse effects are at least in part the result of suppressed activity of sirtuins, particularly Sirtuin1. Deficiency of sirtuin deacetylations is a consequence of reduced bioavailability of its cofactor nicotinamide adenine dinucleotide (NAD
科研通智能强力驱动
Strongly Powered by AbleSci AI