Park Min Hi, Kim Dae Hyun, Lee Eun Kyeong, Kim Nam Deuk, Im Dong Soon, Lee Jaewon, Yu Byung Pal, Chung Hae Young
Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University, Busan, 609-735, Republic of Korea.
Arch Pharm Res. 2014 Dec;37(12):1507-14. doi: 10.1007/s12272-014-0474-6. Epub 2014 Sep 20.
Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER) stress, which lead to insulin resistance. However, some studies show that insulin resistance itself amplifies chronic inflammation. The activity of the insulin-dependent Akt signaling pathway is highlighted because of its decrease in insulin-sensitive organs, like liver and muscle, which may underlie insulin resistance and hyperinsulinemia, and its increased levels in non-metabolic organs, such as kidney and aorta. In that the prevalence of obesity has increased substantially for all age groups in recent years, our review summarizes the data showing the involvement of chronic inflammation in obesity-induced insulin resistance, which perpetuates reciprocal interactions between the chronic inflammatory process and increased adiposity, thereby accelerating the aging process.
慢性炎症是衰老及相关衰老疾病的主要潜在风险因素;衰老过程中的胰岛素抵抗尤其值得关注。慢性炎症会损害正常的脂质蓄积、脂肪组织功能、线粒体功能,并引发内质网(ER)应激,进而导致胰岛素抵抗。然而,一些研究表明,胰岛素抵抗本身会加剧慢性炎症。胰岛素依赖性Akt信号通路的活性备受关注,因为在肝脏和肌肉等胰岛素敏感器官中其活性降低,这可能是胰岛素抵抗和高胰岛素血症的基础,而在肾脏和主动脉等非代谢器官中其水平升高。鉴于近年来所有年龄组的肥胖患病率都大幅上升,我们的综述总结了相关数据,表明慢性炎症参与了肥胖诱导的胰岛素抵抗,这使得慢性炎症过程与肥胖增加之间形成相互作用,从而加速衰老进程。