Age-related inflammation and insulin resistance: a review of their intricate interdependency

• Published in: Archives of pharmacal research Vol. 37; no. 12; pp. 1507 - 1514
• Main Authors: Park, Min Hi, Kim, Dae Hyun, Lee, Eun Kyeong, Kim, Nam Deuk, Im, Dong Soon, Lee, Jaewon, Yu, Byung Pal, Chung, Hae Young
• Format: Journal Article
• Language: English
• Published: Heidelberg Pharmaceutical Society of Korea 01.12.2014; 대한약학회
• Subjects: adipose tissue; adiposity; Aging - immunology; aorta; Cytokines - biosynthesis; Cytokines - immunology; endoplasmic reticulum; Endoplasmic Reticulum Stress - immunology; Humans; hyperinsulinemia; Inflammation; insulin resistance; Insulin Resistance - immunology; kidneys; Lipid Metabolism - immunology; liver; Medicine; muscles; obesity; Obesity - immunology; Pharmacology/Toxicology; Pharmacy; Proto-Oncogene Proteins c-akt - biosynthesis; Proto-Oncogene Proteins c-akt - immunology; Review; risk factors; Signal Transduction; 약학; Aging; Molecular inflammation; Insulin resistance
• ISSN: 0253-6269; 1976-3786; 1976-3786
• DOI: 10.1007/s12272-014-0474-6

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.