期刊
IMMUNITY
卷 55, 期 1, 页码 31-55出版社
CELL PRESS
DOI: 10.1016/j.immuni.2021.12.013
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资金
- Swiss National Foun-dation (SNF) Early Postdoc Mobility grant [P2BSP3_200177]
- U.S. National Institute of Diabetes and Digestive and Kidney Diseases [P30 DK063491, DK101395]
- Swiss National Science Foundation (SNF) [P2BSP3_200177] Funding Source: Swiss National Science Foundation (SNF)
Obesity can cause chronic systemic inflammation, leading to insulin resistance, beta-cell dysfunction, and ultimately type 2 diabetes. This inflammatory state also contributes to long-term complications of diabetes and may be associated with other conditions like Alzheimer's disease and polycystic ovarian syndrome.
Obesity leads to chronic, systemic inflammation and can lead to insulin resistance (IR), b-cell dysfunction, and ultimately type 2 diabetes (T2D). This chronic inflammatory state contributes to long-term complications of diabetes, including non-alcoholic fatty liver disease (NAFLD), retinopathy, cardiovascular disease, and nephropathy, and may underlie the association of type 2 diabetes with other conditions such as Alzheimer's disease, polycystic ovarian syndrome, gout, and rheumatoid arthritis. Here, we review the current understanding of the mechanisms underlying inflammation in obesity, T2D, and related disorders. We discuss how chronic tissue inflammation results in IR, impaired insulin secretion, glucose intolerance, and T2D and review the effect of inflammation on diabetic complications and on the relationship between T2D and other pathologies. In this context, we discuss current therapeutic options for the treatment of metabolic disease, advances in the clinic and the potential of immune-modulatory approaches.
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