Cellular inflammatory responses: novel insights for obesity and insulin resistance.
Type 2 diabetes is rapidly becoming a worldwide epidemic. Obesity and sedentary lifestyle are the main environmental causes for the development of insulin resistance and type 2 diabetes. In the past decade, it has been increasingly recognized that obesity and insulin resistance are associated with chronic, low-grade systemic inflammation. This review will cover the recent advances in this field and provide a working model explaining how cellular inflammatory responses arise to cope with obesity-induced metabolic stresses and how these inflammatory responses underlie insulin resistance.
Chen
Hong
H
Novartis Institutes for BioMedical Research Inc., 100 Technology Square, Cambridge, MA 02139, USA. hong.chen@novartis.com
D000273:Adipose Tissue / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000502:physiology; D006801:Humans; D051550:I-kappa B Kinase / Q000502:physiology; D007249:Inflammation / Q000209:etiology*; D007333:Insulin Resistance; D008264:Macrophages / Q000502:physiology; D048055:Mitogen-Activated Protein Kinase 8 / Q000502:physiology; D009765:Obesity / Q000150:complications*; D011493:Protein Kinase C / Q000502:physiology; D015398:Signal Transduction; D050826:Suppressor of Cytokine Signaling Proteins / Q000502:physiology; D000099221:Protein Kinase C zeta
D051550:I-kappa B Kinase; D048055:Mitogen-Activated Protein Kinase 8; D011493:Protein Kinase C; D050826:Suppressor of Cytokine Signaling Proteins; D000099221:Protein Kinase C zeta; C496560:IKBKB protein, human