Immune and Inflammatory Processes in Obesity, Insulin Resistance, Diabetes, and Related Cardiometabolic Complications
1University of Saskatchewan College of Medicine, Department of Physiology, Saskatoon, SK, Canada S7N 5E5
2Division of Cardiovascular Medicine, Department of Medicine, Henry Ford Heart & Vascular Institute, 2799 West Grand Boulevard, Detroit, MI 48202-2689, USA
3Department of Pharmacology, Center for Integrative Medicine, Center for Molecular Medicine (CIMMBA), University of Florence, Viale Pieraccini 6, 50139 Florence, Italy
Immune and Inflammatory Processes in Obesity, Insulin Resistance, Diabetes, and Related Cardiometabolic Complications
Description
The high prevalence of obesity and diabetes in developed and developing nations poses a great health challenge. Obesity is one of the major causes of insulin resistance and type-2 diabetes. Type-1 diabetes is primarily due to the autoimmune-mediated destruction of pancreatic beta cell leading to insulin deficiency. This is generally accompanied by alterations in lipid metabolism, enhanced hyperglycemia-mediated inflammation and oxidative stress, endothelial cell dysfunction, and apoptosis. Similarly, type-2 diabetes is characterized by elevated inflammation, glucotoxicity, lipotoxicity, and apoptosis that leads to the progressive loss of beta cells and ultimately to insulin insufficiency at later stages of the disease. Thus, in diabetes, inflammation could be triggered by hyperglycemia and/or immune response. Although insulin resistance has traditionally been associated with type-2 diabetes, mounting evidence indicates that insulin resistance in type-1 diabetes is increasing. Therefore, novel mechanistic approaches deciphering the role of inflammation in insulin resistance in type-1 and type-2 diabetes are needed. Many pathophysiological agents are implicated in insulin resistance. Although the exact natures of these factors are not completely understood, a high consensus of opinion suggests that inflammation, oxidative stress, genetic, habitual, environmental, and epigenetic factors are implicated.
Therefore, this special issue will welcome research and review papers that address a wide spectrum of inflammation-related mechanisms associated with insulin resistance, type-1 diabetes, type-2 diabetes, and related cardiometabolic complications. Potential topics include, but are not limited to:
- Role of immune and inflammatory response in epigenetic processes implicated in type-1 and type-2 diabetes
- Novel immune/inflammatory mechanisms of insulin resistance and dysfunctional glucose metabolism in type-1 and type-2 diabetes
- Novel immune/inflammatory prognostic agents
- Novel suppressors of immune/inflammatory events with potential therapeutic application
- Role of immune/inflammatory events in macrovascular and microvascular complications of diabetic complications including atherosclerosis, cardiomyopathy, nephropathy, vasculopathy, and neuropathy
Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/jir/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/jir/oid/ according to the following timetable: