Book Description

The World Health Organization Organization estimates that over 1.9 billion people worldwide are now obese or overweight [body mass index (BMI) > 27 Kg/m2]. Type 2 diabetes (T2D) is now recognized as the most devastating complications of obesity. Intimate relationship exists between obesity, innate (neutrophils, dendritic cells, macrophages, mast cells, and eosinophils) and adaptive (B and T lymphocytes) immune cells. Cells of the innate immune system produce inflammatory cytokines, and other factors leading to impaired insulin secretion and insulin resistance. Likewise, B lymphocytes (mostly B2 cells) are activated in obese adipose tissue and contribute to proinflammatory activation of adipose tissue macrophages and T cells resulting in insulin resistance. Thus, obesity-induced low-grade inflammation in adipose tissue, liver, skeletal muscle, and pancreas not only activates the innate and adaptive systems affecting metabolic homeostasis, it also results in fibrosis and necrosis. It is now becoming increasingly evident that fibrosis is a major contributor to metabolic dysregulation in obese and T2D patients and that advanced liver fibrosis leads to cirrhosis and death. The health risks associated with obesity are further exaggerated by smoking. This research topic consisting of 10 articles (9 reviews and one original) provide a comprehensive assessment of the impact of obesity on immunometabolism, cardiac functions, the connections of nicotine to NAFLD, the expression of hepatic carcinoembryonic antigen related cell adhesion molecule 1 (CEACAM1), the role chromogranin A (CgA) and its peptides pancreastatin (PST) and catestatin (CST) in insulin sensitivity, the loss of skeletal muscle mass and function, and the alternate RNA splicing.