Adipose Tissue And Inflammation

The American Obesity Association identifies obesity's link to numerous medical conditions, including hypertension, type 2 diabetes, cardiovascular disease, several cancers, and a host of inflammatory disorders. Evidence indicates that inflammation has more than a corollary relation with obesity; that in fact, obesity itself manifests a low-grade, m

For decades, scientific efforts have been made to understand obesity and related diseases such as type 2 diabetes and neurodegeneration, and their link with meta-inflammation. Adipose tissue is, at present, viewed as an endocrine organ with important biological effects on metabolism and inflammation, with a possible role in the pathogenesis of obesity-associated metabolic and inflammatory diseases. Chronic systemic low-grade inflammation has gained significant attention as the key player in the pathophysiology of obesity- and aging-associated diseases. Keeping view of this trend, Meta-Inflammation and Obesity offers readers state-of-the-art knowledge on this subject. Chapters cover special topics such as gender differences in obesity-related type 2 diabetes as the consequence of inflammatory response, insights into metabolic changes caused by excessive adipose tissue (which lead to abnormal brain metabolism, neuroinflammation, cognitive decline, development of type 3 diabetes), and the importance of inflammaging in the aging process. Graduate, postgraduate and Ph. D. candidates in medicine, pharmacy, and students of applied medicine, health care professionals as well as scientists involved in adipose tissue research, meta-inflammation analysis, obesity-related medical specialties will find this book a useful reference on the link between inflammation and obesity.

This book presents a comprehensive survey of adipose tissue, its physiological functions, and its role in disease. The volume spans the entire range of adipose tissue studies, from basic anatomical and physiological research to epidemiology and clinical studies. Groundbreaking recent studies are incorporated into traditional models of adipose tissue properties. A description of the role of macrophages in obesity and metabolism in included.

Due to the resultant health consequences and considerable increase in prevalence, obesity has become a major worldwide health problem. “Obesity and Lipotoxicity” is a comprehensive review of the recent researches to provide a better understanding of the lipotoxicity-related mechanisms of obesity and the potential for the development of new treatment strategies. This book overviews the biochemical pathways leading to obesity-related metabolic disorders that occur subsequent to lipotoxicity. Chapters examine the deleterious effects of nutrient excess at molecular level including the cellular and molecular aspects of breast cancer, resistance to leptin, insulin, adiponectin, and interconnection between the circadian clock and metabolic pathways during high-fat feeding. “Lipotoxicity and Obesity” will be a useful resource for clinicians and basic science researchers, such as biochemists, toxicologists, immunologists, nutritionists, adult and pediatric endocrinologists, cardiologists, as well as students who are thought in this field.

Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic disorder such as type 2 diabetes, fatty liver disease and cardiovascular disease. Insulin resistance is an underlying basis for the pathogenesis of these metabolic diseases. Overnutrition or obesity activates the innate immune system with subsequent recruitment of immune cells such as macrophages and T cells, which contributes to the development of insulin resistance. In particular, a significant advance in our understanding of obesity-associated inflammation and insulin resistance has been recognition of the critical role of adipose tissue macrophages (ATMs). ATMs are a prominent source of proinflammatory cytokines, such as TNF-a and IL-6, that can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signaling and cause systemic insulin resistance via endocrine signaling, providing a potential link between inflammation and insulin resistance. All articles in this topic highlight the interconnection between obesity, inflammation, and insulin resistance in all its diversity to the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of insulin resistance and diabetes.

This timely and most comprehensive reference available on the topic covers all the different aspects vital in the fight against the global obesity epidemic. Following a look at adipose tissue development and morphology, the authors go on to examine its metabolic and endocrine functions and its role in disease. The final section deals with comparative and evolutionary aspects of the tissue. The result is an essential resource for cell and molecular biologists, physiologists, biochemists, pharmacologists, and those working in the pharmaceutical industry.

In addition to its metabolic and endocrinologic effects, obesity and adipose tissue have now been shown to be associated with low grade inflammation resulting in cellular and humoral inflammatory factors of which the latter may act by endocrine, paracrine and autocrine mechanisms. These inflammatory mediators have increasingly been suggested as contributing to the obesity link to carcinogenesis and cancer promotion. This volume of Energy Balance and Cancer will focus on recent developments and cutting edge research pointing to inflammation and inflammatory factors as key mediators of this linkage. The volume first provides information on inflammation as an important link between obesity and insulin resistance, which is in itself linked to promotion of cancer through hyperinsulinemia. The volume then covers some of the most important mechanisms by which obesity leads to inflammation, including the novel inflammasome concept, alterations in chromatin structure, circulating inflammatory factors, unique cellular interactions between adipocytes and macrophages and the direct link of dietary fat to inflammation and cancer. Overall, this volume will provide important insight to help understand how inflammation may help modulate the linkage between obesity and cancer and serve as a platform for developing future research in this area.