Meta Inflammation And Obesity

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.

Characterized by obesity, insulin resistance, dyslipidemia, and hypertension, metabolic syndrome is associated with the risks of type 2 diabetes mellitus and cardiovascular disease. Obesity, which increases the incidence of atherosclerotic cardiovascular disease and subsequently leads to increased stress and inflammation, appears to play a central role in the progression of the syndrome. Evidence of inflammatory processes in accumulated fat appears to be an early initiator of metabolic syndrome. Likewise, the more active angiotensin system in obesity may contribute to even greater oxidative stress that serves as a key signaling event in vascular remodeling. These factors strengthen obesity's association with oxidative stress. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome is designed to encourage the development of evidence-based nutritional and pharmacological therapies that can attenuate the impact of obesity-induced insulin resistance and ensuing metabolic syndrome. The book offers a deep understanding of the molecular mechanisms that underlie the process. Edited by leading authorities on oxidative stress, the book's chapters report on cutting-edge research that explores intracellular events mediating or preventing oxidative stress and pro-inflammatory processes in obesity and type 2 diabetes. It also brings together research on the molecular mechanisms inherent in the progression of metabolic stress, includes phenotypic perspectives, and discusses dietary factors, including the role of micronutrients. The chapter authors, each a leading expert in his or her field, discuss different components of metabolic stress and obesity and their associations with oxidative stress and inflammation. The book fills a unique role as a base of knowledge for researchers seeking to develop nutritional and or pharmacological therapies, as well as clinicians seeking a better understanding of this increasingly common disease process.

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.

A comprehensive review of recent work on chromatin and non-histone proteins, this book arises from the interactions of a multidisciplinary group of scientists involved in the study of acetylation. This area of research opens up new and exciting possibilities for drug design, and so the final chapters in the book examine some of the potential applications in the treatment of various diseases.

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

Inflammation and Obesity: A New and Novel Approach to Manage Obesity and its Consequences is a comprehensive and up-to-date exploration of the correlation between obesity and inflammation. From the pathophysiology of obesity and inflammation, to the molecular mechanisms of obesity induced chronic inflammation, the book discusses how obesity and inflammation interact with other diseases. It highlights the hidden risk factors of obesity induced chronic inflammation, provides specific patient management guidelines regarding the higher inflammatory response in patients, and concludes with new therapeutic strategies to address inflammation in obese patients. Identifies the hidden physiological changes that accompany obesity, while also highlighting the challenge of managing obesity with a higher inflammatory response Discusses major hidden health risks of inflammation that accompany obesity, as well as management guidelines for obese patients Links the pathophysiology of inflammation and obesity to the therapeutic strategies that minimizes risk factors, thus opening new areas of research

​According to the World Health Organization, the epidemic of global obesity has nearly tripled since 1975. In 2016, more than 1.9 billion adults were overweight, over 650 million of which were obese. Being overweight and obese has been linked to a number of non-communicable, chronic diseases. Pathophysiology of Obesity-Induced Health Complications is a compilation of review articles dedicated to describe co-morbidities associated with obesity. The wide range that is covered is of significant interest to basic research scientists, clinicians and graduate students who are engaged in studying obesity-induced health complications. Furthermore, this book highlights the potential of novel approaches for the prevention and treatment of obesity and its related illnesses. Nineteen articles in this book are organized in four sections that are designed to provide an overview of obesity-induced health complications. The first section serves as an introductory section on the prevalence, causes, consequences, treatments and preventive approaches for obesity. Section two covers the metabolic disturbances and inflammation due to obesity. The third section is focused on neurological and visceral complications as a consequence of obesity. The final section covers strategies for the prevention of obesity-induced complications. The book illustrates that obesity can result in a diverse range of pathophysiological conditions that adversely affect health.

Macrophages are the sentinels of the immune system whose role has evolved beyond providing aseptic conditions to homeostasis, immune regulation, development, and behaviour. These cells have varied ontogenetic origins which reflects in their phenotypic and functional heterogeneity. Macrophage functions are fine-tuned by exogenous and endogenous signals and once tweaked, the information is included in their genetic makeup, albeit not indefinitely. Subversion of the macrophage functions is the hallmark of many pathogenic organisms and modulation of macrophage activity is pivotal to many therapeutic strategies. Fascinating and rapid developments in this field have necessitated the maintenance of currency of knowledge. This book provides a current account of information on varied topics in macrophage biology. Literature surveys have been presented in a captivating and lucid language. The contributing authors have also provided brief accounts of their own research. Every chapter provides a future perspective of what more could be achieved in the context of the current knowledge. The book will be of interest to students and researchers in microbiology, immunobiology, translational research, pathology, and related fields.