Molecular Mechanisms Underpinning The Development Of Obesity

Obesity is a multi-factorial disease, in which an excess of accumulated body fat can reach levels capable of affecting health. It results from an interplay between environmental factors, eating behavior, genes, epigenetics, and neuronal stimuli. The main aim of this book is to provide a state-of-the-art revision about the molecular mechanisms underpinning the development of obesity, reviewing the current knowledge in areas like monogenic and polygenic obesity forms, but also providing an updated view of the emerging knowledge about epigenetics, nutrigenomics, and neuronal aspects that also contribute to obesity.

Obesity is a worldwide epidemic that affects half a billion people. It has been estimated that, if current trends continue, by 2050, 60% of men and 50% of women worldwide will be obese. Hypertrophy and hyperplasia of white adipose tissue caused by overweight and obesity lead to a chronic inflammatory state, which results in impaired insulin sensitivity and the development of diabetes. Currently, the number of people affected by diabetes globally exceeds 400 million (rising more rapidly in low- and middle-income countries). In 2019, diabetes was the ninth leading cause of mortality, with an estimated 1.5 million direct deaths. This book provides a comprehensive overview of the relationship between inflammation, obesity, and diabetes. It focuses on the pathogenesis and biological mechanisms of obesity, the interaction between adipose tissue and the immune system, the role of genetic and environmental factors, the progression of cardiovascular complications, and the association of obesity and inflammation with type 1 and type 2 diabetes, as well as gestational diabetes. This volume also includes practical recommendations for preventing and managing these conditions using both lifestyle modifications and pharmacological interventions. Written by experts in the field, Obesity, Diabetes and Inflammation: Molecular Mechanisms and Clinical Management addresses the role of inflammation in both obesity and diabetes, its effect on vascular and non-vascular pathologies, oxidative stress, genetics, and epigenetics. This text aims to be a valuable resource for researchers, clinicians, and students of medicine at all levels.

Global health has been challenged with the dawning of the era of the obesity epidemic, and thus as a consequence, strategies to reduce obesity have become public health priorities. According to the United Nations, obesity has been identified as a concern for achieving Sustainable Development Goals. Obesity is a serious health problem with an increased risk of several common diseases including diabetes, cardiovascular disease, and cancer. Although the fundamental cause of obesity and overweight is an imbalance between calorie intake and calorie expenditure, the underlying biochemical and metabolic processes that cause obesity are not fully understood. Two earlier volumes dedicated to the subject of obesity, published in the series “Advances in Biochemistry in Health and Disease” focused on the pathophysiology of obesity-induced health complications and the biochemistry of cardiovascular dysfunction in obesity. This book brings together contributions from international experts in the field to describe advancements on the mechanisms leading to development of obesity and related complications. There are 21 chapters in two different parts in this book, comprising of Part I: Pathophysiologic Mechanisms of Obesity (11 chapters) and Part II: Therapeutic Mechanisms of Obesity (10 chapters). This book will serve as a resource and be of interest to health professionals, medical students, fellows, residents and graduate students. It will also evoke innovative research and effective approaches for the prevention of obesity. This volume will accentuate that obesity is a major health hazard in its own right and that appropriate public health measures should be implemented to prevent or reduce or even reverse the impact of this global chronic disease.

Obesity is a major risk factor for the development of type 2 diabetes and its associated complications, a major socio-economic burden for health care systems. The worldwide prevalence of obesity doubled since 1980 and as a consequence the number of patients with diabetes has been continuously rising with more than 450 Mio. people suffering from this disease at the present time. Substantial progress has been made in understanding the molecular pathways leading from excessive fat accumulation to metabolic perturbation and finally diabetes manifestation. This edition of the "Handbook of Experimental Pharmacology" aims to analyze new insight into the pathophysiology of obesity, to decipher the complex links to diabetes and its complications, and to collect most recent information on new strategies for prevention and treatment of obesity and diabetes.

This book summarizes the effects of obesity on health and its correlation with a wide range of debilitating and life-threatening conditions in humans. It discusses the possible pathological mechanisms that are involved in the development of obesity and highlights obesity-associated molecular mechanisms that contribute to reproductive dysfunctions in men and women. The book provides mechanistic insights on the role of obesity in cardiovascular and respiratory disorders, and examines the role of the complementary molecular mechanism of the gut microbiota in the development of obesity. It also reviews the interaction between the metabolic system and immune cells in the pathogenesis of obesity-associated diseases. Lastly, it assesses the latest advances in nanomedicine as an emerging strategy for the treatment of obesity.

Mitochondria produce the chemical energy necessary for eukaryotic cell functions; hence mitochondria are an essential component of health, playing roles in both disease and aging. More than 80 human diseases and syndromes are associated with mitochondrial dysfunction; this book focuses upon diseases linked to these ubiquitous organelles. Accumulation of mitochondrial DNA damage results in mitochondrial dysfunction through two main pathways. Mutation in mitochondrial DNA causes diseases such as Kearns-Sayre syndrome and Pearson syndrome. Mutation in chromosomal DNA causes diseases such as Parkinson's disease and schizophrenia. These and many other diseases are reviewed in this book. Key Features Presents the detailed structure of mitochondria, mitochondrial function, roles of oxidants and antioxidants in mitochondrial dysfunction. Includes summary of both causes and effects of these diseases. Discusses current and potential future therapies for mitochondrial dysfunction diseases Explores a wide variety of diseases caused by dysfunctional mitochondria.

This book brings a comprehensive treatise about obesity, examining the measures that can be taken to stop and even reduce obesity if these right measures are taken in time. Recent studies show that obesity is on the increase at an alarming rate, especially in the industrialized and affluent countries. A number of reasons have been put forward for this increase, including life style choices, over-eating, over-use of commercially processed food, addiction for fast food, high caloric diet specially containing high levels of sugar and fat, lack of exercise and sedentary life style. Also genetic make up has been associated with obesity. Obesity can lead to a variety of lethal diseases, notably coronary heart disease, cancer and diabetes. These diseases account for the highest number of human death amongst all other causes. There are also a number of other side effects associated with obesity including increased stress, loss of intelligentsia, pancreatitis, premature birth and osteoarthritis. In recent years media have been playing important roles in highlighting the lethality and damage caused by obesity, nevertheless no significant effects can be seen in the population and obesity remains on the increase, especially amongst children. The editors believe that it is important that more education, campaign and research are used to stop this increasing disease.