Preface

With great pleasure, we present you with the publication titled "Meta-inflammation and Obesity." The book represents a state-of-the-art compilation and overview of current scientific evidence on the role of meta-inflammation in obesity and obesity-related disorders. No country in the world has solved the problem of overweight and obesity, and the health and economic consequences of obesity are globally on the rise. We aim to reflect on those variables that we see as potential target points for weight loss and present the best available current data on the overweight and obesity epidemic. The balance between energy intake and expenditure in the body is maintained by complex physiological mechanisms that integrate neuronal activity in various central nervous system structures with signals coming from the gastrointestinal system, adipose tissue, endocrine glands, and the autonomic nervous system. White adipose tissue secretes adipokines that regulate numerous biological processes by autocrine, paracrine, and endocrine mechanisms. Adipokines are essential for the balance between appetite and satiety, regulation of body fat stores and energy expenditure, glucose tolerance, insulin release and sensitivity, cell growth, inflammation, oxidative stress, angiogenesis, and atherosclerosis. The pathophysiological consequences of obesity are largely based on the morphofunctional changes in the visceral adipose tissue. By disrupting all phases of adipogenesis, visceral obesity causes adipocyte dysfunction, with changes in the adipokine secretion pattern, and the onset of meta-inflammation. The term "meta-inflammation" refers to chronic metabolic inflammation, which is said to have a significant role in the pathogenesis of numerous metabolic diseases. The majority of authors agree that inflammation may serve as a link between obesity and numerous diseases. Hence, the role of meta-inflammation in the pathogenesis of obesity-related diseases is currently extensively investigated. Biological and psychosocial differences between men and women affect the epidemiology and pathophysiology of many diseases, including type 2 diabetes mellitus (T2DM). Obesity is a major risk factor for T2DM. Sex hormones (estrogens and androgens) contribute to gender differences in obesity-related T2DM since they regulate not only biological characteristics but also adipose tissue function and metabolism. Current evidence suggests that obesity, in addition to being a contributing factor for cardiovascular and metabolic disorders, also increases the risk of Alzheimer's disease (AD). It is a well-documented fact that the brain is significantly affected by the inflammatory condition of obesity, i.e., meta-inflammation via several pathways. In addition to the role of meta-inflammation, recent research has shown that insulin resistance and impaired insulin signaling can contribute to the development of AD, as well as other neurological disorders. With this in mind, a group of scientists has proposed the term brain diabetes, or diabetes type 3, for cognitive impairment in AD patients, to unify the metabolic inflammatory pathways in the development of the disorder. Obesity is coupled with an altered redox state and increased metabolic risk. Antioxidant defenses in obese patients are decreased, and their concentrations correlate inversely with core adiposity. Moreover, obesity is also defined by increased concentrations of reactive oxygen or nitrogen species. Metabolic changes caused by excessive adipose tissue are associated with damage to the central nervous system, which can result in neuronal death, either through apoptosis or cell necrosis or by modifying the neuron's synaptic plasticity. Adipose tissue dysfunction associated with obesity has been correlated with abnormal brain metabolism, neuroinflammation, brain atrophy, neural impairment, diminished mood, and cognitive decline. The term inflammaging refers to chronic, low-grade systemic inflammation that can be conceptualized as a basis for human aging. Although the importance of inflammaging in the aging process is now well recognized, its etiology remains largely unknown. Given that in the last two decades, the role of chronic systemic low-grade inflammation has gained significant attention as the key player in the pathophysiology of obesity- and aging-associated diseases, future studies should unravel whether inflammatory processes are the cause or consequence of obesity and aging. Furthermore, although some therapeutic interventions alleviate obesity, it seems that they are not sufficient alone and should be reinforced with the use of medications and other therapeutic modalities proven to decrease inflammatory processes.

The preface aims to give insight into the content of our book, and we as the authors sincerely hope that our readers and colleagues will find it interesting and useful in the acquisition of cutting-edge research novelties on the interplay between meta-inflammation and obesity, that has significant clinical consequences.