Pathophysiology of obesity: Endocrine, inflammatory and neural regulators

Abstract

Obesity is a “multi-metabolic and hormonal disease state” that primarily results from an imbalanced physiological energy homeostasis. There is a wide range of factors that play role in the causation of obesity, which can be exogenous or endogenous. Despite significant advances in research to develop knowledge over the development and progression of obesity, the understanding of its exact etiopathology remains incomplete. Complex interplays of hormonal and neural circuitry regulate the energy balance and food intake behavior with peripheral afferent signals conveying the state of energy requirement to the hypothalamus which in turn trigger efferent neuro-endocrine pathways to regulate the food intake behavior and energy expenditure for various physiological functions. Any disruption in neuro-chemical and feedback signaling, that include hormones, cytokines and other regulators derived from the key endocrine glands, adipose tissues, as well as the gastrointestinal tract, lead to metabolic dysfunctions. These metabolic dysregulations in conditions like obesity translate to the systemic level, causing several comorbidities, commonly insulin resistance, diabetes, atherosclerosis, hypertension, cardiovascular diseases, as well as reproductive disorders. The prevalence of obesity is following a steady increasing trend worldwide, and it serves as a common causative of several contemporary diseases. Thus, the present article precisely explains the pathophysiology of obesity emphasizing on different endocrine, chemical and neural regulators involved in the mechanism of its induction and progression.