Impact of Stress on Obesity-Targetted Signaling Pathways for Novel Drug Discovery

Abstract

Obesity is an epidemic that affects millions of people across the world. It is a metabolic disorder that can be characterized by an excess buildup of adipose tissue. Stress can be defined as the organism's false response to any kind of demand or challenge to equilibrium. Whenever an organism comes in contact with any sort of stressor (physical, social, etc.), all the originating internal stress mechanisms are triggered to start a flight or fight response and thereby deal with the stress event. Several animal stress models are thought to exhibit unique metabolic traits, with some animals exhibiting signs of anorexia and a reduction in body weight, while others show an increase in food consumption and body weight and become more prone to disorders of metabolism. Hormones that are released by the endocrine organ gut, such as ghrelin, leptin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), pancreatic polypeptide (PP) as well as cholecystokinin (CCK), have quite an influence on the maintenance of homeostasis and energy balance by generating satiety and food termination. Leptin, a hormone that is released by adipocytes into the bloodstream is necessary for the regulation of body weight and the proper balance of energy. Obesity is caused primarily by leptin deficits or genetic abnormalities in the signaling of the leptin mechanism. A therapeutic approach by the use of probiotics as an external living system for the control of obesity is usually suggested by recent research that examined the relationship of the gut microbiota with obesity. The superfamily of mitogen-activated protein kinases (MAPK) includes the c-Jun N-terminal kinase (JNK) family. In obesity, JNK is a signal transducer that has been extensively studied. This review explores various kinds of rodent stress models and signaling pathways that affect metabolic outcomes to better understand stress-induced obesity.