Obesity due to stress: A change in glucose and lipid metabolism due to altered cortisol levels
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In this literature study different topics concerning stress-induced obesity are described. First of all the dangers and causes of obesity are discussed. Next, the mechanism of stress is explained with among others the HPA axis, which is responsible for the secretion of the glucocorticoid cortisol. Cortisol is able to bind to two different receptors and thereby influence different processes. In this thesis, the effects of cortisol on three systems are thoroughly described. One of these processes is the glucose metabolism. Cortisol influences gluconeogenesis, glycogenolysis and a special enzyme catalyzing the conversion of the inactive form of cortisol to the active form: 11β - hydroxysteroid dehydrogenase type 1. Cortisol also has an effect on the lipid metabolism. Within this metabolism it mainly stimulates the breakdown of adipose tissue (lipolysis), which results in a large amount of free fatty acids in the plasma. This in turn has an effect on other processes which will be inhibited or stimulated. Not only the lipid metabolism and glucose metabolism are affected by cortisol, also the central nervous system. Different parts of the brain respond to cortisol by changing morphology of neurons, which among others leads to "stress eating" and being agitated. All these effects of cortisol can lead to obesity and form a danger for human. Fortunately, there are many ways in which this might be treated and this is discussed in the last chapter of this study.