Neurological And Biochemical Aspects Of Eating Disorders

Abstract

Current studies on the epithalamic nuclei, referring to appetite, have further enriched the doubts about the pathogenesis of anorexia, bulimia and obesity, with the influence on the nuclei of the lateral hypothalamus, which produces lack of appetite thanks to the release of leptin, but which can also be produced by orexin, galanin, or hypocreatine. After food intake and consequent increase in fat levels, leptin - composed of alpha-MSH (an anorectic peptide, melanocyte-stimulating hormone) and CART (peptide regulated by cocaine and amphetamine) - is high in the blood, activating the arcuate nucleus and increasing adrenocorticotropic hormone (ACTH) and thyroid-stimulating hormone (TSH). The metabolic rate is high in obese people, because it is proportional to being overweight: they are less effective in counterbalancing or adjusting their metabolic needs. Modernly, the metabolic phase is valued, in which adenosinotriphosphatase exerts a special power. The mobilization of fat, containing more triglycerides, occurs by the degradation of these into glycerol and free fatty acids, which are transported together with albumin. This transformation is possible because an enzyme, lipase, is activated by epinephrine, glucagon, ACTH, TSH and somatotropin. Mobilization depends on the activation of intracellular lipase. These stimuli are studied, but the influence of glycemic levels - hypo and hyperglycemic - on the action of insulin, or not, and the amount of corticosteroid, lysine, carnitine and the cupric cofactor dopamine-beta-hydrolaxilase, which converts dopamine into norepinephrine, and its low can produce anorexia nervosa, is recognized.