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Desnutrición y amenorrea hipotalámica funcional: Neuropéptidos periféricos (Leptina, Adiponectina, Ghrelina) y su relación con la homeostasis metabólica

Keywords: functional amenorrhea, hypergrelin, energetic metabolic disbalance, insulin.

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Abstract:

functional hypothalamic amenorrhea (fha) is usually associated with an inadequate qualitative and quantitative diet which influences the energetic balance, modifies the body composition and produces hormonal reactions in order to keep metabolic homeostasis. this adaptive process is regulated by a "central circuit" (hypothalamic hormones), a "peripheral circuit" originated by adipocyte tissue (leptin, adiponectin, among other cytokines) and the superior gastrointestinal tract through a neuropetide: ghrelin. leptin acts in the hypothalamus stimulating the synthesis of msh and inhibits the npy and the agrp (agouti-related-peptide) both with orexigen action. npy stimulates crh and both inhibit gnrh in the hypothalamus. low levels of leptin in fha increases npy-crh system blocking gn-rh pulsatility, a key process in fha physiopathology. insulin regulates fatty acids synthesis and inhibits its release from adipocyte tissue. an alteration in insulin secretion in amenorrheic undernou rished women induces lipolisis and increases the availability of fatty acids for its utilization as energetic compounds. insulin and catecholamines regulate the secretion of leptin and free fatty acids levels. caloric restriction induces the reduction of leptin levels, inhibits insulin secretion, produces glucagon release and increases norepinephrine serum levels. both implicated in the regulation and availability of peripheral carbohydrates. lipolysis and release of fatty acids with the eventual presence of ketonuria, indicates that these amenorrheic patients present metabolic acidosis. additionally, adiponectin promotes the oxidation of free fatty acids in skeletal muscle, produces a reduction of triglycerides in these tissues, and inhibits directly the uptake and oxidation of free fatty acids in the liver, decreasing the concentration of triglycerides. these actions also increase the insulin sensibility, characteristic in this pathology. adiponectin reduces the release of glucose from the li

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