Eating Behavior Disorders in Uremia: A Question of Balance in Appetite Regulation

作者: Abelardo Aguilera , Rosa Codoceo , María A Bajo , Pedro Iglesias , Juan J Diéz

DOI: 10.1046/J.0894-0959.2004.16086.X

关键词: Tryptophan transportAnorexiaEndocrinologyMedicineHyperinsulinemiaAppetiteUremiaObesityInternal medicineLeptinNeuropeptide Y receptor

摘要: Eating and appetite disorders are frequent complications of the uremic syndrome which contribute to malnutrition in dialysis patients. The data suggest that anorexia may occur with or without abdominal visceral fat accumulation despite a lower food intake. This form obesity (i.e., low intake malnutrition) is more common patients than high article reviews current knowledge regarding mechanisms responsible for regulation normal conditions Anorexia has been historically considered as sign toxicity due "inadequate" judged by uncertain means ("middle molecule" accumulation, Kt/V, "peak-concentration hypothesis," others). We propose tryptophan-serotonin hypothesis, based on uremia-induced disorder patients' amino acid profile--low concentrations large neutral branched-chain acids tryptophan levels. A rate transport across blood-brain barrier increases synthesis serotonin, major inhibitor. Inflammation also play role genesis malnutrition. For example, silent infection Helicobacter pylori be source cytokines cachectic action; its eradication improves nutrition. evaluation should take into account cultural social aspects. Uremic showed universal trend carbohydrate preference red meat refusal compared healthy people. In contrast, white was less problematic. have remarkable attraction citrics strong flavors general. preferences refusals related predominance some peptide modulators. High levels cholecystokinin (CCK) (a powerful anorexigen) associated early satiety carbohydrates neuropeptide Y (NPY) (an orexigen) repeated Obesity elevated body mass index often falsely good nutritional status. hyperinsulinemia state), distribution (insulin, leptin, insulin-like growth factor [IGF]-1, fatty acids, receptors insulin, lipoprotein lipase, mitochondrial uncoupling protein-2, beta 3 adrenoreceptors) cause an increase appetite. Finally, uremia highly complex. Disorders adipose tissue, gastrointestinal neuropeptides, retained hyperproduced inflammatory end products, central nervous system changes all role. explained hypothalamic hyperserotoninergic state derived from concentration acids.

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