1,721,002 research outputs found
Serotonin and obesity
No full textHuman obesity represents a major threat to global well-being, and a better understanding of its pathogenic mechanisms may lead to the development of effective therapeutic strategies. In this article, we will review the existing literature dealing with the role of serotonin in the pathogenesis of obesity. Using a number of models, we demonstrate that abnormal hypothalamic serotonergic neurotransmission and/or deranged receptor expression/sensitivity exists, and that these are closely associated with changes in the concentrations of dopamine, another hypothalamic monoamine closely involved in the regulation of food intake. However, it is still difficult to ascertain whether these abnormalities are acquired in response to chronic overingestion resulting in obesity, which then drives further increases in food intake to preserve the status quo, or whether these are due to primary factors. The pivotal role of central serotonin in obesity is also strengthened by the evidence that the drugs licensed to interfere with food intake in obese patients involve the serotonergic system. But since their use, including sibutramine, may lead to potentially severe side effects, alternative strategy to increase hypothalamic serotonergic activity is also proposed
Secondary anorexia: a neglected issue in the optimal management of patients suffering from acute and chronic diseases.
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Involvement of plasma leptin, insulin and free tryptophan in cytokine-induced anorexia
No full textBackground- Hypothalamic serotonin, the synthesis of which parallels plasma free tryptophan, contributes to satiety. Plasma free tryptophan, insulin and leptin, all of which can also decrease food intake partly via the hypothalamic serotonergic system, are modulated by cytokines, which decrease food intake. The mechanisms of anorexia induced by cytokines, as related to plasma tryptophan, leptin and insulin, have not been fully determined. Objective.-We determined the plasma concentrations of free as well as total tryptophan, leptin and insulin, and correlations to those of food intake and body weight change after cytokines or tryptophan injection. Design: Interleukin-1alpha and/or tumor necrosis factor-alpha, or tryptophan was injected subcutaneously into male rats for 2 days. Daily food intake, body weight, carcass adiposity, plasma total as well as free tryptophan, plasma leptin and insulin were measured. Results: Interleukin-1alpha injection decreased food intake, body weight, carcass adiposity and plasma leptin, but increased plasma free tryptophan and insulin. Tryptophan injection increased both free and total tryptophan, but did not change food intake, body weight, carcass adiposity or leptin. Plasma free tryptophan, but not total tryptophan, was significantly negatively correlated with food intake. There was a negative correlation between plasma insulin and food intake. Conclusions: Increased plasma free tryptophan may contribute to synthesis of brain serotonin but anorexia may be due to stimulation of its release induced by interleukin-1alpha. Plasma insulin, but not leptin, may partly contribute to anorexia of cytokines. (C) 2003 Elsevier Science Ltd. All rights reserved
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