The mechanisms involved in the control of food intake have been widely studied, since the obesity rates in several countries progressively increase. In long-term, adiposity related factors, such as leptin and insulin, signal the energy status to the central nervous system (CNS) stimulating the synthesis of various anorexigenic neuropeptides and inhibiting the production of orexigenic neuropeptides, in specific areas of the brain. On the other hand, ghrelin, produced by the stomach, stimulates hypothalamic neurons, which express orexigenic neuropeptides, namely neuropeptide Y (NPY) and Agouti related protein (AgRP). AMPK activation has been considered as a mediator of ghrelin in the hypothalamus. As a short-term control, satiety signals, generated during food intake, determine the meal size by activating neurons in the solitary tract (NTS). The primary adrenal insufficiency is characterized, among other clinical manifestations, by anorexia and accentuated body weight loss. Using experimental model of bilateral adrenalectomy (ADX) in rats, it was observed that the activation of NTS neurons increased by feeding, indicating that the increased satiety-related response contributes to the hypophagia induced by ADX. This study aims to evaluate the hypothalamic responsiveness to ghrelin in adrenalectomized rats. For this purpose, we will evaluate the food intake and body weight, as well as the activation of AMPK in the hypothalamus after stimulation with ghrelin in adrenalectomized rats and controls.
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