Glucose is the main energetic source for tissues, including the brain, and can be obtained by diet and also by metabolic processes involving the liver. Uncontrolled levels can be very damaging to the organism, and to prevent it, there are glycemic sensors scattered in regions such as the liver, sympathetic and vagal afferents, and CNS. When activated, the sensors release hormones to normalize blood glucose: mainly glucagon (to increase blood glucose) and insulin (to lower it). In the CNS, mostly in the hypothalamus, the insulin has effects on food behavior and modulation of autonomic nervous system (ANS). Previous studies of our laboratory indicate that the neurons of the paraventricular nucleus of the hypothalamus (PVN) are activated by the central injection of insulin and that these neurons also have projections to the dorsal motor of vagus nucleus (DMV), from which vagal preganglionic neurons innervate the liver, which are part of an important integration pathway on autonomic control of hepatic production of glucose (PHG). Furthermore, it has also been demonstrated in these studies that the central action of insulin in promoting Wistar PHG decrease is dependent of the activation of parasympathetic efferents, and it is a failed mechanism in spontaneously hypertensive rats (SHR), showing us that these animals have some deficiency in this pathway signaling. It is already known that SHR have insulin resistance even before they develop hypertension, and this relationship can contribute to the hypertension development, but this fact has not been explored. Therefore, the subjects of the present study are: to identify the phenotype of the PVN hypothalamic neurons that are projected for DMV and are activated by insulin acting in the CNS and to test the hypothesis that the deficiency in PHG control due to the central action of insulin in SHR is caused by failure on cholinergic neurotransmission in the parasympathetic preganglionic neurons of DMV.
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