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The presence of peripheral signals influences the hypothalamus through actions from afferent neurones and brainstem. The chemoreceptors also play important roles in controlling appetite. These receptors mediate vagal afferent and pass on the signal s to the nucleus of tractus solitaries (NTS) present in the brainstem. Gut hormones also work through this vagal pathway and brainstem (Schwartz et al, 2000). Hence, the orexigenic and anorexigenic neurons in the hypothalamus are mediated by neural and hormonal signals. These neurons will extend to various others in the extra-hypothalamic and intra-hypothalamic regions, such as the hypothalamic paraventricular nucleus (PVN), and lateral hypothalamus (LH) where some of the significant efferent pathways…show more content…
Glucagon-like-peptide-1 (GLP-1):
A pre-proglucagon derived hormone secreted from L-cells of the distal gut in response to glucose ingestion. This hormone is known to decrease food intake in humans and rodents (Turton et al, 1996). GLP-1 binds to its receptor that is present in the gut and pancreas and is found throughout the central nervous system. The anorectic effect of GLP-1 is mediated through central and peripheral mechanisms by a population of neurones located in the brainstem that conveys the signal to the hypothalamus. These areas are significant in the maintenance of energy homeostasis (Navarro et al, 1996).
b. Cholecystokinin (CCK):
The gut peptide, cholecystokinin is released by I cells present in the upper small intestines which function to decrease food intake. There are two forms of CCK receptors: CCK1 and CCK2 receptors and are present throughout the body fulfilling major functions (Dufresne et al, 2006). It interacts with vagal sensory fibres through CCK1 receptors transferring signals to the brainstem to control the intake of food. The anorectic effects of CCK can be reduced through selective damage to these fibres or subdiaphragmatic vagotomy (Heijboer et al, 2006). In case of administration of CCK1 receptor antagonist before meal, large quantities of meals than normal are consumed. This proves that endogenous CCK is necessary to suppress intake of meals (West et al,
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