Abstract:
Hypothalamic neuropeptides, such as neuropeptide Y (NPY) produced by neurons in the arcuate nucleus (ARC) and alpha-melanocyte stimulating hormone (_-MSH, a post-translational cleavage product of proopiomelanocortin, POMC) produced by neurons in both the ARC and the ventromedial nucleus (VMN), appear to be important in regulating food intake and body weight. It has been hypothesised that obesity may be a result of an increase in the activity of hypothalamic NPY neurons and/or a decrease in the activity of hypothalamic POMC neurons. It has been hypothesized that altered hypothalamic neuropeptide signaling may play a role in both genetic obesity (e.g., 'ob'/' ob' mouse) and ypothalamic obesity, which occurs as a result of cellular destruction in the VMN (e.g. gold thioglucose (GTG)-induced obesity). It has been proposed that leptin acts on the hypothalamus to decrease food intake and decrease body weight gain and that these effects are a result of inhibition of hypothalamic NPY neurons and/or stimulation of hypothalamic POMC neurons. Therefore, three studies, employing different mouse models of obesity, were undertaken to examine the roles of NPY neurons, POMC neurons, and leptin in the regulation of food intake and weight gain. (Abstract shortened by UMI.)
