Neuropeptide Y (NPY) is a 36 amino acid protein which acts as a transmitter in the nervous system. NPY is involved in regulation of circadian rhythms, sexual functioning, anxiety and stress response, peripheral vascular resistance and contractility of the heart. Certain data indicate that neuropeptide Y is also involved in the regulation of feeding behavior including food intake and carbohydrate preference as well as metabolic and lipogenic rates. Therefore, NPY may be involved in regulation of body fat and development of obesity. For example, chronic intracerebroventricular administration of neuropeptide-Y to normal rats mimiced hormonal and metabolic changes of obesity. Intracerebroventricular injection of NPY had two effects on energy metabolism. In addition to increased feeding, it led to decreased brown fat thermogenesis and increased white fat lipoprotein lipase (LPL) enzymatic activity. The mRNA of preproneuropeptide Y is increased in the in the hypothalamus of genetically obese Zucker rats. This mRNA can be regulated by food deprivation. In addition, there seems to be a relation between the expression of leptin and NPY gene expression. Systemic administration of leptin inhibits the expression of NPY gene overexpression through a specific action in the arcuate nucleus and exerts a hypoglycemic action that is partly independent of its weight-reducing effects. In part, leptin acts through inhibition of biosynthesis and release of NPY. However, in the May 30, 96 issue of Nature, Erikson et al reported that the lack of expression of NPY gene is not essential for certain feeding responses or leptin actions. The only apparent manifestation of lack of NPY gene expression in mice lacking the gene, was sensitivity to leptin and susceptibility to seizures.
Neuropeptide Y (NPY) is a 36 amino acid protein which acts as a transmitter in the nervous system. NPY is involved in regulation of circadian rhythms, sexual functioning, anxiety and stress response, peripheral vascular resistance and contractility of the heart. Certain data indicate that neuropeptide Y is also involved in the regulation of feeding behavior including food intake and carbohydrate preference as well as metabolic and lipogenic rates. Therefore, NPY may be involved in regulation of body fat and development of obesity. For example, chronic intracerebroventricular administration of neuropeptide-Y to normal rats mimiced hormonal and metabolic changes of obesity. Intracerebroventricular injection of NPY had two effects on energy metabolism. In addition to increased feeding, it led to decreased brown fat thermogenesis and increased white fat lipoprotein lipase (LPL) enzymatic activity. The mRNA of preproneuropeptide Y is increased in the in the hypothalamus of genetically obese Zucker rats. This mRNA can be regulated by food deprivation. In addition, there seems to be a relation between the expression of leptin and NPY gene expression. Systemic administration of leptin inhibits the expression of NPY gene overexpression through a specific action in the arcuate nucleus and exerts a hypoglycemic action that is partly independent of its weight-reducing effects. In part, leptin acts through inhibition of biosynthesis and release of NPY. However, in the May 30, 96 issue of Nature, Erikson et al reported that the lack of expression of NPY gene is not essential for certain feeding responses or leptin actions. The only apparent manifestation of lack of NPY gene expression in mice lacking the gene, was sensitivity to leptin and susceptibility to seizures.
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