We concluded that the hyperphagia of prepuberal LPF animals could account for the HPA axis hyperactivity and for the HPT blocked function due to the altered ARC leptin signaling and impaired NPY regulation on PVN TRH neurons.
At the moment it seems that the p.L7P substitution of preproNPY protein causes altered NPY secretion, which leads to haemodynamic disturbances caused by sympathetic hyperactivity and to various effects caused by altered local signalling by NPY.
Genetically obese rodents also show hyperactivity of the NPY neurones, which is inappropriate to their energy needs and may contribute to their hyperphagia, reduced energy expenditure and excessive weight gain.