Sustained NPY Overexpression in the PVN Results in Obesity via Temporarily Increasing Food Intake
Citations Over TimeTop 18% of 2009 papers
Abstract
Increasing neuropeptide Y (NPY) signaling in the paraventricular nucleus (PVN) by recombinant adeno-associated virus (rAAV)-mediated overexpression of NPY in rats, results in hyperphagia and obesity in rats. To determine the importance of hyperphagia in the observed obesity phenotype, we pair-fed a group of AAV-NPY-injected rats to AAV-control-injected rats and compared parameters of energy balance to ad libitum fed AAV-NPY-injected rats. For 3 weeks, AAV-NPY-injected rats, received the same amount of food as ad libitum-fed rats injected with control rAAV They did not gain more body weight than these controls. When allowed access to food ad libitum, these AAV-NPY-injected rats increased food intake, which subsequently decreased when rats reached the same body weight as AAV-NPY-injected rats that were fed ad libitum for the entire study. These data indicate that overexpression of NPY in the PVN results in obesity by increasing food intake until a certain body weight is achieved.
Related Papers
- → Effect of a selective neuropeptide Y Y2 receptor antagonist, BIIE0246 on neuropeptide Y release(2000)126 cited
- → Pharmacology of neuropeptide Y receptor antagonists(2002)33 cited
- → Neuropeptide Y (NPY)-containing nerves in mammalian ureter(1990)25 cited
- → Pharmacological characterization of neuropeptide Y-(2–36) binding to neuropeptide Y Y1 and Y2 receptors(1996)11 cited
- → Neuropeptide Y in Sympathetic Co‐Transmission: Recent Advances in the Search for Neuropeptide Y Antagonists(1994)21 cited