Effects of intracerebroventricular injection of neuropeptide Y on energy metabolism

Abstract

Our objective was to find out if central injection of neuropeptide Y (NPY) would alter brown fat thermogenesis and white fat lipoprotein lipase activity. The following three groups of Sprague-Dawley rats received five injections over 24 h into the right lateral ventricle: 1) NPY (5 micrograms/injection) and ad libitum food; 2) NPY (5 micrograms/injection) and food restricted to control intake; 3) saline injection and ad libitum food. The NPY ad libitum-fed group consumed more food than the saline controls or NPY food-restricted animals. Brown fat thermogenic activity, assessed by GDP binding, was decreased relative to saline controls in both NPY-treated groups. White fat lipoprotein lipase activity was greatly increased in both NPY treatment groups compared with saline controls. The NPY effects on brown and white fat were not explained by measures of serum insulin, glucagon, glucose, or other metabolites. In a follow-up experiment, we asked whether food was necessary for expression of the NPY effects. Brown fat mitochondrial GDP binding indicated NPY effect even when no food was ingested. We conclude that intracerebroventricular administration of NPY promotes white fat lipid storage and decreases brown fat thermogenesis in addition to its known effect of stimulating food intake.

The impact of the leucine 7 to proline 7 polymorphism of the neuropeptide Y gene on postprandial lipemia and on the response of serum total and lipoprotein lipids to a reduced fat diet

“…It has been suggested that centrally administered NPY increases the expression of LPL mRNA and enhances LPL activity in white adipose tissue thus favoring lipid storage (Billington et al, 1991(Billington et al, , 1994. In the present study, the heparin-releasable LPL activity did not differ among the genotype groups.…”

“…However, disturbed liver uptake or catabolism of LDL could also play a role. NPY has been suggested to regulate LPL activity in adipose tissue of experimental animals (Billington et al, 1991(Billington et al, , 1994. This Table 2 Energy intake, proportion of energy nutrients, and the intake of dietary cholesterol and fiber during the run-in period and the reduced fat diet period, mean AE s.e.m.…”

“…Based on studies in animal models of obesity and type 2 diabetes, it has been suggested that hyperphagia, reduced energy expenditure and obesity in these animal models may be explained by the hypothalamic resistance of insulin inhibition of NPY neurons (Frankish et al, 1995). NPY also seems to favor energy storage through increased lipoprotein lipase (LPL) activity in white adipose tissue (Billington et al, 1991(Billington et al, , 1994. Regarding dietary factors, long term feeding of high-fat diets has been shown to decrease NPY levels in hypothalamus in rats .…”

Effects of acute and chronic relaxin-3 on food intake and energy expenditure in rats

“…Several peptides, such as NPY and AgRP, which stimulate food intake also alter energy expenditure [22][23][24]. We therefore examined the acute effects of H3 on both plasma TSH and other parameters of energy expenditure (VO 2 , RER and ambulatory activity).…”

Neuropeptide Y gene polymorphisms are not associated with obesity in a South Indian population

“…Primary among the functions associated with NPY are its acute effects on feeding behavior and energy expenditure. Injection of NPY into mice results in prolonged increases in food and water intake along with the suppression of metabolic rate (Billington et al, 1991;Schwartz et al, 2000). NPY knockout mice surprisingly experience no alterations in feeding behavior, implying a redundancy and/or multistep process in feeding signaling systems (Erickson et al, 1996a).…”