Neuropeptide Y attenuates satiety: evidence from a detailed analysis patterns ingestion

Effects of hindbrain melanin-concentrating hormone and neuropeptide Y administration on licking for water, saccharin, and sucrose solutions.

“…However, there was no significant main effect of drug for either treatment group and no significant interaction term (Table 2). While the failure of NPY to increase burst size is consistent with previous reports after forebrain ICV NPY stimulation, the failure of MCH to affect burst size observed here stands in contrast to findings noted after 3V administration (7,9,50,78). This failure of MCH was also observed when bursts were expressed in terms of their mean duration (s/burst) rather than mean size [F(1,9) = 0.00, P = 0.99], while the monotonic increase in burst duration across tastants was conserved [F(3,27) = 4.54, P = 0.01; data not shown].…”

“…It would be worthwhile in future studies to evaluate whether progressive ratio or other instrumental responses for food access are increased after 4V NPY delivery. Overall, it appears that hindbrain sites sensitive to 4V NPY stimulation are not involved in the processes that underlie the early meal avidity observed after forebrain NPY infusions.Previous studies have noted that forebrain ICV NPY delivery produces a two-part effect on lick rate such that ingestion rate early in the meal is increased (7,50,78), and the meal is prolonged with a slower ingestion rate in later phases (7,78). Similar results were observed in experiment 3, where meal duration was prolonged for both sucrose solutions, while earlymeal ingestion rate was increased for the 1.0 M sucrose solution but not for the 0.1 M sucrose solution.…”

“…Previous meal pattern studies have reported that NPY delivered to the forebrain primarily increases meal size by prolonging meal duration (48, 51, 76). To date, three studies have evaluated intrameal licking microstructure after forebrain ICV NPY administration, and all report relatively consistent observations (7,50,78), with additional replication of those results also obtained in experiment 3. Collectively, the previous studies and experiment 3 indicated that forebrain NPY infusions increased meal duration and the number of licking bursts, and that 3V NPY reduced the rate of decay in ingestion rate for either sweetened milk or a range of sucrose solutions (0.03-1.0M).…”

Effects of neuropeptide Y on feeding microstructure: Dissociation of appetitive and consummatory actions.

“…Leibowitz and Alexander (1991) showed that NPY injection into the hypothalamic paraventricular nucleus increased the size of macronutrient meals with no accompanying increase in meal frequency, whereas Marin-Bivens, Thomas, and Stanley (1998) reported that perifornical hypothalamic NPY injections increased intake of sweetened rat chow through increases in both meal size and frequency, although most of the effect was due to the increase in meal size. In addition, ICV NPY administration has been shown to alter the rate of ingestion during a liquid sucrose meal (Lynch, Hart, & Babcock, 1994), induce stomach relaxation (Kobashi et al, 2006), and significantly attenuate the magnitude of electrophysiological gastric distension responses in the nucleus of the solitary tract (G. J. Schwartz & Moran, 2002).…”

Neuroendocrine control of satiation

“…When administered into the cerebroventricular system or directly into the hypothalamus, exogenous NPY dose-dependently increases eating [290], and when it is administered chronically, body weight and body fat increase as well [290]. Whether injected into the hypothalamus [291][292][293] or the hindbrain [294][295][296], NPY elicits very-short-latency eating responses, typically seconds to minutes, and also prolongs eating once it has begun, with consequently larger meals being consumed. Thus, NPY both facilitates the onset of meals and delays satiation.…”