Role of NPY and its receptor subtypes in foraging, food hoarding, and food intake by Siberian hamsters

2005 ◽  
Vol 289 (1) ◽  
pp. R29-R36 ◽  
Author(s):  
Diane E. Day ◽  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

Fasting has widespread physiological and behavioral effects such as increases in arcuate nucleus neuropeptide Y (NPY) gene expression in rodents, including Siberian hamsters. Fasting also stimulates foraging and food hoarding (appetitive ingestive behaviors) by Siberian hamsters but does relatively little to change food intake (consummatory ingestive behavior). Therefore, we tested the effects of third ventricular NPY Y1 ([Pro34]NPY) or Y5 ([d-Trp34]NPY) receptor agonists on these ingestive behaviors using a wheel running-based food delivery system coupled with simulated burrow housing. Siberian hamsters had 1) no running wheel access and free food, 2) running wheel access and free food, or 3) foraging requirements (10 or 50 revolutions/pellet). NPY (1.76 nmol) stimulated food intake only during the first 4 h postinjection (∼200–1,000%) and mostly in hamsters with a foraging requirement. The Y1 receptor agonist markedly increased food hoarding (250–1,000%), increased foraging as well as wheel running per se, and had relatively little effect on food intake (<250%). Unlike NPY, the Y5 agonist significantly increased food intake, especially in foraging animals (∼225–800%), marginally increased food hoarding (250–500%), and stimulated foraging and wheel running 4–24 h postinjection, with the distribution of earned pellets favoring eating versus hoarding across time. Across treatments, food hoarding predominated early postinjection, whereas food intake tended to do so later. Collectively, NPY stimulated both appetitive and consummatory ingestive behaviors in Siberian hamsters involving Y1/Y5 receptors, with food hoarding and foraging/wheel running (appetitive) more involved with Y1 receptors and food intake (consummatory) with Y5 receptors.

2005 ◽  
Vol 288 (3) ◽  
pp. R716-R722 ◽  
Author(s):  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

Fasting triggers many effects, including increases in circulating concentrations of ghrelin, a primarily stomach-derived orexigenic hormone. Exogenous ghrelin treatment stimulates food intake, implicating it in fasting-induced increases in feeding, a consummatory ingestive behavior. In Siberian hamsters, fasting also stimulates appetitive ingestive behaviors such as foraging and food hoarding. Therefore, we tested whether systemic ghrelin injections (3, 30, and 200 mg/kg) would stimulate these appetitive behaviors using a running wheel-based food delivery system coupled with simulated burrow housing. We also measured active ghrelin plasma concentrations after exogenous ghrelin treatment and compared them to those associated with fasting. Hamsters had the following: 1) no running wheel access, free food; 2) running wheel access, free food; or 3) foraging requirement (10 revolutions/pellet), no free food. Ghrelin stimulated foraging at 0–1, 2–4, and 4–24 h postinjection but failed to affect wheel running activity not coupled to food. Ghrelin stimulated food intake initially (200–350%, first 4 h) across all groups; however, in hamsters with a foraging requirement, ghrelin also stimulated food intake 4–24 h postinjection (200–250%). Ghrelin stimulated food hoarding 2–72 h postinjection (100–300%), most markedly 2–4 h postinjection in animals lacking a foraging requirement (635%). Fasting increased plasma active ghrelin concentrations in a time-dependent fashion, with the 3- and 30-mg/kg dose creating concentrations of the peptide comparable to those induced by 24–48 h of fasting. Collectively, these data suggest that exogenous ghrelin, similar to fasting, increases appetitive behaviors (foraging, hoarding) by Siberian hamsters, but dissimilar to fasting in this species, stimulates food intake.


2007 ◽  
Vol 292 (4) ◽  
pp. R1728-R1737 ◽  
Author(s):  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

Fasting triggers a constellation of physiological and behavioral changes, including increases in peripherally produced ghrelin and centrally produced hypothalamic neuropeptide Y (NPY). Refeeding stimulates food intake in most species; however, hamsters primarily increase foraging and food hoarding with smaller increases in food intake. Fasting-induced increases in foraging and food hoarding in Siberian hamsters are mimicked by peripheral ghrelin, central NPY, and NPY Y1 receptor agonist injections. Because fasting stimulates ghrelin and subsequently NPY synthesis/release, it may be that fasting-induced increased hoarding is mediated by NPY Y1 receptor activation. Therefore, we asked: Can an Y1 receptor antagonist block fasting- or ghrelin-induced increases in foraging, food hoarding, and food intake? This was accomplished by injecting the NPY Y1 receptor antagonist 1229U91 intracerebroventricularly in hamsters fasted, fed, or given peripheral ghrelin injections and housed in a running wheel-based food delivery foraging system coupled with simulated-burrow housing. Three foraging conditions were used: 1) no running wheel access, free food, 2) running wheel access, free food, or 3) foraging requirement (10 revolutions/pellet) for food. Fasting was a more potent stimulator of foraging and food hoarding than ghrelin. Concurrent injections of 1229U91 completely blocked fasting- and ghrelin-induced increased foraging and food intake and attenuated, but did not always completely block, fasting- and ghrelin-induced increases in food hoarding. Collectively, these data suggest that the NPY Y1 receptor is important for the effects of ghrelin- and fasting-induced increases in foraging and food intake, but other NPY receptors and/or other neurochemical systems are involved in increases in food hoarding.


2008 ◽  
Vol 295 (6) ◽  
pp. R1737-R1746 ◽  
Author(s):  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

Food deprivation stimulates foraging and hoarding and to a much lesser extent, food intake in Siberian hamsters. Leptin, the anorexigenic hormone secreted primarily from adipocytes, may act in the periphery, the brain, or both to inhibit these ingestive behaviors. Therefore, we tested whether leptin given either intracerebroventricularly or intraperitoneally, would block food deprivation-induced increases in food hoarding, foraging, and intake in animals with differing foraging requirements. Hamsters were trained in a running wheel-based food delivery foraging system coupled with simulated burrow housing. We determined the effects of food deprivation and several peripheral doses of leptin on plasma leptin concentrations. Hamsters were then food deprived for 48 h and given leptin (0, 10, 40, or 80 μg ip), and additional hamsters were food deprived for 48 h and given leptin (0, 1.25, 2.5, or 5.0 μg icv). Foraging, food intake, and hoarding were measured postinjection. Food deprivation stimulated food hoarding to a greater degree and duration than food intake. In animals with a foraging requirement, intracerebroventricular leptin almost completely blocked food deprivation-induced increased food hoarding and intake, but increased foraging. Peripheral leptin treatment was most effective in a sedentary control group, completely inhibiting food deprivation-induced increased food hoarding and intake at the two highest doses, and did not affect foraging at any dose. Thus, the ability of leptin to inhibit food deprivation-induced increases in ingestive behaviors differs based on foraging effort (energy expenditure) and the route of administration of leptin administration.


2008 ◽  
Vol 294 (2) ◽  
pp. R321-R328 ◽  
Author(s):  
Megan E. Dailey ◽  
Timothy J. Bartness

Unlike most species, after food deprivation, Siberian hamsters increase foraging and food hoarding, two appetitive ingestive behaviors, but not food intake, a consummatory ingestive behavior. We previously demonstrated (Wood AD, Bartness TJ, Am J Physiol Regul Integr Comp Physiol 272: R783−R792, 1997) that increases in food hoarding are triggered by directly decreasing body fat levels through partial surgical lipectomy; however, we did not test if lipectomy affected foraging, nor if the magnitude of the lipid deficit affected food hoard size. Therefore, we tested whether varying the size of the lipectomy-induced lipid deficit and/or foraging effort affected foraging, food hoarding, or food intake. This was accomplished by housing adult male Siberian hamsters in a foraging/hoarding system and removing (x) both epididymal white adipose tissue (EWATx) pads, both inguinal white adipose tissue (IWATx) pads, or both EWAT and IWAT pads (EWATx + IWATx) and measuring foraging, food hoarding, and food intake for 12 wk. The lipectomy-induced lipid deficit triggered different patterns of white adipose tissue mass compensation that varied with foraging effort. Foraging for food (10 wheel revolutions to earn a food pellet) abolished the EWATx-induced compensation in IWAT pad mass. The magnitude of the lipid deficit did not engender a proportional change in any of the appetitive or consummatory ingestive behaviors. EWATx caused the greatest increase in food hoarding compared with IWATx or EWATx + IWATx, when animals were required to forage for their food. Collectively, it appears that the magnitude of a lipid deficit does not affect appetitive or consummatory behaviors; rather, when energy (foraging) demands are increased, loss of specific (gonadal) fat pads can preferentially stimulate increases in food hoarding.


2013 ◽  
Vol 305 (4) ◽  
pp. R323-R333 ◽  
Author(s):  
Brett J. W. Teubner ◽  
Timothy J. Bartness

Circulating concentrations of the stomach-derived “hunger-peptide” ghrelin increase in direct proportion to the time since the last meal. Exogenous ghrelin also increases food intake in rodents and humans, suggesting ghrelin may increase post-fast ingestive behaviors. Food intake after food deprivation is increased by laboratory rats and mice, but not by humans (despite dogma to the contrary) or by Siberian hamsters; instead, humans and Siberian hamsters increase food hoarding, suggesting the latter as a model of fasting-induced changes in human ingestive behavior. Exogenous ghrelin markedly increases food hoarding by ad libitum-fed Siberian hamsters similarly to that after food deprivation, indicating sufficiency. Here, we tested the necessity of ghrelin to increase food foraging, food hoarding, and food intake, and neural activation [c-Fos immunoreactivity (c-Fos-ir)] using anti-ghrelin Spiegelmer NOX-B11–2 (SPM), an l-oligonucleotide that specifically binds active ghrelin, inhibiting peptide-receptor interaction. SPM blocked exogenous ghrelin-induced increases in food hoarding the first 2 days after injection, and foraging and food intake at 1–2 h and 2–4 h, respectively, and inhibited hypothalamic c-Fos-ir. SPM given every 24 h across 48-h food deprivation inconsistently inhibited food hoarding after refeeding and c-Fos-ir, similarly to inabilities to do so in laboratory rats and mice. These results suggest that ghrelin may not be necessary for food deprivation-induced foraging and hoarding and neural activation. A possible compensatory response, however, may underlie these findings because SPM treatment led to marked increases in circulating ghrelin concentrations. Collectively, these results show that SPM can block exogenous ghrelin-induced ingestive behaviors, but the necessity of ghrelin for food deprivation-induced ingestive behaviors remains unclear.


2012 ◽  
Vol 302 (1) ◽  
pp. R37-R48 ◽  
Author(s):  
Brett J. W. Teubner ◽  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

We previously demonstrated that 3rd ventricular (3V) neuropeptide Y (NPY) or agouti-related protein (AgRP) injection potently stimulates food foraging/hoarding/intake in Siberian hamsters. Because NPY and AgRP are highly colocalized in arcuate nucleus neurons in this and other species, we tested whether subthreshold doses of NPY and AgRP coinjected into the 3V stimulates food foraging, hoarding, and intake, and/or neural activation [c-Fos immunoreactivity (c-Fos-ir)] in hamsters housed in a foraging/hoarding apparatus. In the behavioral experiment, each hamster received four 3V treatments by using subthreshold doses of NPY and AgRP for all behaviors: 1) NPY, 2) AgRP, 3) NPY+AgRP, and 4) saline with a 7-day washout period between treatments. Food foraging, intake, and hoarding were measured 1, 2, 4, and 24 h and 2 and 3 days postinjection. Only when NPY and AgRP were coinjected was food intake and hoarding increased. After identical treatment in separate animals, c-Fos-ir was assessed at 90 min and 14 h postinjection, times when food intake (0–1 h) and hoarding (4–24 h) were uniquely stimulated. c-Fos-ir was increased in several hypothalamic nuclei previously shown to be involved in ingestive behaviors and the central nucleus of the amygdala (CeA), but only in NPY+AgRP-treated animals (90 min and 14 h: magno- and parvocellular regions of the hypothalamic paraventricular nucleus and perifornical area; 14 h only: CeA and sub-zona incerta). These results suggest that NPY and AgRP interact to stimulate food hoarding and intake at distinct times, perhaps released as a cocktail naturally with food deprivation to stimulate these behaviors.


2009 ◽  
Vol 296 (4) ◽  
pp. R877-R892 ◽  
Author(s):  
Megan J. Dailey ◽  
Timothy J. Bartness

Food is acquired (obtained by foraging) and frequently stored (hoarded) across animal taxa, including humans, but the physiological mechanisms underlying these behaviors are virtually unknown. We found that peptides that stimulate food intake in rats stimulate food foraging and/or hoarding more than intake in Siberian hamsters. Neuropeptide Y (NPY) is a potent orexigenic peptide that increases food foraging and hoarding (appetitive behavior) and food intake (consummatory behavior). Given that NPY injections into the hypothalamic paraventricular nucleus (PVH) or perifornical area (PFA) increase food intake by rats, it is possible that these injections may stimulate food foraging or hoarding by Siberian hamsters. We also tested whether antagonism of the NPY Y1 receptor (Y1-R), the agonism of which stimulates hoarding, would inhibit post-food-deprivation increases in foraging and hoarding. We injected one of three doses of NPY or vehicle into the PVH or PFA of animals housed in a simulated foraging-hoarding housing system and measured these behaviors at 1, 2, 4, and 24 h. A subset of animals was subsequently food deprived and then given PVH or PFA Y1-R antagonist microinjections before they were refed. NPY PVH microinjections decreased foraging but increased hoarding and food intake, whereas NPY PFA microinjections increased all three behaviors, but the greatest increase was in hoarding. Y1-R antagonist inhibited post-food-deprivation increases in hoarding when injected into the PVH and PFA and inhibited foraging when injected into the PFA. These results support the view that NPY is involved in appetitive and consummatory ingestive behaviors, but each may be controlled by different brain areas and/or NPY receptor subtypes.


1997 ◽  
Vol 272 (1) ◽  
pp. R118-R125 ◽  
Author(s):  
T. J. Bartness

Food hoarding by male Siberian hamsters (Phodopus sungorus sungorus) is increased only when body mass (fat) is decreased. Pregnancy and lactation result in marked decreases in lipid reserves (approximately 50%) in female Siberian hamsters. Therefore, the present experiments addressed the following questions: 1) Is food hoarding increased after food deprivation in female Siberian hamsters? and 2) How do food hoarding and food intake change during pregnancy, lactation, and their combination? During measurements in a simulated burrow system food hoarding increased after a 32-h fast (approximately 2- to 3-fold) to a level similar to that seen previously in males and was markedly increased during pregnancy (approximately 12- to 18-fold, lactation, and concurrent pregnancy and lactation (approximately 10- to 25-fold for each of the latter 2 conditions). Postfast food intake was not different from prefast baseline measures. Food intake was increased only during the last few days of pregnancy and was elevated throughout lactation. These impressive increases in the level of food hoarding during pregnancy, lactation and their combination suggest that food hoarding may play an important role in supplying easily accessible energy to subserve these reproductive conditions.


1994 ◽  
Vol 266 (4) ◽  
pp. R1111-R1117 ◽  
Author(s):  
T. J. Bartness ◽  
M. R. Clein

Syrian hamsters do not increase their food intake following several metabolic challenges, including food deprivation and blockade of metabolic fuel utilization, in contrast to the response of other small rodents to these challenges. Perhaps hamsters respond to such challenges differently, for example by altering hoarding. In the present experiments, we have begun to question the role of food hoarding in the total energy balance of Siberian hamsters. Therefore, we developed a simulated burrow system, where food was available outside the burrow for consumption and/or hoarding during a 15-h period surrounding the 8-h dark portion of the photocycle. Food hoarding, but not food intake, increased dramatically after 32- and 56-h fasts and was greater following the longer fast. Food-restricted weight-reduced hamsters (80% of ad libitum-fed controls) were refed and given the opportunity to hoard. Initially, when body weights were low, food hoarding was maximal and then decreased gradually to control levels as body weights reached those of the ad libitum-fed controls. Food intake was not affected. Neither hoarding nor food intake was affected by treatment with long-acting protamine zinc insulin, given to enhance the storage of metabolic fuels, at any dose tested. Finally, neither food intake nor hoarding was affected by treatment with the glucose utilization blocker 2-deoxy-D-glucose, the fatty acid utilization blocker methyl palmoxirate, or a combination of the two treatments, all at doses that stimulate food intake in laboratory rats.(ABSTRACT TRUNCATED AT 250 WORDS)


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