Food intake response to modulation of secretion of cholecystokinin in Zucker rats

1983 ◽  
Vol 244 (5) ◽  
pp. R676-R685 ◽  
Author(s):  
C. L. McLaughlin ◽  
S. R. Peikin ◽  
C. A. Baile
Keyword(s):  
Food Intake ◽  
Negative Feedback ◽  
Pancreatic Enzyme ◽  
Meal Size ◽  
Zucker Rats ◽  
Feedback Signal ◽  
Meal Frequency ◽  
Feeding Behaviors ◽  
Endogenous Release ◽  
Cck Release

Exogenous administration of cholecystokinin (CCK) decreases food intake and elicits satiety behaviors. In the present experiments, feeding behaviors of Zucker obese and lean rats were measured in response to treatments that influence endogenous secretion of CCK from the duodenum. Secretion of CCK was increased by administration of phenylalanine, a stimulant of CCK release, and of trypsin inhibitor, which binds to trypsin, a negative-feedback signal for CCK release. Both of these treatments decreased the size of the first meal after a 6-h fast and average daily meal size and increased meal frequency. Administration of trypsin, proported to decrease secretion of CCK, increased average daily meal size and decreased meal frequency. Pancrease, a pancreatic enzyme concentrate, also hypothesized to act as a negative-feedback signal for CCK release, elicited feeding behaviors similar to those of trypsin. Thus the effects of these compounds on the feeding behavior of Zucker obese and lean rats may be related to their effects on CCK secretion. The feeding behaviors of obese rats were affected less than those of lean rats by exogenous administration of CCK, but in these experiments were affected more than in lean rats by modulation of endogenous release of CCK.

Effect of adrenalectomy and corticosterone replacement on meal patterns of Zucker rats

1985 ◽  
Vol 249 (5) ◽  
pp. R584-R594 ◽  
Author(s):  
M. R. Freedman ◽  
T. W. Castonguay ◽  
J. S. Stern
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Meal Frequency ◽  
Light Cycle ◽  
Dark Cycle ◽  
Meal Patterns ◽  
Total Food Intake ◽  
Total Food

Male obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 10 wk of age. Approximately 16 wk later, patterns of food intake were monitored by computer-interfaced top loading balances. Data were collected from ADX rats before, during, and after access to a corticosterone-supplemented saline solution (20 micrograms/ml). Although total food intake during the precorticosterone treatment period was not different between ADX and sham controls, ADX resulted in attenuation of light cycle food intake, primarily via decreased meal frequency. With steroid replacement, light cycle meal frequency and food intake increased. Despite comparable self-administered dose (20.33 +/- 0.89 vs. 17.05 +/- 1.2 mg corticosterone/period, obese vs. lean), obese ADX rats were more responsive to steroid than were lean ADX rats. This increased responsiveness was reflected by a 30% increase in food intake and 60% increase in body weight gain of obese ADX rats during replacement. Lean ADX rats exhibited no change in total food intake or weight gain with replacement. Further, during corticosterone treatment, obese ADX rats increased meal frequency, total food intake, and consumption of large meals (greater than or equal to 4 g) during the dark cycle. Significant postprandial correlations were found only in obese ADX rats, both with and without replacement during the dark cycle. These results suggest adrenal glucocorticoids have a minimal effect on food intake and meal patterns in lean Zucker rats but significantly alter intake and meal patterns in obese rats.

Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats

2001 ◽  
Vol 281 (3) ◽  
pp. R738-R746 ◽  
Author(s):  
Lisa A. Eckel ◽  
Nori Geary
Keyword(s):  
Food Intake ◽  
Neuronal Activity ◽  
Negative Feedback ◽  
Estradiol Benzoate ◽  
Brain Regions ◽  
Meal Size ◽  
Central Nucleus ◽  
Ovariectomized Rats ◽  
Estradiol Treatment ◽  
Multiple Regions

The steroid hormone estradiol decreases meal size by increasing the potency of negative-feedback signals involved in meal termination. We used c-Fos immunohistochemistry, a marker of neuronal activation, to investigate the hypothesis that estradiol modulates the processing of feeding-induced negative-feedback signals within the nucleus of the solitary tract (NTS), the first central relay of the neuronal network controlling food intake, and within other brain regions related to the control of food intake. Chow-fed, ovariectomized rats were injected subcutaneously with 10 μg 17-β estradiol benzoate or sesame oil vehicle on 2 consecutive days. Forty-eight hours after the second injections, 0, 5, or 10 ml of a familiar sweet milk diet were presented for 20 min at dark onset. Rats were perfused 100 min later, and brain tissue was collected and processed for c-Fos-like immunoreactivity. Feeding increased the number of c-Fos-positive cells in the NTS, the paraventricular nucleus of the hypothalamus (PVN), and the central nucleus of the amygdala (CeA) in oil-treated rats. Estradiol treatment further increased this response in the caudal, subpostremal, and intermediate NTS, which process negative-feedback satiation signals, but not in the rostral NTS, which processes positive-feedback gustatory signals controlling meal size. Estradiol treatment also increased feeding-induced c-Fos in the PVN and CeA. These results indicate that modest amounts of food increase neuronal activity within brain regions implicated in the control of meal size in ovariectomized rats and that estradiol treatment selectively increases this activation. They also suggest that estradiol decreases meal size by increasing feeding-related neuronal activity in multiple regions of the distributed neural network controlling meal size.

scholarly journals Amylin receptor blockade stimulates food intake in rats

2004 ◽  
Vol 287 (3) ◽  
pp. R568-R574 ◽  
Author(s):  
Roger D. Reidelberger ◽  
Alvin C. Haver ◽  
Urban Arnelo ◽  
D. David Smith ◽  
Courtney S. Schaffert ◽  
...  
Keyword(s):  
Food Intake ◽  
Intravenous Infusion ◽  
Liquid Diet ◽  
Meal Size ◽  
Meal Frequency ◽  
Energy Reserves ◽  
Selective Blockade ◽  
Inhibit Food Intake ◽  
Hormonal Signal ◽  
The Brain

Amylin is postulated to act as a hormonal signal from the pancreas to the brain to inhibit food intake and regulate energy reserves. Amylin potently reduces food intake, body weight, and adiposity when administered systemically or into the brain. Whether selective blockade of endogenous amylin action increases food intake and adiposity remains to be clearly established. In the present study, the amylin receptor antagonist acetyl-[Asn30, Tyr32] sCT-( 8 – 32 ) (AC187) was used to assess whether action of endogenous amylin is essential for normal satiation to occur. Non-food-deprived rats received a 3- to 4-h intravenous infusion of AC187 (60–2,000 pmol·kg−1·min−1), either alone or coadministered with a 3-h intravenous infusion of amylin (2.5 or 5 pmol·kg−1·min−1) or a 2-h intragastric infusion of an elemental liquid diet (4 kcal/h). Infusions began just before dark onset. Food intake and meal patterns during the first 4 h of the dark period were determined from continuous computer recordings of changes in food bowl weight. Amylin inhibited food intake by ∼50%, and AC187 attenuated this response by ∼50%. AC187 dose-dependently stimulated food intake (maximal increases from 76 to 171%), whether administered alone or with an intragastric infusion of liquid diet. Amylin reduced mean meal size and meal frequency, AC187 attenuated these responses, and AC187 administration alone increased mean meal size and meal frequency. These results support the hypothesis that endogenous amylin plays an essential role in reducing meal size and increasing the postmeal interval of satiety.

Mode of action of OB protein (leptin) on feeding

1998 ◽  
Vol 275 (1) ◽  
pp. R174-R179 ◽  
Author(s):  
Mark C. Flynn ◽  
Thomas R. Scott ◽  
Thomas C. Pritchard ◽  
Carlos R. Plata-Salamán
Keyword(s):  
Food Intake ◽  
Wistar Rats ◽  
Feeding Rate ◽  
Meal Size ◽  
Meal Frequency ◽  
Dependent Manner ◽  
Intracerebroventricular Administration ◽  
Ad Libitum ◽  
Ob Protein ◽  
Dose Dependent

OB protein (leptin) decreases food intake in a variety of species. Here we investigated the effects of the intracerebroventricular administration of recombinant murine OB protein on food consumption and meal parameters in Wistar rats maintained ad libitum. The intracerebroventricular administration of OB protein (0.56–3.5 μg/rat) decreased feeding in a dose-dependent manner. Computer analysis of meal parameters demonstrated that OB protein (3.5 μg/rat, n = 10) decreased nighttime meal size by 42%, whereas meal frequency and meal duration were unaffected. Derived analyses for the nighttime also showed that OB protein decreased the feeding rate (meal size/meal duration) by 30%, whereas the satiety ratio (intermeal intervals/meal size) increased by 100%. A similar profile was observed during the daytime and total daily periods. The intracerebroventricular administration of heat-inactivated OB protein (3.5 μg/rat, n = 10) had no effect on any meal parameter. The results show that OB protein administered intracerebroventricularly inhibits feeding through a specific reduction of meal size.

Intraventricular insulin reduces food intake and body weight of lean but not obese zucker rats

Appetite ◽  
1986 ◽  
Vol 7 (4) ◽  
pp. 381-386 ◽  
Author(s):  
H. Ikeda ◽  
D.B. West ◽  
J.J. Pustek ◽  
D.P. Figlewicz ◽  
M.R.C. Greenwood ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Zucker Rats ◽  
Obese Zucker Rats

Apelin and the proopiomelanocortin system: a new regulatory pathway of hypothalamic α-MSH release

2011 ◽  
Vol 301 (5) ◽  
pp. E955-E966 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Laurence Bodineau ◽  
Nadia De Mota ◽  
Lydie Jeandel ◽  
Nicolas Chartrel ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuronal Cell ◽  
Nerve Fibers ◽  
Zucker Rats ◽  
Direct Stimulation ◽  
Melanocyte Stimulating Hormone ◽  
System A ◽  
Neuronal Cell Bodies ◽  
Hypothalamic Arcuate Nucleus ◽  
Apelin Receptor

Neuronal networks originating in the hypothalamic arcuate nucleus (Arc) play a fundamental role in controlling energy balance. In the Arc, neuropeptide Y (NPY)-producing neurons stimulate food intake, whereas neurons releasing the proopiomelanocortin (POMC)-derived peptide α-melanocyte-stimulating hormone (α-MSH) strongly decrease food intake. There is growing evidence to suggest that apelin and its receptor may play a role in the central control of food intake, and both are concentrated in the Arc. We investigated the presence of apelin and its receptor in Arc NPY- and POMC-containing neurons and the effects of apelin on α-MSH release in the hypothalamus. We showed, by immunofluorescence and confocal microscopy, that apelin-immunoreactive (IR) neuronal cell bodies were distributed throughout the rostrocaudal extent of the Arc and that apelin was strongly colocalized with POMC, but weakly colocalized with NPY. However, there were numerous NPY-IR nerve fibers close to the apelin-IR neuronal cell bodies. By combining in situ hybridization with immunohistochemistry, we demonstrated the presence of apelin receptor mRNA in Arc POMC neurons. Moreover, using a perifusion technique for hypothalamic explants, we demonstrated that apelin-17 (K17F) increased α-MSH release, suggesting that apelin released somato-dendritically or axonally from POMC neurons may stimulate α-MSH release in an autocrine manner. Consistent with these data, hypothalamic apelin levels were found to be higher in obese db/db mice and fa/fa Zucker rats than in wild-type animals. These findings support the hypothesis that central apelin is involved in regulating body weight and feeding behavior through the direct stimulation of α-MSH release.

scholarly journals Negative feedback in ants: crowding results in less trail pheromone deposition

2013 ◽  
Vol 10 (81) ◽  
pp. 20121009 ◽  
Author(s):  
Tomer J. Czaczkes ◽  
Christoph Grüter ◽  
Francis L. W. Ratnieks
Keyword(s):  
Negative Feedback ◽  
Trail Pheromone ◽  
Distribution Networks ◽  
Feedback Mechanism ◽  
Lasius Niger ◽  
Feedback Signal ◽  
Control Mechanisms ◽  
Negative Feedback Mechanism ◽  
Self Organized ◽  
Fold Reduction

Crowding in human transport networks reduces efficiency. Efficiency can be increased by appropriate control mechanisms, which are often imposed externally. Ant colonies also have distribution networks to feeding sites outside the nest and can experience crowding. However, ants do not have external controllers or leaders. Here, we report a self-organized negative feedback mechanism, based on local information, which downregulates the production of recruitment signals in crowded parts of a network by Lasius niger ants. We controlled crowding by manipulating trail width and the number of ants on a trail, and observed a 5.6-fold reduction in the number of ants depositing trail pheromone from least to most crowded conditions. We also simulated crowding by placing glass beads covered in nest-mate cuticular hydrocarbons on the trail. After 10 bead encounters over 20 cm, forager ants were 45 per cent less likely to deposit pheromone. The mechanism of negative feedback reported here is unusual in that it acts by downregulating the production of a positive feedback signal, rather than by direct inhibition or the production of an inhibitory signal.

Involvement of histaminergic system in the regulation of food intake in genetically obese zucker rats

1990 ◽  
Vol 22 ◽  
pp. 20
Author(s):  
R. Arrigo-Reina ◽  
T. Catti ◽  
F. Barbera ◽  
S. Chiecchio ◽  
C. Spadaro
Keyword(s):  
Food Intake ◽  
Zucker Rats ◽  
Histaminergic System ◽  
Obese Zucker Rats
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