Insulin modifies flavor aversions and preferences in real- and sham-feeding rats

1990 ◽  
Vol 259 (4) ◽  
pp. R823-R828
Author(s):  
D. A. Vanderweele ◽  
R. O. Deems ◽  
R. B. Kanarek
Keyword(s):  
Gastric Emptying ◽  
Insulin Injection ◽  
Liquid Diet ◽  
Sweetened Condensed Milk ◽  
Sham Feeding ◽  
Flavor Aversion ◽  
The Real ◽  
Insulin Levels ◽  
Condensed Milk

In separate, parallel experiments, rats were allowed to sham or real feed a flavored sweetened condensed-milk solution after a 17.5-h fast. Coinciding with administration of the milk were injections of insulin or vehicle (saline). Insulin had no effect on intake in the real feeding situation, and flavors paired with insulin (0.8, 2.5, or 5.0 U/rat) were avoided, relative to saline-paired flavors. In sham-feeding rats, insulin (0.8 U/rat) significantly reduced the amount of milk consumed, and flavors paired with insulin injection were preferred, relative to saline-paired ones. Insulin produced a relatively larger hypoglycemia during sham feeding than during real feeding. Thus it appears that insulin-paired flavors of milk may be preferred by animals when they are ingested in sham feeding but not in animals real feeding. Perhaps rapid gastric emptying, as would occur with a liquid diet, accompanied by increased insulin levels, leads to malaise and flavor aversion.

Increase in intake with sham feeding experience is concentration dependent

1999 ◽  
Vol 277 (2) ◽  
pp. R565-R571 ◽  
Author(s):  
John D. Davis ◽  
Gerard P. Smith ◽  
Bramdeo Singh ◽  
Daniel P. McCann
Keyword(s):  
Gastrointestinal Tract ◽  
Negative Feedback ◽  
The Other ◽  
Feedback Signal ◽  
Dilute Solution ◽  
Concentrated Solutions ◽  
Sweetened Condensed Milk ◽  
Sham Feeding ◽  
Feeding Experience ◽  
Condensed Milk

Most sham feeding studies show that about three sham feeding tests are required for intake to reach maximum. One study, however, using a dilute solution, reported maximum sham intake in the first sham feeding test, suggesting that the progressive rise in sham intake may be concentration dependent. We tested this hypothesis with six groups of rats given five sham feeding tests each with one of six concentrations of sweetened condensed milk (0.5:1, 1:1, 2:1, 4:1, 8:1, 16:1, water-to-milk dilutions). It took three sham tests for intake to reach maximum with the three most concentrated solutions, but only one with the three weakest. Thus the intake of concentrated solutions of milk is limited by two negative feedback signals, one derived from the accumulation of fluid in the gastrointestinal tract, the other from a labile signal that loses its effectiveness with sham feeding experience. In contrast, the intake of weak concentrations is limited only by the nonlabile negative feedback signal because the labile signal is missing.

CNS injection of CCK in rats: effects on real and sham feeding and gastric emptying

1990 ◽  
Vol 258 (5) ◽  
pp. R1165-R1169 ◽  
Author(s):  
M. A. Della-Fera ◽  
B. D. Coleman ◽  
C. A. Baile
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gastric Emptying ◽  
Feeding Behavior ◽  
Physiological Role ◽  
Liquid Diet ◽  
Cerebral Ventricles ◽  
Gastric Function ◽  
Sham Feeding ◽  
Gastric Emptying Rate

Cholecystokinin (CCK) released from the intestine during feeding may have a physiological role in satiety. There is also evidence that activation of central CCK-containing pathways is involved in the control of feeding behavior. This study was carried out to determine whether CCK-8 administered into the lateral cerebral ventricles (lv) of rats suppresses both sham feeding (SF) and real feeding (RF). Rats with lv guides and gastric cannulas ate a liquid diet with cannulas open (SF) or closed (RF) after lv (0, 0.05, 0.5 micrograms) or intraperitoneal (ip) (0, 4 micrograms/kg) injection of CCK-8. Both RF and SF were significantly decreased by ip CCK-8. RF was also decreased in a dose-related manner after lv CCK-8, but SF was not affected by lv CCK-8. Decreased feeding after ip CCK-8 may be due in part to its suppression of gastric emptying rate (GER). To determine whether central nervous system (CNS) CCK might also be involved in the control of gastric function, GER was measured after lv (0, 0.05, 0.5 micrograms) or ip (0, 4 micrograms/kg) injection of CCK-8. GER was significantly decreased after ip CCK-8, but lv CCK-8 had no effect on GER. Although both CNS and peripheral CCK peptide systems may be involved in satiety, CNS CCK appears to depend on concurrent peripheral nutrient-related stimuli in eliciting satiety.

5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

2004 ◽  
Vol 287 (4) ◽  
pp. R817-R823 ◽  
Author(s):  
Matthew R. Hayes ◽  
Rachael L. Moore ◽  
Samit M. Shah ◽  
Mihai Covasa
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Feedback Control ◽  
Negative Feedback ◽  
Intraperitoneal Administration ◽  
Liquid Diet ◽  
Solid Meal ◽  
Sham Feeding ◽  
Negative Feedback Control ◽  
Type 3

Serotonin type 3 (5-HT3) receptors have been shown to participate in the negative-feedback control of food intake. We previously reported that cholecystokinin (CCK)-induced suppression of food intake is partly mediated through 5-HT3receptors when rats were tested on a preferred liquid diet, but whether such an effect occurs when they are tested on a solid maintenance diet is unknown. In the present study, we examined the effects of ondansetron, a selective 5-HT3antagonist, on CCK-induced suppression of solid chow intake. Intraperitoneal administration of ondansetron significantly attenuated 30- and 60-min CCK-induced reduction of food intake, with suppression being completely reversed by 120 min. It is not known whether 5-HT3receptors directly mediate CCK-induced satiation or whether their participation depends on CCK acting as part of a feedback cascade to inhibit ongoing intake. Because CCK-induced inhibition of sham feeding does not depend on additive gastric/postgastric-feedback signals, we examined the ability of ondansetron to reverse CCK-induced satiation in sham-feeding rats. Ondansetron did not attenuate reduction of sham feeding by CCK, suggesting that ondansetron does not directly antagonize CCK-satiation signals. CCK suppresses real feeding through a delay in gastric emptying. Ondansetron could attenuate CCK-induced reduction of food intake by reversing CCK-induced inhibition of gastric emptying. We found that blockade of 5-HT3receptors attenuates CCK-induced inhibition of gastric emptying of a solid meal, as well as saline and glucose loads. We conclude that 5-HT3receptors mediate CCK-induced satiation through indirect mechanisms as part of a feedback cascade involving inhibition of gastric emptying.

scholarly journals Diagnosis of experimental stetohepatosis using ultrasound shear wave elastography

2015 ◽  
Vol 26 (1) ◽  
pp. 109-113
Keyword(s):  
Insulin Resistance ◽  
Shear Wave ◽  
Shear Wave Elastography ◽  
Mixed Diet ◽  
Sweetened Condensed Milk ◽  
Non Invasive ◽  
Condensed Milk ◽  
First Time ◽  
Diagnosis Technique

According to available literature data, NAFLD may play crucial role in the pathogenesis of type 2 diabetes and other conditions connected with insulin resistance. In order to study the essence of the NAFLD, we have created an experimental model of the steatohepatosis. The mixed diet for 8 weeks consisting of standard food (47%), sweetened condensed milk (44%), vegetable oil (8%) and vegetable starch (1%) develops non-alcoholic steatohepatosis in the animals undergoing the experiment. The morphological signs of the non-alcoholic steatohepatosis comprised as follows in the hepatocytes of the rats undergoing the experiment: presence of fine-drop fattiness (fine-drop steatosis) and accumulation of fat vacuoles shifting the nucleus towards the cell peripheral. Substantial increase in the liver pulp of the animals undergoing the experiment defined using the ultrasound shear wave elastography technique is indicative of the presence of the non-alcoholic steatohepatosis. The ultrasound shear wave elastography technique can be used as a non-invasive diagnosis marker of the non-alcoholic steatohepatosis. The said diagnosis technique has been recommended for the first time.

Intestinal fat differentially suppresses sham feeding of different gustatory stimuli

1996 ◽  
Vol 270 (5) ◽  
pp. R1122-R1125 ◽  
Author(s):  
L. A. Foster ◽  
K. Nakamura ◽  
D. Greenberg ◽  
R. Norgren
Keyword(s):  
Experimental Period ◽  
Liquid Diet ◽  
Short Term ◽  
Total Consumption ◽  
Sham Feeding ◽  
Entire Experimental Period ◽  
Intermediate Consumption ◽  
Complete Diet ◽  
Bottle Test ◽  
High Concentrations

To determine the intestinal contribution to short-term satiety for solutions of varying palatability, 10 ml of either 0.15 M NaCl or lipid (Intralipid: 0.125, 0.25, 0.5, and 1.0 kcal/ml) was infused at a rate of 0.5 ml/min into the duodenum of rats that were sham feeding either a liquid diet (0.5 kcal/ml), 0.3 M sucrose (0.4 kcal/ml), or a 0.1 M solution of glucose polymers (Polycose 0.4 kcal/ml). Differences in palatability were estimated by the total consumption of each solution over 90 min in a one-bottle test. The intake of solutions maximally ingested during the saline infusions (Polycose > Sucrose > liquid diet) was the most sensitive to the lipid infusions. All four lipid concentrations suppressed intake of Polycose, the solution consumed the most; the three highest concentrations suppressed intake of sucrose (intermediate consumption), and only the two highest concentrations suppressed intake of the complete diet, the solution consumed the least. Nevertheless, the duration of suppression was shorter for the solutions the rats drank the most. For the solution the rats drank the least (liquid diet), the two high concentrations of lipid that suppressed intake did so for the entire experimental period, whereas for Polycose, al lipid infusions suppressed intake, but it recovered to control levels for all but the highest concentration. Other studies have reported that increasing diet palatability shortens the duration of satiety. The current results suggest that this effect may reflect the duration of intake suppression elicited by nutrients in the intestine.

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