Behaviour of Rats During Selfinitiated Pauses in Feeding and Drinking, and during Periodic Response-Independent Delivery of Food and Water

1980 ◽  
Vol 32 (3) ◽  
pp. 459-472 ◽  
Author(s):  
T. J. Roper
Keyword(s):  
Good Predictor ◽  
Temporal Pattern ◽  
Baseline Level ◽  
Fixed Time ◽  
Interreinforcement Interval ◽  
Free Access ◽  
Periodic Response ◽  
Access To Food ◽  
Schedule Induction

In Experiment I rats deprived of either food or water were given free access to food or water respectively, and their behaviour was observed during self-imposed pauses in feeding or drinking. In Experiment II food or water were delivered according to fixed-time 30-s and fixed-time 60-s schedules, and the behaviour of the rats was observed during the interreinforcement intervals imposed by these schedules. In both experiments the temporal pattern of those activities that occurred during pauses in eating differed from the pattern of activities occurring during pauses in drinking; and with both food and water the temporal pattern of activities during self-imposed pauses in consummatory behaviour in Experiment I proved a good predictor of the pattern of activities during schedule-imposed interreinforcement intervals in Experiment II. This suggests that intermittent schedules permit the occurrence of those activities that are normally closely associated with the consummatory behaviour in question. In Experiment II certain activities that occurred towards the end of the interreinforcement interval were found to be enhanced relative to baseline level, but there was no enhancement of activities occurring near the beginning of the interval. This is contrary to Staddon's (1977) account of schedule-induced behaviour, and suggests that schedule-induction is not as common as has sometimes been supposed.

Changes in body composition attendant on force feeding

1959 ◽  
Vol 196 (5) ◽  
pp. 965-968 ◽  
Author(s):  
Clarence Cohn ◽  
Dorothy Joseph
Keyword(s):  
Body Weight ◽  
Metabolic Pathways ◽  
Male Rats ◽  
Free Access ◽  
Carbohydrate Diet ◽  
Experimental Animals ◽  
Force Feeding ◽  
Feeding Regimen ◽  
Ad Libitum ◽  
Access To Food

Normal young adult male rats were either force-fed or allowed to eat ad libitum a moderate carbohydrate diet for 3–4 weeks. The force-fed animals were given either the amount of diet consumed by the animals eating ad libitum (pair-fed) or 80% of this amount (underfed). After a 2-week period of observation, we found that the rats eating ad libitum gained 65 gm of body weight, the pair-fed, force-fed 62 gm and the underfed, force-fed 40 gm. On the basis of the water, fat and protein content of the skin, viscera and carcass of control animals killed at the beginning of the feeding regimen and of similar constituents of the experimental animals after 2 weeks of feeding, the composition of the newly formed tissues of the various groups of animals consisted of the following: a) the rat with free access to food—water = 67.8%, fat = 7.8% and protein = 22.4%; b) the pair-fed, force-fed animal—water = 55.5%, fat = 23.6% and protein = 17.7%; c) the underfed, force-fed animal—water = 64.4%, fat = 7.9% and protein = 20.0%. The ratio of calories retained in newly formed tissue to the calories ingested over the 2-week period was 11.9% for the animals eating ad libitum, 20.6% for the pair-fed, force-fed animals and 9.5% for the underfed, force-fed rats. Force feeding appears to change intermediary metabolic pathways in the direction of increased ‘efficiency’ with resultant greater fat deposition.

Cholecystokinin suppresses food intake by a nonendocrine mechanism in rats

1994 ◽  
Vol 267 (4) ◽  
pp. R901-R908 ◽  
Author(s):  
R. D. Reidelberger ◽  
G. Varga ◽  
R. M. Liehr ◽  
D. A. Castellanos ◽  
G. L. Rosenquist ◽  
...  
Keyword(s):  
Food Intake ◽  
Pancreatic Enzyme ◽  
Free Access ◽  
Amylase Secretion ◽  
Receptor Antagonists ◽  
Feeding Experiments ◽  
Pancreatic Enzyme Secretion ◽  
Endocrine Mechanism ◽  
Access To Food ◽  
Cck Receptor Antagonists

A cholecystokinin monoclonal antibody (CCK MAb) was used to immunoneutralize CCK to test the hypothesis that CCK produces satiety by an endocrine mechanism. We first characterized the effects of CCK MAb on pancreatic secretion. Conscious rats with jugular vein and bile-pancreatic duct cannulas received CCK MAb or control antibody intravenously 30 min before a 2-h maximal dose of CCK-8 (200 pmol.kg-1.h-1 i.v.) or access to food. CCK MAb caused dose-related inhibition of amylase secretion. CCK MAb (2 mg/kg) completely blocked the response to CCK-8 and inhibited the response to food by 89%. In feeding experiments, rats with free access to food received CCK MAb or control antibodies (2 mg/kg iv) 2 h after lights off. CCK MAb had no effect on 1.5- or 3.5-h food intake. Another group of rats received CCK MAb (4 mg/kg i.v.) or a combined injection of type A and type B CCK receptor antagonists devazepide and L-365,260 (1 mg/kg each i.v.). CCK MAb had no effect on feeding, whereas the receptor antagonists stimulated 1-, 2-, 3-, and 4-h intake by 62, 45, 43, and 29%. These results suggest that endogenous CCK stimulates pancreatic enzyme secretion at least partially by an endocrine mechanism and produces satiety by a nonendocrine mechanism.

scholarly journals Effects of infusions of lysine, leucine and ammonium chloride into the hepatic portal vein of chickens on voluntary food intake

1987 ◽  
Vol 58 (2) ◽  
pp. 325-331 ◽  
Author(s):  
Audrey A. Rusby ◽  
J. M. Forbes
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Ammonium Chloride ◽  
Jugular Vein ◽  
Free Access ◽  
Delayed Effect ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Access To Food ◽  
Portal Infusion

1. Adolescent cockerels of a laying strain were prepared with catheters whose tip lay in the hepatic portal vein, to study the effect of 3-h infusions of nutrients on food intake.2. Lysine, infused into the hepatic portal vein at rates of 150–450 mg/3 h reduced 3-h food intake by up to 58%, for a period of 6 h in previously starved birds, but had no effect on birds allowed free access to food. Infusions made into the jugular vein had no effect, suggesting a role for the liver in monitoring lysine levels.3. Portal infusion of leucine had a delayed effect while ammonium chloride, infused at isomolar rates to those of the lysine infusions, had very little effect on intake.4. The results support the concept of liver sensitivity to amino acids, but the mode of action is not clear; it appears not to be via the effects of ammonia.

scholarly journals Histological Effect of Allium sativum (Garlic) on the Liver of White Rabbits

2021 ◽  
pp. 28-35
Author(s):  
Osuloye Oluwaseum Olayemi ◽  
Olojo Oluwatobi Omotola ◽  
Philip Abutu
Keyword(s):  
Allium Sativum ◽  
Cell Damage ◽  
Basal Diet ◽  
Liver Glycogen ◽  
Treated Group ◽  
Control Group ◽  
Free Access ◽  
Glycogen Depletion ◽  
Garlic Powder ◽  
Access To Food

Allium sativum commonly referred to as garlic has been known over the years for its medicinal and culinary purposes. It has also been reported to have several toxic effects when used excessively. However, the purpose of this study was to determine the histological effects of Allium sativum (garlic) powder on the liver of white rabbits at different dosages. Twenty rabbits were randomly divided int.o five groups with free access to food and water for a period of four weeks. Four groups B, C, D, and E were fed with garlic supplemented basal diet containing different concentrations of garlic powder i.e. 100mg, 200mg, 500mg, and 1000mg respectively. These groups were called the treated group. Group A was fed with basal diet only and was considered as the control group. The results obtained showed some histological changes such as the presence of cellular necrosis, vacuolations, lipofuscin pigments, pyknosis and nuclear hypertrophy which were as a result of liver glycogen depletion and hepatic cell damage which may be due to relatively high dosage of garlic used in some of the groups.

PHOSPHORUS METABOLISM IN COLD-EXPOSED RATS

1963 ◽  
Vol 41 (11) ◽  
pp. 2209-2214 ◽  
Author(s):  
John R. Beaton
Keyword(s):  
Urinary Excretion ◽  
Cold Exposure ◽  
Inorganic Phosphorus ◽  
Male Rats ◽  
Free Access ◽  
Lipid Phosphorus ◽  
Blood Concentrations ◽  
Adenosine Phosphates ◽  
Access To Food ◽  
Phosphorus Levels

Male rats weighing 207 ± 2.38 g were exposed to cold (2–3 °C) for a period of 7 days during which urine and faeces were collected daily and analyzed for phosphorus. As a consequence of cold exposure, urinary excretion of phosphorus is increased. With free access to food, the increased food (and hence phosphorus) intake of the animals compensates for the increased urinary excretion and a normal phosphorus balance results. Cold exposure was without significant effect upon blood concentrations of acid-soluble, inorganic, organic, or lipid phosphorus. Increased inorganic and decreased organic, non-lipid phosphorus levels were observed in livers of cold-exposed rats. These observations suggest the breakdown of organic phosphates (e.g. hexose and triose phosphates, adenosine phosphates, phosphocreatine) to inorganic phosphorus.

Resistance to the phosphaturic effect of parathyroid hormone in the hamster

1979 ◽  
Vol 237 (3) ◽  
pp. F175-F181
Author(s):  
C. A. Harris ◽  
J. F. Seely
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Free Access ◽  
Calcium Excretion ◽  
Renal Tubular Cell ◽  
Acid Base ◽  
Significant Difference ◽  
Renal Tubular ◽  
Fractional Excretion Of Phosphate ◽  
Access To Food

The renal effects of parathyroid hormone (PTH) and dibutyryl 3'5'-cyclic AMP (DBcAMP) were studied in thyroparathyroidectomized hamsters. The hamsters were permitted free access to food and water or fasted for 16 h. PTH caused a phosphaturia in the fed hamster (fractional excretion of phosphate (FEPO4) increased from 5.8 +/- 1.3 to 27.4 +/- 4.6%, P less than 0.001) but not in the fasted hamster (from 9.9 +/- 2.5 to 12.4 +/- 2.5%, NS), whereas calcium excretion decreased significantly in both groups. There was no significant difference in blood acid-base or phosphate levels between the two groups. Insulin did not restore the phosphaturic response to PTH (FEPO4 from 7.7 +/- 2.6 to 5.3 +/- 1.7%), whereas phosphate or NH4Cl infusion did, FEPO4 increasing from 20.9 +/- 3.1 to 38.1 +/- 5.4% (P less than 0.02) and from 19.5 +/- 3.8 to 39.0 +/- 7.5%, respectively. DBcAMP caused a phosphaturia both in the fasted (from 9.6 +/- 2.7 to 20.1 +/- 4.5%, P less than 0.01) and fed (from 2.5 +/- 0.5 to 10.7 +/- 1.5%, P less than 0.02) hamster. A fasting state of up to 64 h did not produce resistance to PTH in the rat. It is concluded that fasting produces resistance to the phosphaturic but not the calcium-retaining effects of PTH in the hamster. The resistance may occur, at least partly, prior to the production of cAMP within the renal tubular cell.

Abstract P164: The Role of the Adrenoreceptors Beta 3 on Metabolic Syndrome Induced by Fructose

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Eduardo Dias ◽  
Alexandre Tavolari ◽  
Marina Souza ◽  
Renata Oliveira ◽  
Patricia Fiorino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Visceral Fat ◽  
Blood Pressure Variability ◽  
Free Access ◽  
Fat Deposits ◽  
Sympathetic Modulation ◽  
Access To Food

The aim of this study was to evaluate the role of the adrenoreceptor beta 3 (ARβ3) in the cardiovascular function on Metabolic Syndrome (MS) induced by fructose overload. Male mice after weaning (8-10g) were divided into 4 groups (n=7/group): FVB Control (C) and ARβ3 Knockout Control (Kβ3C), with free access to food and water for 8 weeks; FVB fructose (F) and ARβ3 Knockout fructose (Kβ3F), with free access to food and fructose added to the drinking water (10%) for 8 weeks. At the end of the protocol, intraperitoneal glucose tolerance test was performed. Triglycerides and HDL fractions were evaluated by colorimetric methods. The animals were submitted to catheterization of carotid artery. This catheter was connected to a transducer and continuous signals of blood pressure (BP) was recorded. The variability of the resultant signal was evaluated in frequency domain. Visceral fat deposits were collected, weighted and normalized as fat (mg)/body weight (g). Results: fructose increased the fasting glycemia in the knockout group (Kβ3C=93±3 vs. Kβ3F=122±7 mg/dL) and decreased the glucose tolerance in both fructose groups. Fructose increased the triglycerides and decreased HDL cholesterol. The uric acid increased in the knockout animals. There was an increase on visceral fat deposits only in FVB animals (C=10±2 vs. F=16±1 mg/g), as well as on blood pressure (C=123±4 vs. 136±2 mmHg) There was an increase on blood pressure variability for all experimental groups compared to Control (C=10.7±1 vs. F=36±11; Kβ3C=50±7; Kβ3F=24±4 mmHg 2 ) as well as on peripheral sympathetic modulation (C=3.3±0.4 vs. F=8.1±0.1; Kβ3C=22.9±3; Kβ3F=9.2±2 mmHg 2 ). Furthermore, Kβ3F showed a decrease on blood pressure variability and peripheral sympathetic modulation. Our data suggest that the hypertension induced by fructose is related with adiposity. Moreover, the blood pressure variability and its sympathetic modulation are dependent of the ARB3. The association between fructose and ARβ3 knockout leads to the loss of the sympathetic modulation.

scholarly journals VIRUS-INDUCED DIABETES MELLITUS

1973 ◽  
Vol 137 (5) ◽  
pp. 1226-1239 ◽  
Author(s):  
D. Wark Boucher ◽  
Abner Louis Notkins
Keyword(s):  
Blood Glucose ◽  
Encephalomyocarditis Virus ◽  
Immunoreactive Insulin ◽  
Free Access ◽  
Abnormal Glucose Tolerance ◽  
Male Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Access To Food ◽  
Rapid Drop

Infection of DBA/2N male mice with encephalomyocarditis virus resulted in a diabeteslike syndrome characterized by hyperglycemia, glycosuria, hypoinsulinemia, polydipsia, and polyphagia. Blood glucose levels were elevated within 4 days after infection and reached a maximum mean level of 320 mg/100 ml within 12 days. Approximately 60–80% of the animals developed a transient hyperglycemia while 10–15% of the animals remained hyperglycemic for well over 6 mo. The remaining animals failed to become hyperglycemic but many had abnormal glucose tolerance curves. Hyperglycemia was most pronounced when animals were allowed free access to food, and the incidence of byperglycemia was related both to the strain and sex of the animals, with few females developing hyperglycemia. The amount of immunoreactive insulin in the plasma of infected hyperglycemic mice was significantly lower than in appropriate controls, and injection of exogenous insulin resulted in a rapid drop in the blood glucose levels. Despite the fact that certain animals were hyperglycemic for many months, virus could not be recovered from the pancreas after the first 10 days of the infection.

PHOSPHORUS METABOLISM IN COLD-EXPOSED RATS

1963 ◽  
Vol 41 (1) ◽  
pp. 2209-2214
Author(s):  
John R. Beaton
Keyword(s):  
Urinary Excretion ◽  
Cold Exposure ◽  
Inorganic Phosphorus ◽  
Male Rats ◽  
Free Access ◽  
Lipid Phosphorus ◽  
Blood Concentrations ◽  
Adenosine Phosphates ◽  
Access To Food ◽  
Phosphorus Levels

Male rats weighing 207 ± 2.38 g were exposed to cold (2–3 °C) for a period of 7 days during which urine and faeces were collected daily and analyzed for phosphorus. As a consequence of cold exposure, urinary excretion of phosphorus is increased. With free access to food, the increased food (and hence phosphorus) intake of the animals compensates for the increased urinary excretion and a normal phosphorus balance results. Cold exposure was without significant effect upon blood concentrations of acid-soluble, inorganic, organic, or lipid phosphorus. Increased inorganic and decreased organic, non-lipid phosphorus levels were observed in livers of cold-exposed rats. These observations suggest the breakdown of organic phosphates (e.g. hexose and triose phosphates, adenosine phosphates, phosphocreatine) to inorganic phosphorus.

scholarly journals Sleep Restriction Is Associated With Increased Morning Plasma Leptin Concentrations, Especially in Women

2010 ◽  
Vol 12 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Norah S. Simpson ◽  
Siobhan Banks ◽  
David F. Dinges
Keyword(s):  
Body Mass Index ◽  
Sleep Restriction ◽  
Free Access ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Race Ethnicity ◽  
Ad Libitum ◽  
Access To Food ◽  
Plasma Leptin ◽  
Healthy Participants

Study Objectives: We evaluated the effects of sleep restriction on leptin levels in a large, diverse sample of healthy participants, while allowing free access to food. Methods: Prospective experimental design. After 2 nights of baseline sleep, 136 participants (49% women, 56% African Americans) received 5 consecutive nights of 4 hours time in bed (TIB). Additionally, one subset of participants received 2 additional nights of either further sleep restriction (n = 27) or increased sleep opportunity (n = 37). Control participants (n = 9) received 10 hr TIB on all study nights. Plasma leptin was measured between 10:30 a.m. and 12:00 noon following baseline sleep, after the initial sleep-restriction period, and after 2 nights of further sleep restriction or recovery sleep. Results: Leptin levels increased significantly among sleep-restricted participants after 5 nights of 4 hr TIB (Z = -8.43, p < .001). Increases were significantly greater among women compared to men (Z = -4.77, p < .001) and among participants with higher body mass index (BMI) compared to those with lower (Z = -2.09, p = .036), though participants in all categories (sex, race/ethnicity, BMI, and age) demonstrated significant increases. There was also a significant effect of allowed TIB on leptin levels following the 2 additional nights of sleep restriction (p < .001). Participants in the control condition showed no significant changes in leptin levels. Conclusions: These findings suggest that sleep restriction with ad libitum access to food significantly increases morning plasma leptin levels, particularly among women.

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