Hyperreactivity to aversive diets in rats produced by injections of insulin or tolbutamide, but not by food deprivation

Vasselli, Joseph R.; Sclafani, Anthony

doi:10.1016/0031-9384(79)90056-8

Cited by 54 publications

(10 citation statements)

References 25 publications

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“…The results from the current studies also cannot be attributed to a general debilitating effect of OBX on feeding behavior because body weight and daily food intake of the rats with OBX were similar to SHAM rats throughout the study. Rats injected with insulin or 2-DG are hyperreactive to aversive diets (e.g., see Vasselli and Sclafani, 1979), but the normal daily food intake of OBX rats in the present study suggests that the animals did not find their standard rat chow diet to be aversive.…”

Section: Discussioncontrasting

confidence: 47%

Olfactory bulbectomy impairs the feeding response to 2-deoxy-d-glucose in rats

et al. 2011

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An early study reported that, unlike sham-operated rats, rats made anosmic by olfactory bulbectomy (OBX) failed to compensate for the dilution of their diet with nonnutritive bulk by increasing their food intake. In the present study, the effects of a glucoprivic challenge, intraperitoneal-administered 350 mg/kg 2-deoxy-D-glucose (2-DG), on food intake were measured in OBX and sham-operated female rats. Sham-operated rats significantly increased their food intake, but in two separate experiments OBX rats displayed no increase in food intake during the first 2 h following administration. Blood glucose levels were nearly identical in both groups. Body weights and daily food intakes of OBX rats did not differ from the sham-operated controls throughout the studies. Bulbectomized rats also displayed a normal drinking response after an intraperitoneal injection of 1 M hypertonic saline. Hypothalamic nuclei and the neural pathways mediating taste have been implicated in the feeding response to 2-DG. The present results suggest that olfactory input and olfactory neural pathways also mediate, at least in part, the feeding response to a glucoprivic challenge induced by intraperitoneal injection of 2-DG.

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Section: Discussioncontrasting

confidence: 47%

Olfactory bulbectomy impairs the feeding response to 2-deoxy-d-glucose in rats

et al. 2011

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“…Recent experiments examining the role of diet palatability on feeding following the administration of either insulin or 2-DG ( Brandes 1977;Kanarek & Mayer 1978;Vasselli & Sclafani 1979) call into question the supposedly clearcut effects of hypoglycemia and cellular glucopenia on food intake. In these experiments, rats maintained for extended periods of time on diets adulterated with aversive-tasting substances, such as quinine, sucrose-octa-acetate, or curry powder, in contrast to animals given unadulterated diets, did not increase food intake following the administration of either insulin (Brandes 1977;Vasselli & Sclafani 1979) or 2-DG (Kanarek & Mayer 1978). In fact, in one instance, following insulin injections animals would not eat any of the adulterated diet and died as a result of hypoglycemia (Vasselli & Sclafani 1979).…”

Section: Department Of Psychology Tufts University Medford Mass 0mentioning

confidence: 99%

“…In these experiments, rats maintained for extended periods of time on diets adulterated with aversive-tasting substances, such as quinine, sucrose-octa-acetate, or curry powder, in contrast to animals given unadulterated diets, did not increase food intake following the administration of either insulin (Brandes 1977;Vasselli & Sclafani 1979) or 2-DG (Kanarek & Mayer 1978). In fact, in one instance, following insulin injections animals would not eat any of the adulterated diet and died as a result of hypoglycemia (Vasselli & Sclafani 1979).…”

Section: Department Of Psychology Tufts University Medford Mass 0mentioning

confidence: 99%

The metabolic basis of dual periodicity of feeding in rats

Magnen

1981

Behav Brain Sci

183

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This article examines how the depletion and replenishment of various energy stores give rise to periodic eating and how constant body-energy levels are maintained over time.Measures of the energy expended throughout the 24-hour feeding pattern in rats indicate that two different energy stores (one of small capacity and one of large) determine two superimposed feeding periodicities: one from meal to meal (prandial), the other from day to night (nycthemeral). The article reviews how experimental overrepletion or overdepletion of gastrointestinal content, blood glucose, or body fats affect food intake. These data suggest that gastrointestinal content determines both meal size and meal-to-meal periodicity. Other evidence indicates that glucose uptake rate in tissues, which is modulated by fat synthesis and fat mobilization, affects the periodic onset of feeding and the difference between nocturnal and diurnal postprandial satiety.There follows an examination of the neuroendocrine bases for the interacting mechanisms governing energy input and output balance and of the role of the ventromedial hypothalamus in body-fat regulation and the lateral hypothalamus in feeding.

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“…Rats injected with high doses of insulin die unless they eat sufficient carbohydrate to counteract hypoglycaemia (Lotter & Woods, 1977;Vasselli & Sclafani, 1979). Treated animals must, therefore, have continuous access to food.…”

Section: Discussionmentioning

confidence: 99%

“…Treated animals must, therefore, have continuous access to food. Acclimation to the diet is also required, since insulin treatment causes hyper-reactivity to novel or aversive feeds (Vasselli & Sclafani, 1979). In the present study an incremental-dose regimen was used to reduce stress and mortality.…”

Section: Discussionmentioning

confidence: 99%

Energy balance in rats given chronic hormone treatment

Woodward

Emery

1989

Br J Nutr

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1. Sprague-Dawley rats were injected for 16 d with long-acting insulin, and energy balance was calculated using the comparative carcass technique. Two experiments were carried out with females (starting weights 150 and 90 g respectively), and one with males (starting weight 150 8). In a fourth experiment, cytochrome c oxidasc (EC 1 .9.3.1) activity was measured as an indicator of the capacity for substrate oxidation. 2.Insulin increased weight gain by up to 57% ( P < 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P < 0.01 for all studies). The excess weight gained by the insulin-treated rats was predominantly due to fat deposition.3. Energy expenditure, calculated as the difference between metabolizable intake and carcass energy gain. was expressed on a whole-body basis, or relative to either metabolic body size (kg body-weight"75) or fat-free mass. Insulin consistently raised energy expenditure, regardless of the method of expression, but this change reached statistical significance in only two of the nine comparisons.4. Cytochrome c oxidase activity was not affected by insulin treatment in either interscapular brown adipose tissue or gastrocnemius muscle. In liver, total enzyme activity (U/tissue) was increased from 2928 (SF 162) in the controls to 3940 (SE 294) in the treated group ( P i 002), but specific activity (U/mg protein) was unchanged.5. It is concluded that, despite causing substantial hyperphagia, insulin treatment only slightly increases energy expenditure in rats. The costs of increased tissue deposition may account for this change.

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Hyperreactivity to aversive diets in rats produced by injections of insulin or tolbutamide, but not by food deprivation

Cited by 54 publications

References 25 publications

Olfactory bulbectomy impairs the feeding response to 2-deoxy-d-glucose in rats

Olfactory bulbectomy impairs the feeding response to 2-deoxy-d-glucose in rats

The metabolic basis of dual periodicity of feeding in rats

Energy balance in rats given chronic hormone treatment

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