Effects of enterostatin in non-food-deprived rats with limited or continuous access to oil or sucrose

Rebecca L. Corwin, H. B. Rice

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The peptide enterostatin has been proposed to function as a selective signal for fat-induced satiety. In the majority of enterostatin studies, however, rats were food-deprived, and the test food was also the maintenance diet. The present study sought to determine if enterostatin would selectively reduce consumption of oil that was provided in addition to a standard diet in non-food-deprived rats. Rats had either continuous (24-h/day) or limited access (120-min/day) to either a 32% sucrose solution or 100% corn oil. In addition to the sucrose and the oil, rats also had 22-h access to a standard pelleted rodent diet. Control rats had unlimited access to the standard diet but no access to oil or sucrose. Rats were maintained on their respective diets for 3 weeks before enterostatin testing. Food intake and body weight were monitored. Rats with continuous access to oil or sucrose consumed more calories and gained more weight than control rats. Caloric intake and body weight of the rats with limited access to oil or sucrose did not differ significantly from controls. Enterostatin, administered intraperitoneally (i.p.) at doses of 0 (vehicle), 89, 178, and 356 μg/kg, had no effect on consumption of oil, sucrose, or standard diet in these non-food-deprivation paradigms; however, 356 μg/kg reduced standard-diet intake when rats were overnight food-deprived, thus verifying peptide activity. These results do not support a role for enterostatin in the regulation of fat intake when optional high-fat foods are provided in addition to a readily available standard diet. Copyright (C) 1998 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalPhysiology and Behavior
Volume65
Issue number1
DOIs
StatePublished - Jan 1 1998

Fingerprint

Sucrose
Oils
Diet
Food
Fats
Body Weight
procolipase
Peptides
Corn Oil
Energy Intake
Rodentia
Eating
Maintenance
Weights and Measures

All Science Journal Classification (ASJC) codes

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

Cite this

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abstract = "The peptide enterostatin has been proposed to function as a selective signal for fat-induced satiety. In the majority of enterostatin studies, however, rats were food-deprived, and the test food was also the maintenance diet. The present study sought to determine if enterostatin would selectively reduce consumption of oil that was provided in addition to a standard diet in non-food-deprived rats. Rats had either continuous (24-h/day) or limited access (120-min/day) to either a 32{\%} sucrose solution or 100{\%} corn oil. In addition to the sucrose and the oil, rats also had 22-h access to a standard pelleted rodent diet. Control rats had unlimited access to the standard diet but no access to oil or sucrose. Rats were maintained on their respective diets for 3 weeks before enterostatin testing. Food intake and body weight were monitored. Rats with continuous access to oil or sucrose consumed more calories and gained more weight than control rats. Caloric intake and body weight of the rats with limited access to oil or sucrose did not differ significantly from controls. Enterostatin, administered intraperitoneally (i.p.) at doses of 0 (vehicle), 89, 178, and 356 μg/kg, had no effect on consumption of oil, sucrose, or standard diet in these non-food-deprivation paradigms; however, 356 μg/kg reduced standard-diet intake when rats were overnight food-deprived, thus verifying peptide activity. These results do not support a role for enterostatin in the regulation of fat intake when optional high-fat foods are provided in addition to a readily available standard diet. Copyright (C) 1998 Elsevier Science Inc.",
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Effects of enterostatin in non-food-deprived rats with limited or continuous access to oil or sucrose. / Corwin, Rebecca L.; Rice, H. B.

In: Physiology and Behavior, Vol. 65, No. 1, 01.01.1998, p. 1-10.

Research output: Contribution to journalArticle

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