Open Access
Caruso, Christopher
Area of Honors:
Nutritional Sciences
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Gary J Fosmire, Thesis Supervisor
  • Mihai Covasa, Thesis Supervisor
  • Gary J Fosmire, Honors Advisor
  • CCK
  • DIO and DR rats
  • satiation
  • gastric peptides
  • neural signaling
  • obesity
ABSTRACT Over the past several decades, obesity in the United States has been on the rise and has turned into a serious national health problem. In simplistic terms, the etiology of obesity arises from an imbalance between energy input and expenditure, leading to an excessive build up of stored energy in the form of fat. This imbalance between energy input and expenditure is directly correlated to meal size and frequency. The size of the meal consumed has been linked to certain digestive hormones and their interaction between the digestive system and the brain. One hormone produced by the small intestinal endocrine cells and controls meal size is cholecystokinin (CCK). The objective of the study presented in this thesis was to determine whether dietary-induced obesity leads to changes in CCK sensitivity and whether these changes were associated with alteration in food intake, body weight, adiposity and glucose impairments. The diet-induced obese prone (DIO) and diet-induced obese resistant (DR) rat models were used because they exhibit a polygenic phenotype similar to obesity in humans. The results show that, compared to DR, DIO rats were more sensitive to low doses of CCK and less sensitive to high doses of CCK. At the end of the experiment, DIO rats were heavier than DR rats, and consumed more food during 24h. However, DIO rats ate less grams of food per body weight than DIO rats. In addition, there was a significant difference in raw fat deposit weight (epididymal, retroperitoneal and visceral). The DR rats had larger fat pads as proportion of their body weight, compared to DIO rats. The findings suggest that, in addition to other reported deficits, DIO rats may have a deficit in CCK signaling leading to significant weight gain, even in the absence of energy store deficits.