Location: Children's Nutrition Research Center
Project Number: 6250-51000-055-10-S
Project Type: Specific Cooperative Agreement
Start Date: Apr 1, 2009
End Date: Mar 31, 2014
Objective 1: Determine the role of the circadian clock in regulation of food intake and the interaction between diet composition and circadian rhythms of food intake on body weight control during post-weaning and adult life; determine the specific role of central and peripheral clocks, as well as the circadian output pathways in maintaining the homeostasis of food intake. Sub-objective 1.A. Determine the role of the circadian clock in controlling food intake and the development of obesity. Sub-objective 1.B. Study the role of central and peripheral clocks, as well as the circadian output pathways in maintaining the homeostasis of food intake.
Children's Nutrition Research Center researchers will determine how the disruption of circadian rhythm disrupts energy homeostasis by measuring food-intake and energy expenditure of wt and Period2-mutant adult mice (10-12 weeks of age) using the Comprehensive Lab Animal Monitoring System (CLAMS). We will study whether disruption of circadian rhythm abolishes the homeostasis of energy homeostasis by measuring serum metabolic parameters in wt and Period2-mutant mice at post-weaning (3-7 weeks of age) and in adulthood (10-12 weeks of age). The interaction of diet composition and food-intake homeostasis will be evaluated by studying the effect of high energy food on body weight and food-intake of wt and Period2-mutant mice. The effect of restricted feeding on the homeostasis of serum metabolic parameters and body weight of wt and Period2-mutant mice will also be analyzed. Our scientists will determine how the disruption of circadian rhythm leads to deregulation of long-term peripheral adiposity signal leptin by investigating the role of the peripheral circadian clock in controlling leptin transcription, the role of the central circadian clock in controlling leptin transcription, and the role of the circadian output pathways in controlling leptin transcription in adipose tissues.