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Inhibition of hypothalamic TRH neurons is a well-established adaptation to caloric restriction that suppresses pituitary secretion of thyroid hormone, but may also participate in modulation of autonomic function. Central TRH, downstream of leptin signaling in the arcuate nucleus of the hypothalamus, is decreased by fasting. We hypothesized that decreased TRH contributes to the bradycardia and decreased thermogenesis seen during caloric restriction (CR). Male Sprague Dawley rats were instrumented with telemetry devices for measurement of heart rate (HR) and blood pressure (BP) and a lateral intracerebroventricular (ICV) guide cannula for central infusions. After recovery, rats were given either ad libitum (AD-LIB) or CR treatments for seven days; half of each diet group was then given continuous infusions of TRH (25 nmol/hr) or saline (.25ìL/hr) for seven days. In AD-LIB rats, TRH produced reductions in food intake and slight increases in MAP and HR. The CR rats receiving saline continued to exhibit bradycardia while the TRH rats exhibited significant increase in HR to a magnitude greater than that observed in AD-LIB rats infused with TRH. These data support the hypothesis that TRH is involved in the metabolic and cardiovascular responses to negative energy balance.
Respiratory Quotient, Oxygen Consumption, Metabolism, Body Weight, Nutrition, Physiology, Homeostasis, Energy Balance, Blood Pressure, Heart Rate, Rodent, Rat, Energy Expenditure, Food Intake
Date of Defense
October 11, 2005.
A Thesis submitted to the Department of Nutrition, Food, and Exercise Sciences in partial fulfillment of the requirements for the degree of Master of Science.
Includes bibliographical references.
J. Michael Overton, Professor Directing Thesis; Marc E. Freeman, Outside Committee Member; Cathy W. Levenson, Committee Member.
Florida State University
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