According to one theory, some types of human obesity can beexplained by impaired activity of the sympathetic nervous system. A new study using an animal model of obesity, the Zucker rat, adds direct supporting evidence to this idea. Peter J. Havel, a graduate student pursuing dual degrees in endocrinology and veterinary medicine, injected obese and lean Zucker rats with a substance which produces a state of glucose insufficiency in the central nervous system. This condition is termed "neuroglucopenia" and is known to activate the sympathoadrenal (fight-or-flight) system. The sympathetic nervous systems of the obese rats reacted by releasing significantly lower amounts of the neurohormone epinephrine (also called adrenaline) and the neurotransmitter norepinephrine than those of the lean rats. "We know that the sympathetic nervous system can inhibit insulin secretion and stimulate thermogensis by brown adipose tissue, which is a way in which the impairment of sympathetic activity could contribute to obesity," Havel said. "The idea is not new, but this is a direct demonstration of the impairment, looking directly at the sympathetic mediators." Havel will present his findings at 2:45 p.m. Monday, Oct. 21, in the Carmel B Room during a session titled "Food Intake: Neuromodulators."