Obesity and the Central Nervous System
Sponsored by The APS Central Nervous System Section
Supported by The Journal of Physiology
Metabolic Abnormalities Track

The past decade has witnessed an explosion of information regarding the role of the central nervous system in the development of obesity and the influence of peripheral, hormonal signals that regulate CNS function to regulate food intake and metabolism. The goal of this symposium is to provide a series of talks by leaders in the field to discuss state-of-the-art data and models regarding the brain as an initiator of obesity and as a target organ of peripheral feedback signals that regulate feeding and drinking behavior. This will provide interested APS members with an overview of the most current concepts in this area. Speakers have been chosen to provide consideration of integrative, genetic, cellular/molecular and clinical aspects of the topic. Given the wide interest in the topic of obesity it is anticipated that this symposium will be of interest to a wide range of APS members from virtually all sections. The speakers have provided titles and a short summary of their talks as follow:

Only some individuals become obese when placed in an obesogenic environment. Studies in animal models with a genetic propensity to develop diet-induced obesity (DIO) suggest that some may have a reduced responsiveness to signals such as leptin and insulin which normally inhibit the development obesity when dietary fat and calorie contents are increased. Since obesity is almost impossible to reverse once it develops in such individuals, prevention is probably the best treatment for the emerging obesity epidemic. Both manipulations of the perinatal maternal environment and early onset exercise can have long lasting effects on preventing the development of DIO and/or its complications such as insulin resistance. Such manipulations are associated with altered development of brain pathways which regulate energy homeostasis and may hold promise for prevention of obesity in human beings.

Mary Dallman. “Glucocorticoids and insulin both modulate caloric intake through actions on the brain.”  Glucocorticoids act primarily in a feed-forward fashion on brain to activate CNS pathways that implement wanting that is appropriate to physiological needs. Although glucocorticoids stimulate intake of chow, fat and sucrose, insulin appears to act at liver to indirectly sculpt the calorie-associated desires toward foods high in fat and sucrose. Both conditions of reduced food allowance and chronic stress excite glucocorticoid-augmented CNS networks leading toward ultimate abdominal obesity.

Greg Morton.  “Hypothalamic Leptin Regulation of Energy Homeostasis and Glucose Metabolism.”  Obesity and type 2 diabetes are growing health concerns. Two hormones thought to play a critical role in both energy homeostasis and glucose metabolism are the adiposity hormones insulin and leptin. Both these hormones circulate in proportion to body fat stores and interact with their respective receptors expressed in key brain areas such as the hypothalamic arcuate nucleus (ARC) that regulate food intake and glucose metabolism. We have recently shown that leptin signaling selectively in this brain area is sufficient to reduce food intake and body weight and also improve insulin sensitivity, even when the effects of feeding are controlled for. Taken together, these findings indicate that leptin signaling in the arcuate nucleus is an important determinant of both energy homeostasis and glucose metabolism.

Michael Tuck “Sympathetic Nervous System in Obesity” will review clinical studies and critique them, including various methods used to measure sympathetic nervous system function in humans. The talk will not discuss animal models.