Experimental obesity: a homeostatic failure due to defective nutrient stimulation of the sympathetic nervous system.
The basic hypothesis of this review is that studies on models of experimental obesity can provide insight into the control systems regulating body nutrient stores in humans. In this homeostatic or feedback approach to analysis of the nutrient control system, we have examined the afferent feedback signals, the central controller, and the efferent control elements regulating the controlled system of nutrient intake, storage, and oxidation. The mechanisms involved in the beginning and ending of single meals must clearly be related to the long-term changes in fat stores, although this relationship is far from clear. Changes in total nutrient storage in adipose tissue can arise as a consequence of changes in the quantity of nutrients ingested in one form or another or a decrease in the utilization of the ingested nutrients. A change in energy intake can be effected by increased size of individual meals, increased number of meals in a 24-hour period, or a combination of these events. Similarly, a decrease in utilization of these nutrients can develop through changes in resting metabolic energy expenditure which are associated with one of more of the biological cycles such as protein metabolism, triglyceride for glycogen synthesis and breakdown, or maintenance of ionic gradients for Na+ + K+ across cell walls. In addition, differences in energy expenditure related to the thermogenesis of eating or to the level of physical activity may account for differences in nutrient utilization.
Bray
G A
GA
York
D A
DA
Fisler
J S
JS
D000818:Animals; D004032:Diet; D004195:Disease Models, Animal; D006706:Homeostasis; D006801:Humans; D009765:Obesity / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*