Author:
Himms-Hagen J.,Hogan S.,Zaror-Behrens G.
Abstract
Feeding female genetically obese (ob/ob) mice a palatable "cafeteria" diet results in increased sympathetic nervous system activity in brown adipose tissue and hypertrophy and increased thermogenesis of this tissue. There is an associated increase in the capacity of the ob/ob mouse to respond thermogenically to noradrenaline, prolongation of its survival in the cold, and an increase in body temperature at all times of day. Thus the cafeteria diet overcomes the usual refractoriness of brown adipose tissue of the ob/ob mouse to noradrenaline and to sympathetic stimulation, increases the low capacity for a thermogenic response to noradrenaline, almost normalizes resistance to cold, and increases the "set point" at which the ob/ob mouse regulates its body temperature. It is concluded that the repetitive sympathetic nervous stimulation engendered by the high-fat cafeteria diet has a trophic action on brown adipose tissue that improves its atrophied functional state and that the low sympathetic nervous system activity usually seen in brown adipose tissue of ob/ob mice eating chow under animal house conditions results in secondary atrophy of the tissue. The results point to a central location for the defect in the ob/ob mouse, perhaps in the control of the sympathetic nervous system in relation to diet availability and composition and to environmental temperature.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism
Cited by
37 articles.
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