CENTRAL REGULATION OF SYMPATHETIC ACTIVITY TO BROWN FAT

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Balancing energy expenditure with energy intake, metabolic requirements and energy storage is critical for maintenance of body weight, for sustained responsiveness to metabolic signals such as glucose, insulin and leptin and for homeostatic regulation of many body systems. Our experiments are defining and testing the hypothesis that energy expenditure in BAT is a potential sink for the consumption of surplus energy intake to prevent excess energy storage in white adipose tissue. Defining energy afferent signaling pathways, as well as those efferent neural pathways controlling the BAT energy expenditure effector will contribute to our understanding of the regulation of body weight and of energy substrate availability and to the design of therapeutic strategies to control disturbances in body energy homeostasis that result in diseases such as obesity, diabetes and hypertension. Recent findings include the identification of neurons in the ventrolateral medulla as having a potent sympathoinhibitory effect on BAT sympathetic outflow and the demonstration that application of neuropeptide Y into the rostral raphe pallidus elicits a potent excitation of BAT sympathetic nerve activity and BAT thermogenesis and increases in body temperature.