Stress and appetite/Bibliography

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Revision as of 06:58, 11 October 2010 by imported>Emelie Gustafson (New page: {{subpages}} '''Journal Articles''' Dallman, M., Akana, S., Strack, A., Hanson, S., Sebastian, R. 1995. The neural network that regulates energy balance is responsive to glucocorticoids a...)
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A list of key readings about Stress and appetite.
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Journal Articles

Dallman, M., Akana, S., Strack, A., Hanson, S., Sebastian, R. 1995. The neural network that regulates energy balance is responsive to glucocorticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. Ann N Y Acad Sci. 771:730-42. ” What follows is a review first of our more recent studies that suggest strongly that the HPA axis serves as one arm of a two-hormone system (corticosteroids and insulin) that regulates energy balance over the long term. Next, we will describe our results on the effect of the diurnal rhythm and of caloric intake on the magnitude of ACTH responses to stress, corticosteroid feedback, and prior stress-induced facilitation in acutely restrained rats…we observe that NPY may be the major integrator of activities in the feeding and adrenocortical system.”


Foster, M., Warne, J., Ginsberg, A., Horneman, H., Pecoraro, N., Akana, S., Dallman, M. 2009. Palatable Foods, Stress, and Energy Stores Sculpt Corticotropin-Releasing Factor, Adrenocorticotropin, and Corticosteron Concentrations after Restraint. Endocrinology. 150(5): 2325-2333. “ In this study we tested the effects of prior access to chow-only, sucrose/chow, lard/chow, or sucrose/lard/chow diets on central CRF expression on rats…in response to acute stress and chronic stress… The results suggest strongly that ingestion of highly palatable foods reduces activity in the central stress response network, perhaps reducing the feeling of stressors.”


Schwartz, M., Woods, S., Porte, D Jr., Seely, R., Baskin, D. 2000. Central nervous system control of food intake. Nature. 404: 661-671. “To better understand how energy homeostasis can be achieved, we described a model that delineates the roles of individual hormonal and neuropeptide signaling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.”