High-fat feeding alters both basal and stress-induced hypothalamic
-pituitary-adrenal activity in the rat.
Tannenbaum, Beth M., Gloria S. Tannenbaum, David N. Brindley, M. Dawn
McArthur, Mary F. Dallman, and Michael J. Meaney.
Developmental Neuroendocrinology Laboratory, Douglas Hospital
Research Center, and Department of Neurology and Neurosurgery, McGill
University, Montreal, Canada H4H-1R3; Neuropeptide Physiology
Laboratory, Montreal Children's Hospital Research Institute and
Department of Pediatrics, McGill University, Montreal, Canada H3H-1P3
; Signal Transduction Laboratories, Department of Biochemistry,
University of Alberta, Edmonton, Canada T6G-2S2; 5Department of
Physiology, University of California, San Francisco, CA 94143.
APStracts 4:0199E, 1997.
High-fat feeding induces insulin resistance and increases the risk for
the development of diabetes and coronary artery disease.
Glucocorticoids exacerbate this hyperinsulinemic state, rendering an
individual at further risk for chronic disease. The present studies
were undertaken to determine whether dietary fat-induced increases in
corticosterone (B) reflect alterations in the regulatory components
of the hypothalamic-pituitary-adrenal (HPA) axis. Adult male rats
were maintained on a high fat (20%) or control (4%) diet for varying
periods of time. Marked elevations in light-phase spontaneous basal B
levels were evident as early as 7 days after fat diet onset and B
concentrations remained significantly elevated up to 21 days post fat
diet onset, compared to controls. In contrast, there were no
significant effects on any parameters of spontaneous growth hormone
secretory profiles, thus providing support for the specificity of the
effects on the HPA axis. In a second study, all groups of rats fed
the high fat diet for either 1, 9 or 12 weeks exhibited significantly
elevated levels of plasma adrenocorticotropic hormone, B, fatty acid
and glucose either prior to, during and/or at 20, 60 and/or 120
minutes following the termination of a restraint stress. Furthermore,
12 week fat-fed animals showed a significant resistance to insulin
compared to normal-fed controls. There were no differences in
negative feedback efficacy in high-fat fed rats vs controls. Taken
together, these results suggest that dietary fat intake acts as a
background form of chronic stress, elevating basal B levels and
enhancing HPA responses to stress.
Received 9 January 1997; accepted in final form 22 August 1997.
APS Manuscript Number E10-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997