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Psychosomatic Medicine, Vol 51, Issue 4 441-448, Copyright © 1989 by American Psychosomatic Society
ORIGINAL ARTICLES |
JA McCubbin, RS Surwit, CM Kuhn, C Cochrane and MN Feinglos
Department of Psychiatry, Duke University Medical Center, Durham, North Carolina.
The genetically obese mouse (C57BL/6J ob/ob) is a commonly used animal model of non-insulin-dependent diabetes mellitus. These mice show exaggerated glycemic responses during behavioral stress and adrenergic stimulation, but the precise glucoregulatory mechanisms are not well characterized. The ob/ob mice have multiple endocrine abnormalities, including elevated pituitary and circulating beta-endorphin levels; and a relationship between hyperglycemia and altered opioid function has been suspected. We now report that opiate antagonism with naltrexone potentiates hyperglycemic responses during stress and epinephrine challenge in obese mice. This effect of opioid blockade suggests that endogenous opioids inhibit stress- and epinephrine-induced hyperglycemia in the genetically obese mouse.
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