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Submitted on November 7, 2003
Accepted on March 18, 2004
Laboratory of Neuroendocrinology, National Institute of Agrobiological Sciences (S.O., T.I., H.O.), Tsukuba 305-8602, Japan; Department of Animal Physiology and Nutrition, National Institute of Livestock and Grassland Science (F.I.), Tsukuba 305-0901, Japan; and Laboratory of Animal Reproduction, Nagoya University (S.M.), Nagoya 464-8601, Japan
* To whom correspondence should be addressed. E-mail: ohkura{at}affrc.go.jp.
The present study examined the relative importance of blood glucose vs. free fatty acids as a metabolic signal regulating GnRH release as measured electrophysiologically by multiple-unit activity (MUA) in the arcuate nucleus/median eminence region in ovariectomized, estradiol-treated goats. MUA was recorded before, during, and after 1) cellular glucoprivation by peripheral infusion of 2-deoxy-D-glucose (2DG; 25, 50, and 75 mg/kg/h, iv), 2) peripheral hypoglycemia in response to various doses (15-195 mU/kg/h, iv) of insulin infusion, and 3) cellular lipoprivation induced by peripheral infusion of sodium mercaptoacetate (MA; 2.4 mg/kg/h alone or combined with 25 mg/kg/h of 2DG, iv), and effects on the interval of characteristic increases in MUA (MUA volleys) were examined. Infusion of the highest dose of 2DG increased the mean interval between MUA volleys, whereas the lower doses of 2DG had no effect on volley interval. The MUA volley intervals lengthened as insulin-induced hypoglycemia became profound. There was a negative correlation between MUA volley intervals and blood glucose concentrations during insulin infusion, and co-infusion of glucose with insulin returned the MUA volley interval to a normal frequency. Infusion of MA alone or MA with 2DG did not increase MUA volley intervals. These findings demonstrate that glucose availability, but not fatty acids, regulates the GnRH pulse generator activity in the ruminant. Glucose is considered to be a key metabolic regulator that fine-tunes pulsatile GnRH release.
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