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Neuroendocrine mechanism mediating energetic regulation of gonadotropin release in female rats

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Energy level is a critical factor controlling gonadal activity at various phases of reproduction. A female rat model has revealed that fasting-induced luteinizing hormone (LH) suppression is mediated by a specific neural pathway, such as noradrenergic neurons originating in the A2 region and projecting to the hypothalamic paraventricular nucleus and corticotropin-releasing hormone neurons. The pathway is shared with that mediating glucoprivic suppression of LH pulses. Among the peripheral signals altered by energy deficiency, glucose could be a signal molecule conveying the peripheral information to the brain to regulate feeding and gonadotropin-releasing hormone/LH release through the noradrenergic pathway during undernutrition. The brain detects the energy availability to control feeding and reproductive function at various phases of an animal’s life. It is most likely that the central glucose-sensing mechanism could be similar to the pancreatic one, involving a glucokinase-mediated process to detect glucose availability. Further studies are needed to elucidate the mechanism integrating the energy signals.
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Keywords: fasting; feeding; glucose; luteinizing hormone; sensing

Document Type: Research Article

Publication date: June 1, 2006

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