Abstract
Reproduction is accurately regulated by metabolic states in mammals. Adiponectin regulates luteinizing hormone (LH) secretion in the pituitary and energy homeostasis in the hypothalamus. We further investigated the gonadotropin-releasing hormone (GnRH) secretion regulation by adiponectin and its related molecular and electrophysiological mechanisms. The results showed that adiponectin receptors (AdipR1 and 2) were expressed in GT1-7 cells derived from hypothalamus neurons. GnRH secretion was inhibited via activation of AMP-activated protein kinase (AMPK). Moreover, we revealed that hyperpolarization of plasma membrane potentials and reduction of calcium influx was also caused by adiponectin.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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AMP-Activated Protein Kinase Kinases
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Adiponectin / pharmacology
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Adiponectin / physiology*
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Animals
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Calcium / metabolism
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Cell Line
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Enzyme Activation
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Gonadotropin-Releasing Hormone / antagonists & inhibitors
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Gonadotropin-Releasing Hormone / metabolism*
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Hypothalamus / cytology
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Hypothalamus / drug effects
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Hypothalamus / metabolism*
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Membrane Potentials* / drug effects
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Mice
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Neurons / drug effects
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Neurons / metabolism
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Protein Kinases / metabolism
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Receptors, Adiponectin / metabolism
Substances
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Adiponectin
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Receptors, Adiponectin
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adiponectin receptor 1, mouse
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adiponectin receptor 2, mouse
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Gonadotropin-Releasing Hormone
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Protein Kinases
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AMP-Activated Protein Kinase Kinases
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Calcium