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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, METHODS, METHODS, METHODS, METHODS, RESULTS. Meshes: Androgens, Animals, Apoptosis, Fertility, Ghrelin, Infertility, Male, Leptin, Male, Mice, Mice, Inbred C57BL, Mice, Obese, Phenotype, Receptors, Ghrelin, Signal Transduction, Testis, Testosterone, Up-Regulation.
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Does inhibition of ghrelin signaling improve the reproductive phenotype of male ob/ob mouse? Context: To investigate whether ghrelin signaling is involved in the pathogenesis of male factor infertility induced by leptin deficiency. Experimental study. University academic medical center. Ten-week-old C57BL/6J mice and ob/ob mice. Western blotting, (quantitative) reverse transcription-polymerase chain reaction (qRT-PCR), immunohistochemistry, and in situ end labeling of fragmented DNA. Expression levels of ghrelin and its functional receptor growth hormone (GH) secretagogue receptor 1a (GHS-R1α) were examined by Western blotting and immunohistochemistry. Ob/ob mice were injected IP with specific GHS-R1α antagonist, and thereafter germ cell apoptosis and steroidogenic capability were assessed by TUNEL assay, (q) RT-PCR, and radioimmunoassay. Expression of GHS-R1α and its endogenous ligand ghrelin was both up-regulated in ob/ob testis. Inhibition of the ghrelin pathway restored androgen synthesis, reduced germ cell apoptosis, and thereby resulted in improved sperm production in ob/ob mice.
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Ghrelin, as an antagonistic partner of leptin in the endocrinic/paracrine circuit, may be involved in the pathogenesis of male factor infertility induced by leptin deficiency. Final Decision: yes