Regulation of hypothalamic expression of KiSS-1 and GPR54 genes by metabolic factors: analyses using mouse models and a cell line - PubMed (original) (raw)
. 2007 Oct;148(10):4601-11.
doi: 10.1210/en.2007-0500. Epub 2007 Jun 26.
Affiliations
- PMID: 17595226
- DOI: 10.1210/en.2007-0500
Regulation of hypothalamic expression of KiSS-1 and GPR54 genes by metabolic factors: analyses using mouse models and a cell line
Raul M Luque et al. Endocrinology. 2007 Oct.
Abstract
It is well established that reproductive function is metabolically gated. However, the mechanisms whereby energy stores and metabolic cues influence fertility are yet to be completely deciphered. Recently, the hypothalamic KiSS-1/GPR54 system has emerged as a fundamental regulator of the gonadotropic axis, which conveys the modulatory actions of sex steroids to GnRH neurons. Evidence is also mounting that KiSS-1 neurons may also represent the link between systemic metabolic signals and central control of reproduction. To further explore this possibility, we examined the impact of changes in energy status and key metabolic regulators on the hypothalamic expression of KiSS-1 and GPR54 genes, using different mouse models and the hypothalamic cell line N6. Time-course analysis of the effects of short-term fasting revealed a rapid (12- and 24-h) decline in KiSS-1 and GPR54 mRNA levels, which preceded that of GnRH (48 h). In contrast, diet-induced obesity or obesity associated with leptin deficiency (ob/ob vs. wild-type mice) failed to induce overt changes in hypothalamic expression of KiSS-1 and GPR54 genes. However, leptin infusion of ob/ob mice evoked a significant increase in KiSS-1 and GPR54 mRNA levels compared with pair-fed controls. Moreover, leptin, but not insulin or IGF-I, stimulated KiSS-1 mRNA expression in the mouse hypothalamic cell line N6. In addition, neuropeptide Y (NPY) null mice showed decreased KiSS-1 mRNA levels at the hypothalamus, whereas exposure to NPY increased expression of KiSS-1 in hypothalamic N6 cells. In sum, our present data further characterize the functional relevance and putative key mediators (such as leptin and NPY) of the metabolic regulation of the hypothalamic KiSS-1 system in the mouse.
Similar articles
- Developmental and hormonally regulated messenger ribonucleic acid expression of KiSS-1 and its putative receptor, GPR54, in rat hypothalamus and potent luteinizing hormone-releasing activity of KiSS-1 peptide.
Navarro VM, Castellano JM, Fernández-Fernández R, Barreiro ML, Roa J, Sanchez-Criado JE, Aguilar E, Dieguez C, Pinilla L, Tena-Sempere M. Navarro VM, et al. Endocrinology. 2004 Oct;145(10):4565-74. doi: 10.1210/en.2004-0413. Epub 2004 Jul 8. Endocrinology. 2004. PMID: 15242985 - Sex steroids and leptin regulate the "first Kiss" (KiSS 1/G-protein-coupled receptor 54 system) in human gonadotropin-releasing-hormone-secreting neuroblasts.
Morelli A, Marini M, Mancina R, Luconi M, Vignozzi L, Fibbi B, Filippi S, Pezzatini A, Forti G, Vannelli GB, Maggi M. Morelli A, et al. J Sex Med. 2008 May;5(5):1097-1113. doi: 10.1111/j.1743-6109.2008.00782.x. Epub 2008 Mar 4. J Sex Med. 2008. PMID: 18331266 - KiSS-1 and reproduction: focus on its role in the metabolic regulation of fertility.
Tena-Sempere M. Tena-Sempere M. Neuroendocrinology. 2006;83(5-6):275-81. doi: 10.1159/000095549. Epub 2006 Aug 29. Neuroendocrinology. 2006. PMID: 16940711 Review. - KiSS-1 neurones are direct targets for leptin in the ob/ob mouse.
Smith JT, Acohido BV, Clifton DK, Steiner RA. Smith JT, et al. J Neuroendocrinol. 2006 Apr;18(4):298-303. doi: 10.1111/j.1365-2826.2006.01417.x. J Neuroendocrinol. 2006. PMID: 16503925 - KiSS-1/kisspeptins and the metabolic control of reproduction: physiologic roles and putative physiopathological implications.
Castellano JM, Roa J, Luque RM, Dieguez C, Aguilar E, Pinilla L, Tena-Sempere M. Castellano JM, et al. Peptides. 2009 Jan;30(1):139-45. doi: 10.1016/j.peptides.2008.06.007. Epub 2008 Jun 21. Peptides. 2009. PMID: 18634841 Review.
Cited by
- IGF-1 Acts through Kiss1-expressing Cells to Influence Metabolism and Reproduction.
Wang M, Pugh SM, Daboul J, Miller D, Xu Y, Hill JW. Wang M, et al. bioRxiv [Preprint]. 2024 Jul 4:2024.07.02.601722. doi: 10.1101/2024.07.02.601722. bioRxiv. 2024. PMID: 39005405 Free PMC article. Preprint. - Kisspeptin a potential therapeutic target in treatment of both metabolic and reproductive dysfunction.
Sliwowska JH, Woods NE, Alzahrani AR, Paspali E, Tate RJ, Ferro VA. Sliwowska JH, et al. J Diabetes. 2024 Apr;16(4):e13541. doi: 10.1111/1753-0407.13541. J Diabetes. 2024. PMID: 38599822 Free PMC article. Review. - Dietary Protein Regulates Female Estrous Cyclicity Partially via Fibroblast Growth Factor 21.
Cao Y, Yang M, Song J, Jiang X, Xu S, Che L, Fang Z, Lin Y, Jin C, Feng B, Wu D, Hua L, Zhuo Y. Cao Y, et al. Nutrients. 2023 Jul 6;15(13):3049. doi: 10.3390/nu15133049. Nutrients. 2023. PMID: 37447375 Free PMC article. - Food deprivation differentially modulates gene expression of LPXRFa and kisspeptin systems in the brain-pituitary axis of half-smooth tongue sole (Cynoglossus semilaevis).
Wang B, Cui A, Xu Y, Zhang Y, Jiang Y, Liu X. Wang B, et al. Front Endocrinol (Lausanne). 2023 Mar 24;14:1099832. doi: 10.3389/fendo.2023.1099832. eCollection 2023. Front Endocrinol (Lausanne). 2023. PMID: 37033260 Free PMC article. - Agouti-related peptide neuronal silencing overcomes delayed puberty in neonatally underfed male mice.
Decourt C, Connolly GADP, Ancel C, Inglis MA, Anderson GM. Decourt C, et al. J Neuroendocrinol. 2022 Oct;34(10):e13190. doi: 10.1111/jne.13190. Epub 2022 Aug 19. J Neuroendocrinol. 2022. PMID: 36306199 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
Miscellaneous