Hypothalamic kiss1 mRNA and kisspeptin immunoreactivity are reduced in a rat model of polycystic ovary syndrome (PCOS)

Kisspeptin mRNA expression is increased in the posterior hypothalamus in the rat model of polycystic ovary syndrome

“…Androgen-induced rat models of PCOS are mostly used to study pathophysiological mechanisms of PCOS. However, these models might not be suitable for the study of GnRH secretion, because hypothalamic Kiss1 mRNA expression is decreased in DHT treated rats [25]. For the present study, we selected letrozole-induced PCOS model rats, which show elevated serum T and LH levels, polycystic ovarian morphology and enlarged ovaries [11][12][13], because these hormonal and histologic findings are similar findings to human PCOS except for the relatively lower serum E 2 level.…”

Leptin-Responsive GABAergic Neurons Regulate Fertility through Pathways That Result in Reduced Kisspeptinergic Tone

“…Food deprivation can delay, and even prevent, sexual maturation and disrupt fertility across species (Frisch, 1985;Ahima et al, 1996). In humans, starvation is associated with menstrual cycle disruption in females, mediated by a decrease in luteinizing hormone (LH) secretion (Welt et al, 2004) that reflects reduced activity of gonadotropin-releasing hormone (GnRH) neurons in response to metabolic cues (Mantzoros et al, 2011).…”

“…Cre/ϩ were generated by insertion of an internal ribosome entry site (IRES)-Cre recombinase cassette downstream of the stop codon of endogenous genes Vgat (vesicular GABA transporter) and Vglut2 (synaptic vesicular glutamate transporter), respectively (Vong et al, 2011). The Lepr lox/ϩ mice were generated by the insertion of two loxP sites and an frt site flanking the coding exon 17 of the leptin receptor gene (Balthasar et al, 2004;McMinn et al, 2004). This modification (Meyers et al, 1998) permits the conditional ablation of Lepr driven by the IRES-Cre recombinase cassettes described above (Balthasar et al, 2004;McMinn et al, 2004).…”

“…The Lepr lox/ϩ mice were generated by the insertion of two loxP sites and an frt site flanking the coding exon 17 of the leptin receptor gene (Balthasar et al, 2004;McMinn et al, 2004). This modification (Meyers et al, 1998) permits the conditional ablation of Lepr driven by the IRES-Cre recombinase cassettes described above (Balthasar et al, 2004;McMinn et al, 2004). The mice were genotyped by PCR using the following primers to identify expression of the Cre amplicon (5Ј-GCC CTG GAA GGG ATT TTT GAA GCA-3Ј and 5Ј-ATG GCT AAT CGC CAT CTT CCA GCA-3Ј), endogenous ghrelin (Ghrl ) as internal amplification control (5Ј-GGT CAG CCT AAT TAG CTC TGT-3Ј and 5Ј-GAT CTC CAG CTC CTC CTC TGT C-3Ј), and primers recognizing the loxP site (5Ј-AAT GAA AAA GTT GTT TTG GGA CGA-3Ј and 5Ј-CAG GCT TGA GAA CAT GAA CAC AAC AAC-3Ј (1) changes in body weight, (2) progression to vaginal opening, and (3) timing of first estrus.…”

Prenatal Exposure of Kisspeptin Antagonist on the GonadotropinReleasing Hormone (GnRH) Expression in Rat Model of Polycystic Ovary Syndrome

“…Although PCOS symptoms generally become obvious during puberty, clinical and experimental evidence suggest an intrauterine origin for the syndrome [7]. Exposure to excess androgen during the critical period of early life leads to the development of a PCOS-like phenotype in adulthood, which is associated with reduced hypothalamic kiss1 (a male-typical kiss1 pattern) and unresponsive to sex steroid feedback actions; however there is enhanced GnRH neuron activity and LH secretion [9,10]. Experimental studies demonstrate that kisspeptin antagonists decrease LH pulse frequency and amplitude but do not appear to affect basal LH secretion [11,12].…”