Acceleration of pubertal development following central blockade of the Y1 subtype of neuropeptide Y receptors

Pralong, François P.; Voirol, Marie-Jeanne; Giacomini, Marco; Gaillard, Rolf C.; Grouzmann, Eric

doi:10.1016/s0167-0115(00)00130-0

Cited by 39 publications

(20 citation statements)

References 36 publications

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“…Development of selective agonists/antagonists for different receptors and utilization of knockout animals have improved our understanding of the role of different receptor subtypes for NPY in the control of reproductive axis, although at the moment the characterization of the specific role of the different receptor subtypes is scarce. Recent experiments have shown that the NPY Y 1 receptor inhibits the gonadotrope axis (22) and that its blockade accelerates the onset of puberty (49). In addition, NPY Y 4 receptors have been involved in the NPY effects on LH release (25), and experimental evidence suggests that the inhibition of LH secretion exerted by central administration of NPY in the rats is predominantly mediated by Y 5 receptors (51).…”

mentioning

confidence: 99%

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Pinilla¹,

Fernández²,

Vigo³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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] is a gastrointestinal secreted molecule recently shown to be involved in the control of food intake with agonistic activity on neuropeptide Y (NPY) receptor subtypes Y2 and Y5. Notably, PYY-(3-36) has been recently demonstrated as putative regulator of gonadotropin secretion in the rat. However, the "reproductive" facet of this factor remains to be fully elucidated. In this context, we report herein our analyses of the influence of the nutritional status on the effects of PYY-(3-36) upon GnRH and gonadotropin secretion. The major findings of our study are 1) the stimulatory effect of central administration of PYY-(3-36) on LH secretion was significantly enhanced after fasting and blocked by a GnRH antagonist; 2) besides central effects, PYY-(3-36) elicited LH and FSH secretion directly at the pituitary level, a response that is also augmented by fasting; 3) PYY-(3-36) inhibited GnRH secretion by hypothalamic fragments from male rats fed ad libitum, whereas a significant stimulatory effect was observed after fasting; and 4) the increase in the gonadotropin responsiveness to PYY-(3-36) in fasting was not associated with changes in the expression of Y2 and Y5 receptor genes at hypothalamus and/or pituitary. In conclusion, our study extends our previous observations suggesting a relevant, mostly stimulatory, role of PYY-(3-36) in the control of gonadotropin secretion. Strikingly, such an effect was significantly enhanced by fasting. Considering the proposed decrease in PYY-(3-36) levels after fasting, the possibility that reduced PYY-(3-36) secretion might contribute to defective function of the gonadotropic axis after food deprivation merits further investigation.polypeptide YY-(3-36); gonadotropin-releasing hormone; luteinizing hormone; follicle-stimulating hormone; fasting; pituitary ALTHOUGH IT IS KNOWN that conditions of negative energy balance are frequently linked to lack of puberty onset and reproductive failure, at the moment the mechanisms involved in fitting the reproductive function to body energy stores remain incompletely defined. Compelling evidence has recently demonstrated that central and peripheral endocrine signals governing energy homeostasis, such as the adipocytederived hormone leptin, the stomach-derived hormone ghrelin, orexins, and neuropeptide Y (NPY), are also involved in the control of reproductive function by acting at different levels of hypothalamic-pituitary-gonadal axis.In this context, it has been demonstrated that NPY, a member of the pancreatic polypeptide family (54), is involved in the control of food intake, reproductive function, and pituitary secretion (26,27,30,33). In rats, central administration of NPY advances puberty (43), whereas immunoneutralization of NPY reduced the magnitude of the LH surge during the afternoon of first proestrus (42). A facilitatory role of NPY on the onset of puberty has been also reported in the female rhesus monkey (23) and in chicks (18). Secretion of NPY to portal vasculature is increased on the afternoon of proestrus and serves to amplify...

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confidence: 99%

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Pinilla¹,

Fernández²,

Vigo³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…These effects of NPY are largely due to inhibition of GnRH release (Gazal et al 1998) and may be mediated by a direct action on GnRH neurons (Klenke et al 2010). In addition, central infusion of NPY in prepubertal rats is followed by a delay of pubertal maturation similar to that observed in food-restricted animals (Pralong et al 2000). Thus, we reasoned that increased leptin secretion may facilitate pubertal maturation of the hypothalamic-adenohypophysealgonadal axis by suppressing hypothalamic NPY release.…”

Section: Introductionmentioning

confidence: 95%

Reciprocal changes in leptin and NPY during nutritional acceleration of puberty in heifers

Cardoso¹,

Alves²,

Prezotto³

et al. 2014

Journal of Endocrinology

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Feeding a high-concentrate diet to heifers during the juvenile period, resulting in increased body weight (BW) gain and adiposity, leads to early-onset puberty. In this study, we tested the hypothesis that the increase in GnRH/LH release during nutritional acceleration of puberty is accompanied by reciprocal changes in circulating leptin and central release of neuropeptide Y (NPY). The heifers were weaned at 3.5 months of age and fed to gain either 0.5 (Low-gain; LG) or 1.0 kg/day (High-gain; HG) for 30 weeks. A subgroup of heifers was fitted surgically with third ventricle guide cannulas and was subjected to intensive cerebrospinal fluid (CSF) and blood sampling at 8 and 9 months of age. Mean BW was greater in HG than in LG heifers at week 6 of the experiment and remained greater thereafter. Starting at 9 months of age, the percentage of pubertal HG heifers was greater than that of LG heifers, although a replicate effect was observed. During the 6-h period in which CSF and blood were collected simultaneously, all LH pulses coincided with or shortly followed a GnRH pulse. At 8 months of age, the frequency of LH pulses was greater in the HG than in the LG group. Beginning at 6 months of age, concentrations of leptin were greater in HG than in LG heifers. At 9 months of age, concentrations of NPY in the CSF were lesser in HG heifers. These observations indicate that increased BW gain during juvenile development accelerates puberty in heifers, coincident with reciprocal changes in circulating concentrations of leptin and hypothalamic NPY release.

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“…Çocukluk çağındaki dişi sıçanlarda kronik olarak intraserebroventriküler olarak NPY1R antagonisti verilmesinin endojen hipotalamik NPY'yi baskılayarak puberteyi hızlandırdığı görülmüş-tür. [73] NPY'nin büyüme üzerinde de etkisi bulunmaktadır. Önceki çalışmalar stresin büyümenin düzenlenmesinde önemli rolü olduğunu ortaya koymuştur.…”

Section: Büyüme Ve Ergenlik (Puberte)unclassified

Neuropeptide Y and Stress

Gülsün¹,

Tamam²

2012

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychia

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ÖZETStres ve bireysel baş etme yetilerinin nörobiyolojik yönü birçok araştırmacının ilgi odağı olmuştur. Bir dizi çalışmada genetik değişkenler ile strese tepki düzeyleri ve yaşam olayları arasında bir ilişki olduğu gösterilmiştir. Nöropeptid Y stres esnekliğini düzenleyen sistemlerden biridir. Uzun süreli ya da tekrarlayan stres durumlarında nöropeptid Y beynin anahtar bölgelerinden salınır. Bu sistem stresle ilgili bozukluklara yatkınlığı farklı kişilerde farklı esneklikte işleyiş gösterir. Gen-çevre etkileşimleri için özellikle ilgi çekici olan strese duyarlı sinyal moleküllerini kodlayan genlerin değişimidir. Bu durum strese yatkınlığa ya da esnekliğe katkıda bulunabilir. Nöropeptid Y sistemi de strese davranışsal uyumda anahtar rol oynamaktadır. Nöropeptid Y düzeyinin azalmış olması tedaviye dirençli depresyonda ve travma sonrası stres bozukluğunda da gözlenmiştir. Düşük nöropeptid Y ekspresyonunun ya da strese yanıt olarak nöropeptid Y sisteminin yeterince işlevsel olmaması ve sonucunda ortaya çıkan stres esnekliğinin az olması stresle ilişkili bozukluklara yatkınlığı arttırabilmektedir. Anahtar Sözcükler: Nöropeptid Y, stres, stres esnekliği ABSTRACTThe neurobiological aspects of stress and coping skills has been the focus of interest for many researchers. Some of the studies has shown that there is a significant relationship among genetically variables, stress response and life events. Neuropeptide Y is one of the systems regulating the stress response. Under the prolonged or repeated trauma neuropeptide Y is released from the brain's key areas. This system shows different levels of functioning in individuals with different levels of resilience. There is particular interest in the variations of genes that encode stress-sensitive signaling molecules during geneenvironment interaction. This condition may contribute to susceptibility of stress or stress resilience. Neuropeptide Y system plays a key role in the adaptation to behavioral stress. The reduced levels of neuropeptide Y have also been observed in treatment-resistant depression and posttraumatic stress disorder. Lower level of neuropeptide Y expression and dysfunctional neuro-

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Acceleration of pubertal development following central blockade of the Y1 subtype of neuropeptide Y receptors

Cited by 39 publications

References 36 publications

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Reciprocal changes in leptin and NPY during nutritional acceleration of puberty in heifers

Neuropeptide Y and Stress

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