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

Abstract

] 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...

Enteroendocrine Changes Facilitating Weight Loss Following Gastric Bypass

“…Similar results have been noted in rodents [78,79]. The exact mechanisms are not known, but may be attributed to earlier and more intense subjection of the distal gut mucosa to nutrients or, alternatively, be due to a decrease in levels of peptides such as leptin, thought to suppress PYY secretion and the hypothalamic response [80][81][82]. In addition, constant high levels of DPP-IV have been identified after weight loss operations [80], a factor probably augmenting the anorexic effects of PYY itself.…”

Selective role of neuropeptide Y receptor subtype Y2 in the control of gonadotropin secretion in the rat

“…polypeptide YY3-36; luteinizing hormone-releasing hormone; luteinizing hormone; follicle-stimulating hormone; fasting; pituitary IT IS KNOWN THAT THE INITIATION OF PUBERTY and the integrity of reproductive function are physiologically coupled to nutritional status. A large body of evidence accumulated over the last several years (14,23,24,40,42) indicates that feeding behavior and activity of the gonadotropic axis are linked and that the pancreatic polypeptide family may be pivotal in this relationship. The pancreatic polypeptide family consists of a series of related peptides composed of 36 amino acids termed neuropeptide Y (NPY) 1-36 , peptide YY (PYY) , and pancreatic peptide (PP) 1-36 (47).…”

“…A large body of evidence accumulated over the last several years (14,23,24,40,42) indicates that feeding behavior and activity of the gonadotropic axis are linked and that the pancreatic polypeptide family may be pivotal in this relationship. The pancreatic polypeptide family consists of a series of related peptides composed of 36 amino acids termed neuropeptide Y (NPY) , peptide YY (PYY) , and pancreatic peptide (PP) (47).…”

“…Thus, for NPY (preferential Y 1 and Y 5 agonist), discrepant stimulatory or inhibitory effects on sexual maturation and reproduction have been observed de-pending upon species, steroid environment (26), the site of NPY administration into the brain (37), and a chronic (18,38,39) vs. acute (32) pattern of infusion. Likewise, PYY (preferential Y 2 and Y 5 agonist) has been reported to be stimulatory or inhibitory or to have no effect on gonadotropinreleasing hormone (GnRH) and gonadotropin secretion depending upon the age, sex, steroidal environment, and in vivo vs. in vitro studies (14,40,43). PP (preferential Y 4 agonist) has been reported to increase or not affect gonadotropin secretion depending upon the species and steroidal environment (21,43,44).…”

Peptide YY (PYY)3–36 modulates thyrotropin secretion in rats

“…In fasting conditions, there is a higher NPY inhibitory tonus on TRH neurons (Fekete et al 2001) and, in addition, fasting was associated with reduced PYY 3-36 serum levels, as reported by others (Tovar et al 2004, Chan et al 2005, which may render the tissues more sensitive to PYY 3-36 action. Other reports support the concept that fasting enhances PYY 3-36 effects, such as those concerning the peptide action on gonadotropin secretion (Pinilla et al 2006) and on food intake (Challisa et al 2003, Riediger et al 2004.…”