neuropeptide-y--leu(31)-pro(34)- and Body-Weight

The effect of chronic administration of exogenous neuropeptide Y (NPY) and specific NPY receptor agonists and antagonists on reproductive function was examined in lactating rats. As previously demonstrated in our laboratory, chronic (7-day) intracerebroventricular (i.c.v.) NPY infusion (6 microg/day) from days 8-15 postpartum (pp) caused a significant decrease in milk production and an early termination of lactational diestrus. Similar application of the mixed Y1/Y4/Y5 receptor agonist (Leu31, Pro34) NPY (at 3, 6 and 9 microg/day) reproduced the effect of chronic NPY infusion on milk production in a dose-independent manner. Consistent with this effect, the potent Y1 antagonist/Y4 agonist, 1229U91, given concomitantly with NPY eliminated the decline in milk production. The Y2 receptor agonist, NPY13-36, had no effect on milk production at any of the doses used. Length of lactational diestrus was reduced following administration of the Y2 agonist at 18 microg/day but not at 9 microg or 27 microg/day whereas (Leu31, Pro34) NPY infusion had no effect on this parameter at any of the doses used. However, the group that was treated with NPY plus 1229U91 exhibited the usual length of lactational diestrus, indicating that there is at least some Y1 involvement in the effects of NPY on lactational infertility. To test the possibility that the effects of NPY infusion are mediated through changes in circulating prolactin and progesterone, plasma concentrations of these hormones were measured on day 15 pp in NPY-, (Leu31, Pro34) NPY- and vehicle-treated females. NPY-infused females had lower plasma prolactin concentrations than vehicle-infused dams but progesterone concentrations were similar across groups. Overall, these data indicate that chronic exogenous NPY-infusion in lactating females disrupts milk production and shortens lactational diestrus, most likely through reducing prolactin secretion, and that this effect is mediated via Y1 receptor activity.

Topics: Animals; Animals, Newborn; Body Weight; Diestrus; Dose-Response Relationship, Drug; Drug Combinations; Eating; Female; Lactation; Neuropeptide Y; Neuropeptides; Peptides, Cyclic; Postpartum Period; Progesterone; Prolactin; Rats; Rats, Wistar; Receptors, Neuropeptide Y

The effects of neuropeptide Y (NPY), peptide YY (PYY), [Leu31, Pro34]NPY, and NPY (13-36) on adipocyte lipolysis have been studied in subcutaneous (inguinal) and visceral (parametrial) rat adipose tissues. A 48-h fasting period and chemical sympathectomy were used to evaluate the regulation of Y1 and Y2 pathways in rat adipocytes. NPY, PYY, and [Leu31, Pro34]NPY significantly inhibited fat cell lipolysis by about 25% in both tissues (p < or = 0.05). This inhibition was achieved mainly through the Y1 pathway. No significant response to NPY (13-36) was observed, suggesting a lack of involvement of the Y2 pathway in the antilipolytic effect of NPY and PYY. The 48-h fasting period led to the loss of the Y1 inhibitory effect previously observed in control rats. On the other hand, the chemical sympathectomy induced a 35% increase of fat cell lipolysis (p < or = 0.05). The latter involved the Y2 pathway as stimulated by NPY (13-36), and was observed in the parametrial tissue exclusively. These results suggest that: a) rat Y receptors reported to exhibit Gi responses can also express Gs-like responses, and b) visceral and subcutaneous adipose tissues exhibit specific regulation of fat cell lipolysis.

Topics: Adipocytes; Animals; Appetite Stimulants; Body Weight; Cell Size; Eating; Fasting; Female; Lipolysis; Neuropeptide Y; Oxidopamine; Peptide Fragments; Peptide YY; Rats; Rats, Wistar; Receptors, Neuropeptide Y; Sympathectomy, Chemical; Sympatholytics