Disease relevance of NPY

• Thus the hypoleptinemia of lactation may activate NPY orexigenic pathways and attenuate anorexigenic melanocortin and CART pathways in the hypothalamus to promote the hyperphagia of lactation [1].
• In control animals, there was a significant increase in the NPY concentration in fetal, but not maternal, plasma during hypoxemia [2].
• In control fetuses, acute hypoxaemia led to transient bradycardia, femoral vasoconstriction and significant increases in plasma concentrations of catecholamines, vasopressin and NPY [3].
• These data show: 1) differences between the maternal and fetal plasma NPY response to maternal inhalation hypoxia; 2) that NPY may play a role in mediating fetal defense responses to acute hypoxemia; and 3) that fetal exposure to glucocorticoids modifies the fetal plasma NPY response to acute hypoxemia [2].
• During saline infusion, hypoxaemia induced hypertension, bradycardia, femoral vasoconstriction, hyperglycaemia and an increase in haemoglobin, catecholamines and neuropeptide Y (NPY) [4].

Psychiatry related information on NPY

• The possible roles of the central noradrenergic and NPY systems in the etiology of the hypercortisolemia of endogenous depression and anorexia nervosa are discussed [5].

High impact information on NPY

• Studies were performed to determine the effects of intracerebroventricular norepinephrine (NE) or neuropeptide Y (NPY) on the ovine hypothalamic-pituitary-adrenal (HPA) axis [5].
• When added to cultured ovine anterior pituitary cells, NPY neither increased basal ACTH release nor augmented CRF- or AVP-induced ACTH release [5].
• Glucose infusion increased mRNA expression for POMC, but not for the anorectic neuropeptide CART, or the orexigenic neuropeptides NPY and AGRP, in the arcuate nucleus of the fetal hypothalamus [6].
• In contrast, CGRP antagonism markedly diminished the femoral vasoconstrictor and glycaemic responses to hypoxaemia, and attenuated the increases in haemoglobin, catecholamines and NPY [4].
• The appearance of NPY in GHRH cells of lean animals may be a mechanism for regulation of increasing GH secretion with reduced adiposity [7].

Chemical compound and disease context of NPY

• Fetal treatment with dexamethasone significantly enhanced the fetal NPY response to acute hypoxemia but had no effects on basal NPY levels in the fetal or maternal plasma or on the maternal response to acute hypoxemia [2].
• 5. In the rings containing endothelium, NPY enhanced the contraction caused by U46619 during hypoxia only [8].
• We have characterized the localization and the ontogenetic changes in Neuropeptide tyrosine (NPY) before birth and investigated the regulation of NPY expression by cortisol and undernutrition in the fetal sheep hypothalamus during late gestation [9].
• Plasma concentrations of noradrenaline, NPY and vasopressin were not measured during hypotension in lambs [10].
• In foals, there were significant increases in plasma concentrations of noradrenaline, neuropeptide Y (NPY), vasopressin, adrenocorticotrophic hormone (ACTH) and cortisol in response to hypotension (P<0.05) [10].

Biological context of NPY

• Levels of gene expression of NPY and MCH were higher in THIN ewes [11].
• The appetite stimulators, NPY and MCH, appear to be involved in the metabolic response to altered adiposity, whereas ENK in the periventricular region may be linked to the secretion of GH and possibly LH [11].
• Both, percent area and the optical density of NPY immunostaining measured in this area were higher (P < 0.01) in the preovulatory than in the follicular phase [12].
• Plasma concentrations of neuropeptide Y (NPY) were measured in pregnant ewes and their fetuses under basal conditions and in response to acute hypoxemia during late gestation [2].
• High levels of NPY expression during the luteal phase of the oestrous cycle may be caused by progesterone [13].

Anatomical context of NPY

• In the study reported here, we tested the hypothesis that long-term food restriction suppresses tonic release of LH as a result of 1) an increase in biosynthetic activity of NPY neurons in the arcuate nucleus of the hypothalamus, 2) an increase in activity of neurons that secrete beta-endorphin, and 3) a decrease in biosynthesis of LHRH [14].
• Two populations of the NPY-positive neurons were detected and evaluated in the infundibular and periventricular nuclei of the hypothalamus [12].
• For NPY, the number of cells counted in the arcuate nucleus/median eminence region and the number of silver grains per cell was significantly lower in animals killed during August than in animals killed in February or December [15].
• These studies indicate that changes in photoperiod may regulate ER expression within the preoptic area and suggest that hypothalamic NPY and betaE neurons are involved in the seasonal regulation of reproductive activity in the ewe [16].
• Following at least 5 days of recovery, one group of fetuses (n = 9) was subjected to a 30 min treatment period with exogenous NPY (17 microg kg(-1) bolus plus 0.85 microg kg(-1) min(-1) infusion) [17].

Associations of NPY with chemical compounds

• Influence of food restriction on neuropeptide-Y, proopiomelanocortin, and luteinizing hormone-releasing hormone gene expression in sheep hypothalami [14].
• Early decrease of proopiomelanocortin but not neuropeptide Y mRNA expression in the mediobasal hypothalamus of the ewe, during the estradiol-induced preovulatory LH surge [18].
• Hypothalamic gene expression in sheep for cocaine- and amphetamine-regulated transcript, pro-opiomelanocortin, neuropeptide Y, agouti-related peptide and leptin receptor and responses to negative energy balance [19].
• To address the mechanisms underlying these responses, chemoreflex function and plasma concentrations of catecholamines, neuropeptide Y (NPY) and vasopressin were measured [3].
• The effects of fetal treatment with dexamethasone on these NPY responses were also examined [2].

Regulatory relationships of NPY

• Basal episodic profiles (pre-E beta) of LH, GH, and PRL were similar in ovx ewes infused with control or anti-NPY serum [20].
• Since dietary restrictions and exogenous NPY have similar influence on the activation of GH secretion, we suggest that NPY could be a neuromodulatory link between nutritional cues and somatotropic axis in sheep [21].

Other interactions of NPY

• The current study sought to define the effects of altered adiposity on the expression of genes for neuropeptide Y (NPY), POMC, enkephalin (ENK), and melanin-concentrating hormone (MCH) [11].
• Fasting up-regulated gene expression for OB-Rb and for the orexigenic neuropeptides NPY and AGRP in the ARC [19].
• The HPD lesion effectively destroyed the entire median eminence [no nerve terminals immunostained for tyrosine hydroxylase (TH) and gonadotropin-releasing hormone] and the adjacent arcuate nucleus (no perikarya immunostained for proopiomelanocortin or TH, and no cells expressed neuropeptide Y mRNA) [22].
• We conclude that lowering body weight leads to increased expression of Ob-Rb, ghrelin/GHS-R expression and proportion of NPY cells that express Ob-Rb in the arcuate nucleus [23].
• Furthermore, the coexistence of these peptides within neurons of the NI is very limited, as from all possible permutations checked, only SRIF and NPY were found together in a small number of cells [24].

Analytical, diagnostic and therapeutic context of NPY

• Also the density of NPY- and CPON-immunoreactive nerve fibers decreased in the animals after the ganglionectomy [25].
• Immunohistochemistry revealed projections into the external zone of the median eminence for NPY, GAL and SP [26].
• In situ hybridization for NPY was performed in OVX and OVX ewes treated with progesterone [13].
• Finally, perfusion of NPY antiserum during an ongoing LH surge disrupted LH release [27].
• Microinjections of NPY into the POA decreased (P < 0.01) average plasma LH levels during the non-breeding season at a dose of 10 micrograms but did not significantly affect pulse frequency or amplitude [28].

References