Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the effects of dietary leucine supplementation in lactating dams, particularly on energy homeostasis through signaling mechanisms in the central nervous system. Dams were fed ad libitum with standard diet during pregnancy (control dams) or supplemented with 2% leucine (leucine-supplemented dams) from delivery onwards. Food intake, body weight and composition were periodically recorded. Hypothalamus was collected at the end of lactation, and the expression of neuropeptide Y (NPY), agouti-related protein (AgRP) pro-opiomelanocortin (POMC), cocaine and amphetamine regulated transcript (CART), insulin receptor (InsR), ghrelin receptor (GSHR), melanocortin receptor (MCR4), leptin receptor (Ob-Rb) and suppressor of cytokine signaling 3 (SOCS3) were analyzed. Dietary leucine supplementation to lactating rats increased plasma leucine by 56%, modulated body composition and contributed to a tendency of higher ratio of lean/fat mass content of dams during lactation, without affecting food intake, thermogenesis capacity or body or tissue/organs weights. No differences in body weight of offspring from control and leucine-supplemented dams were found. The expression of orexigenic peptides (NPY and AgRP) decreased in leucine-dams, whereas the expression of anorexigenic peptides (POMC and CART), the hypothalamic receptors of insulin, ghrelin, melanocortin and leptin and SOCS3 did not change by leucine supplementation. In conclusion, increased leucine intake during lactation may contribute to a healthier profile of body composition in dams, without compromising the growth and development of the progeny by a mechanism associated with lower expression of orexigenic neuropeptides in hypothalamus.
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PMID:Dietary l-leucine supplementation of lactating rats results in a tendency to increase lean/fat ratio associated to lower orexigenic neuropeptide expression in hypothalamus. 2034 2

Increasing number of evidence suggest that gastric mucosal protection can be induced also centrally. Several neuropeptides, such as TRH, amylin, adrenomedullin, enkephalin, beta-endorphin, nociceptin, nocistatin, ghrelin or orexin given centrally induce gastroprotection and the dorsal vagal complex and vagal nerve may play prominent role in this centrally initiated effect. Since also cannabinoid receptors are present in the dorsal vagal complex, we aimed to study whether activation of central cannabinoid receptors result in gastric mucosal defense and whether there is an interaction between cannabinoids and endogenous opioids. Gastric mucosal damage was induced by 100% ethanol in rats. The cannabinoids were given intravenously (i.v.) or intracerebroventricularly (i.c.v.), while the antagonists were given i.c.v or intracisternally (i.c.). Gastric lesions were evaluated macroscopically 60 min later. Anandamide, methanandamide and WIN55,212-2 reduced ethanol-induced mucosal lesions after both peripheral (0.28-5.6 micromol/kg, 0.7-5.6 micromol/kg and 0.05-0.2 mumol/kg i.v., respectively) and central (2.9-115 nmol/rat, 0.27-70 nmol/rat and 1.9-38 nmol/rat i.c.v., respectively) administration. The gastroprotective effect of anandamide and methanandamide given i.c.v. or i.v.was reversed by the CB(1) receptor antagonist SR141716A (2.16 nmol i.c.v.). Naloxone (27.5 nmol i.c.v.) also antagonized the effect of i.c.v. or i.v. injected anandamide and WIN55,212-2, but less affected that of methanandamide. The gastroprotective effect of anandamide was diminished also by endomorphin-2 antiserum. In conclusion it was first demonstrated that activation of central CB(1) receptors results in gastroprotective effect. The effect is mediated at least partly by endogenous opioids.
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PMID:Analysis of the effect of neuropeptides and cannabinoids in gastric mucosal defense initiated centrally in the rat. 2038 51

Leptin and ghrelin are known to be the main hormones involved in the control of food intake, with opposite effects. Here we aimed to assess whether changes in leptin and ghrelin systems can be involved in the different satiating capacities of carbohydrates (CHO) and fat. Adult male Wistar rats were studied under 24h fasting conditions and after 24h fasting followed by a 12h re-feeding period with 64 kcal of CHO or fat, consisting of a mixture of wheat starch and sucrose or bacon, respectively. Serum levels of leptin and ghrelin, and mRNA levels of leptin and ObRb in the retroperitoneal and inguinal adipose tissue and of NPY, POMC, ObRb and GSHR in the hypothalamus were measured. CHO re-feeding resulted in higher leptin mRNA expression levels in the retroperitoneal adipose tissue and in higher circulating leptin levels compared with those after fat re-feeding. Moreover, circulating ghrelin levels and ghrelin/leptin ratio were significantly higher after fat re-feeding compared with CHO re-feeding, and hypothalamic expression levels of ghrelin receptor increased after fat, but not after CHO, re-feeding. Hence, expression levels of hypothalamic neuropeptides involved in food intake control and regulated by these hormones, particularly the orexigenic NPY and the anorexigenic pro-opiomelanocortin (POMC)-derived alpha-melanocyte-stimulating hormone, were also differently affected by CHO and fat re-feeding, resulting in a significantly lower NPY/POMC ratio after CHO re-feeding than after fat re-feeding. In conclusion, different effects on the leptin and ghrelin systems can account, at least in part, for the lower satiating capacity of fat compared to CHO.
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PMID:The different satiating capacity of CHO and fats can be mediated by different effects on leptin and ghrelin systems. 2045 Sep 38

Ghrelin, a 28-amino-acid octanoylated peptide predominantly produced by the stomach, was discovered to be the natural ligand of the type 1a GH secretagogue receptor. Thus, it was considered as a natural GH secretagogue (GHS) additional to GHRH, although later on ghrelin has mostly been considered a major orexigenic factor. The GH-releasing action of ghrelin takes place both directly on pituitary cells and through modulation of GHRH from the hypothalamus; some functional anti-somatostatin action has also been shown. However, even at the neuroendocrine level, ghrelin is much more than a natural GHS. In fact, it significantly stimulates prolactin secretion in humans, independent of both gender and age and probably involving a direct action on somatomammotroph cells. Above all, ghrelin and synthetic GHS possess an acute stimulatory effect on the activity of the hypothalamus-pituitary-adrenal axis in humans, which is, at least, similar to that of the opioid antagonist naloxone, arginine vasopressin and even corticotropin-releasing hormone. Also, ghrelin plays a relevant role in the modulation of the hypothalamic-pituitary-gonadal function, with a predominantly CNS-mediated inhibitory effect upon the gonadotropin pulsatility both in animals and in humans.
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PMID:Ghrelin and anterior pituitary function. 2061 13

Energy homeostasis and fuel metabolism undergo significant modifications in the course of aging. This presents in elderly subjects either as increased body mass and glucose intolerance - which may lead to obesity and type 2 diabetes - or loss of appetite, which may also seriously compromise health. The hypothalamic expression of neuropeptide Y (NPY), the most potent orexigen, and its receptors, was highly suppressed in old rats. Moreover, induction of the NPY-dependent responses was severely blunted in old animals. Similar reductions, although of a lower magnitude, were reported for other hypothalamic orexigens, A and orexins. Orexigenic activity of ghrelin, the only peripheral orexigen, was clearly suppressed in old humans and rats. However, aging did not alter hypothalamic expression of key anorexigens, alpha-MSH and CART. Age-related decrease of central anorexigenic action of leptin was likely caused by the impaired leptin signal transduction. Thus, aging in rodents is associated with the general down-regulation of orexigenic hypothalamic pep-tides - and unchanged expression of anorexigenic hypothalamic peptides - which may lead to weight loss at the end of life. If similar changes at the level of CNS underlie the 'anorexia of aging' observed in some elderly, therapeutic interventions at this regulatory level may be possible in the future.
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PMID:Central control of food intake in aging. 2070 54

Recent studies have demonstrated a role for appetite- and volume-regulating neuropeptides in alcohol dependence, particularly in association with alcohol craving. The peptides leptin, ghrelin, adiponectin, vasopressin and the atrial natriuretic peptide (ANP) have been of particular interest because of their central effects on various brain circuits, including the hypothalamic-pituitary-adrenocortical (HPA) axis. In addition, pro-opiomelanocortin (POMC) plays an important role in linking appetite regulation with the HPA axis. Recent research has also demonstrated that the expression of these peptides in alcohol dependence is, at least partially, regulated by genetic and epigenetic mechanisms. These peptides and their associated circuits provide an intriguing new field for future pharmacological approaches for treating depression, anxiety and, potentially, addictive disorders such as alcohol dependence.
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PMID:Appetite- and volume-regulating neuropeptides: Role in treating alcohol dependence. 2087 12

Animals chronically exposed to stressors with access to diets high in fat and sugar consume and prefer these diets, a result consistent with the association between stress and comfort food ingestion in humans. As social subordination in rhesus monkeys provides an ethologically relevant translational model of psychosocial stress, we tested the hypothesis that differences in food intake between dominant and subordinate female monkeys are due to corticotropin-releasing hormone-(CRH) induced alteration in sensitivity to ghrelin, a potent orexigenic signal. We assessed food intake of animals given a choice between a low (LCD) and high calorie diet (HCD) in response to 4-day treatment with the CRH receptor antagonist, astressin B, and to an acute treatment of ghrelin. Ghrelin stimulated intake of LCD in subordinates but did not further increase consumption of HCD, whereas ghrelin decreased LCD consumption without affecting HCD intake in dominant females. Astressin B decreased cortisol levels and increased preference for and intake of the HCD in subordinates and decreased calorie intake and HCD preference in dominant animals. These results suggest that increased caloric intake by subordinates may, in part, be explained by a greater sensitivity to postprandial increases in ghrelin and that CRH receptor antagonism leading to a decrease in cortisol has mixed effects on food choice depending on an individual's stress background.
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PMID:Increased ghrelin sensitivity and calorie consumption in subordinate monkeys is affected by short-term astressin B administration. 2098 8

1. Obesity is a metabolic disease of pandemic proportions largely arising from positive energy balance, a consequence of sedentary lifestyle, conditioned by environmental and genetic factors. Several central and peripheral neurohumoral factors (the major ones being the anorectic adipokines leptin and adiponecin and the orexigenic gut hormone ghrelin) acting on the anorectic (pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript) and orexigenic (neuropeptide Y and agouti gene-related protein) neurons regulate energy balance. These neurons, mainly in the arcuate nucleus of the hypothalamus, project to parts of the brain modulating functions such as wakefulness, autonomic function and learning. A tilt in the anorectic-orexigenic balance, perhaps determined genetically, leads to obesity. 2. Excess fat deposition requires space, created by adipocyte (hypertrophy and hyperplasia) and extracellular matrix (ECM) remodelling. This process is regulated by several factors, including several adipocyte-derived Matrix metalloproteinases and the adipokine cathepsin, which degrades fibronectin, a key ECM protein. Excess fat, also deposited in visceral organs, generates chronic low-grade inflammation that eventually triggers insulin resistance and the associated comorbidities of metabolic syndrome (hypertension, atherosclerosis, dyslipidaemia and diabetes mellitus). 3. The perivascular adipose tissue (PVAT) has conventionally been considered non-physiological structural tissue, but has recently been shown to serve a paracrine function, including the release of adipose-derived relaxant and contractile factors, akin to the role of the vascular endothelium. Thus, PVAT regulates vascular function in vivo and in vitro, contributing to the cardiovascular pathophysiology of the metabolic syndrome. Defining the mechanism of PVAT regulation of vascular reactivity requires more and better controlled investigations than currently seen in the literature.
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PMID:Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint. 2108 97

We have previously identified that peripherally administered cholecystokinin (CCK) exerts an anorexigenic action via the vagal afferent, and subsequently the brain melanocortin- and corticotropin-releasing hormone-neuronal pathways in goldfish. N-Methyl-d-aspartate (NMDA) receptors have been shown to be involved in the regulations of locomotor activity and food intake in mammals. Although several neuropeptides and other factors exert similar effects in fish and mammals, the role of NMDA receptor in the control of locomotor activity and feeding behavior in fish is still unclear. In the present study, we examined the effect of the NMDA receptor antagonist, MK-801, on locomotor activity and food intake in the goldfish. Intraperitoneal (IP) injection of MK-801 at 0.15nmol/g body weight (BW) increased locomotor activity, but did not affect food consumption. IP injection of MK-801 at same dose attenuated peripheral CCK (100pmol/g BW)-induced anorexigenic, but not peripheral acyl ghrelin (10pmol/g BW)-induced orexigenic actions. These data show for the first time that the NMDA receptor-signaling pathway is involved in the regulation of locomotor activity and feeding behavior through modulation of the peripheral CCK-induced satiety signal, but not the orexigenic effect of ghrelin.
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PMID:Effect of the N-methyl-d-aspartate receptor antagonist on locomotor activity and cholecystokinin-induced anorexigenic action in a goldfish model. 2109 16

Ghrelin plays an important role in energy metabolism by regulating food intake, body weight and glucose homeostasis. In this review, we highlight recent developments describing how ghrelin stimulates neuropeptide Y (NPY) neurons, but not pro-opiomelanocortin neurons, to regulate food intake. We describe a novel signaling modality, in which ghrelin activates NPY/agouti-related protein (AgRP) neurons through fatty acid oxidation, reactive oxygen species buffering and mitochondrial function. We hypothesize that this unique system may serve to maintain NPY/AgRP cell function during prolonged negative energy balance. We discuss the idea that the metabolic status plays a key role in ghrelin function. For example, our recent studies illustrate that diet-induced obesity causes ghrelin resistance in arcuate NPY/AgRP neurons. On the other side of the metabolic coin, ghrelin and GOAT knockout models show that ghrelin is required to maintain blood glucose during severe calorie restriction. We propose the hypothesis that ghrelin primarily functions during negative energy balance to maintain whole-body energy homeostasis.
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PMID:Metabolic status regulates ghrelin function on energy homeostasis. 2112 19


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