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)

Chronic naloxone treatment of schedule-fed guinea pigs caused an initial anorexia followed by a resumption of food and water intake, despite the continued presence of the narcotic antagonist. During this state of chronic naloxone treatment, amphetamine exerted a similar degree of anorexia to that in animals not pretreated with naloxone. In contrast, amphetamine tolerant guinea pigs exhibited supersensitivity to naloxone with respect to feeding behavior. Since chronic amphetamine exposure results in an increased level of beta-endorphin in the hypothalamus it is suggested that an enhanced endorphinergic activity compensates for the effect of amphetamine on feeding mechanisms.
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PMID:Interaction of amphetamine and naloxone in feeding behavior in guinea pigs. 738 14

Plasma and cerebrospinal fluid (CSF) concentrations of three well-known satiety neuropeptides, cholecystokinin (CCK), somatostatin and calcitonin gene-related peptide (CGRP), along with two powerful orexigenic neuropeptides, neuropeptide Y (NPY) and beta-endorphin have been measured in elderly persons with idiopathic anorexia and normal weight healthy subjects in a similar age range. Plasma and CSF immunoreactivity levels of the two main fractions of CCK (CCK8s and CCK33) after being separated by HPLC were measured by a radioimmunoassay (RIA) developed in our laboratory, whereas the other neuropeptides were assayed by commercially available RIA kits. Elderly underweight anorectic patients had significantly lower levels of beta-endorphin but increased concentrations of NPY in both plasma and CSF when compared to controls. In addition to significantly higher levels of CCK8s but not CCK33 in plasma, we found a trend to higher CSF concentrations of CCK8s and a positive correlation between the body mass index and either beta-endorphin (r = 0.58, P < 0.05) or CCK8s (r = 0.69, P < 0.01) concentrations in CSF in the anorectic group. CSF somatostatin concentrations were decreased significantly, but plasma somatostatin levels and plasma and CSF concentrations of CGRP were similar in senile anorectics and controls. Treatment of five anorectic patients with megestrol acetate, 480 mg daily for 6 months, reversed only the decrease in CSF beta-endorphin levels but did not normalize the body weight or the fat body mass. On the basis of our findings, we hypothesize that a decrease in CSF beta-endorphin concentration along with a rise in plasma levels of CCK8s might be accounted for the primary anorexia of aging.
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PMID:Alterations in plasma and cerebrospinal fluid levels of neuropeptides in idiopathic senile anorexia. 790 1

The carboxyl-terminal tripeptide of alpha-MSH(1-13), Lys-Pro-Val, antagonizes anorexia induced by interleukin-1 beta (IL-1). The present studies were undertaken to determine if the Lys-Pro dipeptide portion of this tripeptide likewise antagonizes anorexia induced by ICV administration of 0.5 pmol IL-1 in rats previously deprived of food. This dose of Lys-Pro did significantly attenuate the IL-1-induced anorexia, but only for 1 h after infusion. Simultaneous administration of a larger dose (5.0 pmol) of Lys-Pro reversed the IL-1-induced anorexia during both the 0-1-h and 2-4-h periods. In addition, both 0.5 and 5.0 pmol of the D-substitute tripeptide, Lys-D-Pro-Thr (LDPT), similarly attenuated the IL-1-induced anorexia. The ICV administration of 5.0 pmol Lys-Pro also did not have any significant effects on food consumption. These results indicate that the dipeptide Lys-Pro may have a short-term antagonistic action against the anorexia induced by IL-1, and it is possible that this action may be partially mediated by the blockade of IL-1 on its own receptor.
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PMID:The dipeptide Lys-Pro attenuates interleukin-1 beta-induced anorexia. 838 84

Hypothalamic neuropeptides are thought to contribute to the pathophysiology of eating disorders. In an animal model with chronic abnormalities of energy expenditure, appetitive behavior, and body weight, without acute food restriction, we found alterations in peripheral levels of adrenocorticotropic hormone and corticosterone, but no alterations in the expression of neuropeptides genes that are known to regulate ingestive behavior and food intake acutely. Our data suggest that activation of hypothalamic-pituitary-adrenal function in activity anorexia may not be due to increased transcription of corticotropin-releasing hormone gene, but might be related to posttranscriptional events or to other neuropeptides, such as arginine vasopressin. Furthermore, we suggest that abnormalities in neuropeptides observed in eating disorders may be caused by acute food restriction, rather than by chronic hyperactivity, anorexia, and low weight.
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PMID:Activity-induced anorexia in rats does not affect hypothalamic neuropeptide gene expression chronically. 838 55

We examined a hypothesis that alpha-Melanocyte Stimulating Hormone (MSH) can antagonizes the anorexia induced by intracerebroventricular injection of corticotropin releasing factor (CRF). Food intake of the rats deprived of food for 18 h was significantly inhibited by 4 h after intracerebroventricular injection of CRF. alpha-MSH also suppressed food consumption by 4 h after the treatment. However, simultaneous administration of alpha-MSH attenuated the anorexic effect of CRF at 0-2 h period and food consumption for 4 h was equal to controls. In addition, simultaneous administration of alpha-MSH deleted the stimulatory effects of CRF on serum corticosterone levels. The present experiment demonstrated that alpha-MSH can antagonizes the anorexia and activation of hypothalamo-pituitary-adrenal axis by CRF, suggesting that the processing step of proopiomelanocortin may be important for the induction of anorexia elicited by CRF.
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PMID:Alpha-melanocyte stimulating hormone (MSH) antagonizes the anorexia by corticotropin releasing factor (CRF). 841 10

Infections are associated with increased plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone. Hypothalamo-pituitary-adrenal (HPA) responses have also been observed with immunological stimuli that are not infective. Although such responses have been suggested to be mediated by ACTH secreted by lymphocytes, adrenocortical activation by immunological stimuli requires a functional pituitary. The most likely mechanism by which immunological stimuli activate the HPA axis involves production of cytokines by lymphocytes. The prime candidate is interleukin 1 (IL-1), because IL-1 production follows activation of the immune system and IL-1 administration is a potent activator of the HPA axis. However, other cytokines, such as tumour necrosis factor, may also be involved. Most immunological stimuli and IL-1 also activate both peripheral and central noradrenergic neurons. IL-1-induced activation of the HPA axis in vivo depends upon secretion of corticotropin-releasing factor (CRF), an intact pituitary, and the ventral noradrenergic bundle which innervates the CRF-containing neurons in the paraventricular nucleus (PVN) of the hypothalamus. Besides elevating body temperature, administration of IL-1 elicits a number of behavioural responses in rats and mice, including anorexia, increased sleep time, decreased investigation of novel objects and other animals, increased defensive withdrawal and other behaviours characteristic of sickness. Some of these responses can be reversed by CRF-antagonists and mimicked by CRF administration. Thus, endogenous production of IL-1 can account for a range of physiological and behavioural responses characteristic of sickness. Nevertheless, definitive evidence that IL-1 mediates these responses in sick animals is lacking.
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PMID:Infection as a stressor: a cytokine-mediated activation of the hypothalamo-pituitary-adrenal axis? 849 Oct 88

In this paper a new immunological model of anorexia and bulimia nervosa will be presented in which the inflammatory cytokines are conceived as the fundamental regulators of body metabolism. This conception differs from the conventional view in which the inflammatory cytokines are perceived primarily as peptide molecules utilized by the immune system to control infection, inflammation and tissue or neuronal damage. Given that the inflammatory cytokines are also fundamental regulators of body metabolism, when they become dysregulated they create physiological chaos which results in the development of a number of autoimmune, metabolic and psychiatric disorders. In this proposed immunological model of anorexia and bulimia nervosa, elevated tumor necrosis factor-alpha features as the primary cause of these conditions. Pathophysiological parallels are drawn between anorexia nervosa and cancer cachexia in terms of the causal role the cytokines, neuropeptides and neurotransmitters play in the manifestation of shared symptoms. These shared symptoms include elevated tumour necrosis factor-alpha, down-regulated interleukin-2 and interleukin-4 and depletion of lean body mass. Furthermore, the following neuropeptides are dysregulated in both anorexia nervosa and cancer cachexia: vasoactive intestinal peptide, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, peptide YY and beta-endorphin. In addition, in anorexia and bulimia nervosa, secretion of the neurotransmitter serotonin is inhibited while norepinephrine is enhanced. It will be argued that the causal interplay between the cytokines, neuropeptides and neurotransmitters initiates a cascade of biochemical events which may result in either anorexia or bulimia nervosa, or cancer cachexia. The extent to which these inflammatory cytokines, neuropeptides and neurotransmitters are causally efficacious in the pathogenesis of other autoimmune disorders, such as diabetes mellitus and rheumatoid arthritis, will also be addressed.
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PMID:The role of tumor necrosis factor-alpha in the pathogenesis of anorexia and bulimia nervosa, cancer cachexia and obesity. 896 Dec 38

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
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PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

Young female rats of 160-180 g were implanted with osmotic minipumps releasing 3.0 micromol/day per kg of oleoyl-oestrone in liposomes (Merlin-2) into the bloodstream for up to 14 days. Merlin-2 induced a loss of appetite in the first days, later recovered, and a decrease in body weight of 7%, which contrasts with the 15% increase in controls during the 2-week period. Neither plasma glucose nor urea was affected by treatment, but liver glycogen increased by 50% in 14 days. Insulin decreased slightly with Merlin-2 treatment. Plasma corticotropin (ACTH) and corticosterone showed a transient increase by day 6 of treatment. The expression of the ob gene in adipose tissue fell during the period studied to practically nil on day 14; circulating leptin levels decreased more than 70% from day 1 to day 14. Oestrone levels increased from 0.3 nM (controls) to a maintained 40-60 nM level for the rest of the experiment. Oleoyl-oestrone levels first increased 4-fold, to decrease again to the initial levels on day 10, increasing later to 100-fold on day 14. The three phases observed in food intake, weight loss and oleoyl-oestrone levels match fairly well, which supports the direct involvement of oleoyl-oestrone in body-weight control. However, the control of oleoyl-oestrone levels seems to be mediated in part by corticosterone. The practical disappearance of leptin synthesis coincides with the massive accumulation of oleoyl-oestrone in plasma. The results presented suggest the involvement of oleoyl-oestrone in the main mechanisms of control of body weight and its regulation by glucocorticoids and leptin.
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PMID:Short-term treatment with oleoyl-oestrone in liposomes (Merlin-2) strongly reduces the expression of the ob gene in young rats. 929 Nov 5

We investigated the effectiveness of lipopolysaccharide (LPS) and muramyl dipeptide (MDP) administered into the brain to induce anorexia in acutely fasted Wistar rats allowed to refeed. We also assayed for changes in mRNA levels of IL-1 system components, TNF-alpha, TGF-beta1, glycoprotein 130 (gp 130), leptin receptor (OB-R), pro-opiomelanocortin (POMC), neuropeptide Y (NPY), glucocorticoid receptor (GR), and CRF receptor (CRF-R) in selected brain regions. The data show that LPS and MDP induced anorexia differentially during refeeding. LPS-induced anorexia was of a stronger magnitude and duration than that of MDP. RNase protection assays showed that LPS and MDP significantly increased the expression of IL-1beta, IL-1 receptor type I, and TNF-alpha mRNAs in the cerebellum, hippocampus, and hypothalamus; LPS was more potent in all cases. MDP treatment, on the other hand, induced a stronger increase in hypothalamic levels of IL-1 receptor antagonist (IL-1Ra) and TGF-beta1 mRNAs relative to LPS. In addition, competitive RT-PCR analysis showed that LPS induced an eleven-fold increase in IL-1alpha mRNA in the hypothalamus relative to vehicle. These findings suggest that LPS and MDP mediate anorexia through different cytokine mechanisms. A stronger up-regulation of anti-inflammatory cytokines (IL-1Ra and TGF-beta1) mRNA expression by MDP may be involved in the weaker MDP-induced anorexia relative to LPS. No significant changes were observed in the peptide components examined except for an up-regulation in cerebellar gp 130 mRNA and down-regulation of hypothalamic GR mRNA expression in response to LPS or MDP. This study shows that LPS and MDP induce anorexia in fasted rats allowed to refeed, and suggests an important role for endogenous cytokine-cytokine interactions.
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PMID:Lipopolysaccharide (LPS)- and muramyl dipeptide (MDP)-induced anorexia during refeeding following acute fasting: characterization of brain cytokine and neuropeptide systems mRNAs. 962 98


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