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)

Seventy-two long-surviving liver transplant recipients were evaluated prospectively, including a baseline allograft biopsy for weaning off of immunosuppression. Thirteen were removed from candidacy because of chronic rejection (n = 4), hepatitis (n = 2), patient anxiety (n = 5), or lack of cooperation by the local physician (n = 2). The other 59, aged 12-68 years, had stepwise drug weaning with weekly or biweekly monitoring of liver function tests. Their original diagnoses were PBC (n = 9), HCC (n = 1), Wilson's disease (n = 4), hepatitides (n = 15), Laennec's cirrhosis (n = 1), biliary atresia (n = 16), cystic fibrosis (n = 1), hemochromatosis (n = 1), hepatic trauma (n = 1), alpha-1-antitrypsin deficiency (n = 9), and secondary biliary cirrhosis (n = 1). Most of the patients had complications of long-term immunosuppression, of which the most significant were renal dysfunction (n = 8), squamous cell carcinoma (n = 2) or verruca vulgaris of skin (n = 9), osteoporosis and/or arthritis (n = 12), obesity (n = 3), hypertension (n = 11), and opportunistic infections (n = 2). When azathioprine was a third drug, it was stopped first. Otherwise, weaning began with prednisone, using the results of corticotropin stimulation testing as a guide. If adrenal insufficiency was diagnosed, patients reduced to < 5 mg/day prednisone were considered off of steroids. The baseline agents (azathioprine, cyclosporine, or FK506) were then gradually reduced in monthly decrements. Complete weaning was accomplished in 16 patients (27.1%) with 3-19 months drug-free follow-up, is progressing in 28 (47.4%), and failed in 15 (25.4%) without graft losses or demonstrable loss of graft function from the rejections. This and our previous experience with self-weaned and other patients off of immunosuppression indicate that a significant percentage of appropriately selected long-surviving liver recipients can unknowingly achieve drug-free graft acceptance. Such attempts should not be contemplated until 5-10 years posttransplantation and then only with careful case selection, close monitoring, and prompt reinstitution of immunosuppression when necessary.
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PMID:Weaning of immunosuppression in long-term liver transplant recipients. 783 42

The genetic loci agouti and extension control the relative amounts of eumelanin (brown-black) and phaeomelanin (yellow-red) pigments in mammals: extension encodes the receptor for melanocyte-stimulating hormone (MSH) and agouti encodes a novel 131-amino-acid protein containing a signal sequence. Agouti, which is produced in the hair follicle, acts on follicular melanocytes to inhibit alpha-MSH-induced eumelanin production, resulting in the subterminal band of phaeomelanin often visible in mammalian fur. Here we use partially purified agouti protein to demonstrate that agouti is a high-affinity antagonist of the MSH receptor and blocks alpha-MSH stimulation of adenylyl cyclase, the effector through which alpha-MSH induces eumelanin synthesis. Agouti was also found to be an antagonist of the melanocortin-4 receptor, a related MSH-binding receptor. Consequently, the obesity caused by ectopic expression of agouti in the lethal yellow (Ay) mouse may be due to the inhibition of melanocortin receptor(s) outside the hair follicle.
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PMID:Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor. 793 41

The relationship between maternal plasma levels of beta-endorphin (beta-Ep) during labor and various obstetrical factors was investigated in 115 healthy pregnant women. beta-Ep was determined by radioimmunoassay using double-antibody RIA kit (INCSTAR Corporation, Stillwater, M'S.). The results were as follows: (1) The primiparous women showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with the multiparous women. In addition, the group of women whose Bishop's score at the onset of labor was 5 points or less showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with that in the group of women whose Bishop's score was 6 points or more. (2) The increase in maternal plasma levels of beta-Ep during the first and the second stage of labor was significantly higher in obese women (pre-pregnancy BMI > or = 24) than in normal weight women (pre-pregnancy BMI < 24). In normal weight women in pre-pregnancy, the group of women whose weight gain during pregnancy was 11kg or more showed a significantly higher increase of beta-Ep compared with that in the group of women whose weight gain was less than 11 kg. These results suggest that a stressful delivery caused a significant increase of maternal plasma levels of beta-Ep during labor. Moreover, obesity and marked weight gain during pregnancy caused a remarkable increase in beta-Ep probably due to latent dystocia.
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PMID:[Maternal plasma beta-endorphin levels during labor in relation to maternal obesity]. 795 97

Ingestion of highly palatable diets (HPDs), rich in sucrose and fat, has been shown to lead to obesity and alterations in cardiovascular function in animal models. A hypothesis has been advanced which suggests that ingestion of an HPD increases hypothalamic beta-endorphin release, an effect which results in an increase in sympathetic nerve outflow during the development of obesity. The hypothesis was tested by chronic (10 weeks) feeding of male spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs) with the HPD or normal rat chow (ND). Cardiovascular function (systolic blood pressure, heart rate) and body weight gain were monitored during the feeding period. Pain sensitivity was tested weekly by measuring tail-flick latency. Body weight gain was greater in WKY rats than in SHRs, but ingestion of the HPD had no effect in either strain. Terminal organ analysis indicated differences between strains of SHRs and WKYs in the heart, the adrenal and pituitary glands, peri-testicular fat pad, and testis weights expressed by organ weight/body weight. The heart weight was greater in SHRs on the HPD than in SHRs on the ND. The ingestion of the HPD significantly increased blood pressure only in SHRs, following 10 weeks of dietary intervention. However, tail-flick latency was prolonged in both SHRs and WKYs during ingestion of the HPD. Increases in tail-flick latency suggest that the HPD increases brain opiate levels in both SHRs and WKYs. Exaggerated increases in heart weight and blood pressure were noted in SHRs following feeding with the HPD, indicating enhanced sensitivity of SHRs to HPD-induced hypertension.
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PMID:Cardiovascular and analgesic effects of a highly palatable diet in spontaneously hypertensive and Wistar-Kyoto rats. 802 5

The concentrations of beta-endorphin, ACTH, insulin (IRI), glucagon (IRG), cortisol and growth hormone were determined by radioimmunoassay during oral glucose tolerance test (OGTT) performed in 13 obese patients with normal glucose tolerance and without arterial hypertension. The test was performed in random, before and after intravenous administration of 0.8 mg of naloxone. Six persons with normal body weight served as controls. Higher basal concentrations of beta-endorphin and significant increase in beta-endorphin levels during OGTT, without concomitant increase in ACTH concentrations, have been found in obese patients. No effect of naloxone on beta-endorphin liberation during OGTT was observed, though the drug caused lowering in maximal increment of beta-endorphin and paradoxically lowered the concentrations of ACTH and cortisol. The basal concentrations of beta-endorphin did not correlate with the concentrations of insulin, ACTH, cortisol and growth hormone. Elevated concentrations of insulin, lowered concentration of growth hormone and normal levels of glucose and glucagon were observed in basal conditions, and excessive responses of insulin, glucose and glucagon were observed in obese patients during OGTT. Naloxone lowered insulin response and inhibited the fall of growth hormone during OGTT but did not influence the concentrations of glucose and glucagon. No correlation was found during OGTT after naloxone between insulin and beta-endorphin, ACTH or cortisol, whereas negative correlation was observed between insulin and growth hormone. The obtained results suggest that the elevated concentrations of beta-endorphin in simple obesity may be of both hypophyseal and peripheral origin. Hyper-beta-endorphinemia observed in obesity is probably not directly responsible for hyperinsulinemia, it may, however, be responsible for lower sensitivity of tissues to the action of insulin.
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PMID:[Effect of naloxone on beta-endorphin and insulin concentrations during glucose tolerance testing in patients with simple obesity]. 805 20

We examined the effects of an oral glucose load on plasma insulin, androgens, and beta-endorphin (beta EP) concentrations in patients carefully selected as having polycystic ovary syndrome (PCOS) and normal glucose tolerance. Our aim was to verify whether insulin resistance is a common feature of PCOS and to differentiate the metabolic abnormalities related to PCOS from those associated with obesity. Plasma immunoreactive insulin (IRI), C-peptide (C-PR), testosterone, androstenedione, dehydroepiandrosterone sulfate, ACTH, and beta EP responses to a 3-h oral glucose tolerance test (OGTT) were evaluated in 10 obese (OB-PCOS) and 10 nonobese (NO-PCOS) patients with PCOS and in 7 obese and 7 nonobese ovulatory controls. OB-PCOS and NO-PCOS did not differ significantly from weight-matched controls in the IRI response, but had a significantly higher C-PR response in terms of mean postglucose load levels and mean incremental areas. During OGTT, mean plasma levels of testosterone, androstenedione, and dehydroepiandrosterone sulfate declined in both PCOS groups as well as in controls, and no significant correlation between the plasma androgen and IRI or C-PR responses was found. The ACTH response in OB-PCOS and NO-PCOS was similar to that in controls, with a progressive decrease until 180 min. A similar decline in plasma beta EP was found in controls, whereas no change in plasma beta EP was observed in OB-PCOS and NO-PCOS. These findings indicate that independently of the presence of obesity, PCOS patients have enhanced insulin secretion in response to OGTT and show a peculiar pattern of changes in plasma beta EP.
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PMID:Insulin, C-peptide, androgens, and beta-endorphin response to oral glucose in patients with polycystic ovary syndrome. 810 16

Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, beta-endorphin, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.
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PMID:[Hormonal aspects of the pathogenesis of arterial hypertension in young obese patients]. 810 42

Acute effects of intracerebroventricularly administered corticotropin-releasing hormone (CRH) on deprivation-induced food intake, whole-body oxygen consumption, brown adipose tissue metabolism, and several locomotive behaviors were examined in 6- to 7-wk-old female genetically obese (ob/ob) and lean mice. Corticotropin-releasing hormone depressed food intake in a dose-dependent manner, with a tendency for greater suppression of intake in intact ob/ob mice than in lean mice. Adrenalectomy abolished this tendency for CRH to be more potent in ob/ob mice than in lean mice. Corticotropin-releasing hormone also lowered the oxygen consumption of ob/ob and lean mice, without affecting brown adipose tissue metabolism as assessed by measurement of GDP binding to brown adipose tissue mitochondria. Grooming activity was lowered in CRH-injected mice. The CRH-induced lowering of oxygen consumption and grooming activity in mice contrasts with CRH-induced elevations of oxygen consumption and grooming in rats, suggesting species-specific responses to this peptide. Because effects of CRH were similar in adrenalectomized ob/ob and lean mice, it is unlikely that obesity-producing abnormalities in ob/ob mice are related to abnormal CRH action mechanisms. However, potential abnormalities in CRH synthesis and/or release cannot be excluded.
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PMID:Corticotropin-releasing hormone decreases feeding, oxygen consumption and activity of genetically obese (ob/ob) and lean mice. 814 74

Obesity, the most frequent nutritional problem throughout the rich nations, can have a vast and significant influence on different aspects of endocrinology, in particular on ovulation disfunction, on hyperandrogenemia, on hormone-sensitive carcinomas. Our study proposes to value the response to adrenal cortex to stimulation with adrenocorticotropin (ACTH) hormone in obese patients, with particular attention to the behavior of adrenocortical androgens and their precursor. We recruited 30 female patients so divided: 12 obese, nonhirsute, eumenorrheic patients (group A); 10 normal weight, hirsute patients in situation of secondary amenorrhea (group B); 8 normal weight, nonhirsute, eumenorrheic patients (group C). Cortisol, progesterone, 17 OH progesterone, dehydroepiandrosterone sulfate, androstenedione, testosterone were measured at 60, 120, 180, 240, 300 min during continual infusion i.v., for 5 h, of ACTH 1-17 at 100 mcg dose, in physiological sodium chloride solution. All the women with monthly menstruation were studied between the IV and VIII day of their cycle. In the patients with secondary amenorrhea the value of basic progesterone was used to completely exclude an eventual luteal phase and the relationship LH/FSH was so as to logically exclude a diagnosis of polycystic ovary. This exclusion was also confirmed from the report of the ultrasonography. The basic concentration of hormone dosage is not significantly different between the patients of the three groups, except for T. This hormone is different because it is found to be significantly (p < 0.01) increase in the hirsute patients, in respect of the patients in group A and group C. Also P and 17OHP have been found to be higher, if only in insignificant measure, in hirsute patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Probable role of obesity on the adrenal response to acute stimulation with adrenocorticotrophic hormone in eumenorrheic and hirsute, non-eumenorrheic women]. 823 17

The basal and hyperglycaemia-stimulated secretion of glucose, IRI and beta-endorphin (BE) were studied in subjects who had gone surgical treatment for obesity few years ago and the results were compared with those of obese subjects and lean controls. 58 persons were divided into the following groups: A-obese subjects BMI > 30, B--obese subjects 25 < BMI < 30, C--subjects treated by truncal vagotomy and gastric banding, D--subjects treated by jejunoileostomy, E--control group BMI < 25. Oral glucose (75 g) tolerance test was performed in all subjects. Blood concentration of glucose, and serum concentration of IRI and BE were studied before and 30, 60, 90 and 120 minutes after ingestion of glucose. The basal levels and areas over basal values (AOBV) of investigated parameters were evaluated. Both the basal and glucose stimulated levels of IRI and BE were higher in the obese subjects than in the control group. Truncal vagotomy and gastric banding or jejunoileostomy resulted in reduction of IRI secretion without any decrease in BE levels. The alteration of the opioid system may play some role in the pathogenesis of obesity.
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PMID:[Level of beta endorphins and insulin in blood of obese subjects. Effect of surgical treatment for obesity on higher exchange parameters]. 823 1


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