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)

Postburn galactorrhea, although relatively uncommon, is a complex problem to treat. Three of 25 female premenopausal patients who were admitted during the years 1995 to 2001 with more than 40% TBSA burns developed this problem. All three patients were obese according to body mass index and other clinical criteria. It was observed that the additional disturbance of equilibrium of hypothalamus because of burn injury, which is already disturbed as per se in obese patients, precipitates sustained release of prolactin, leading to galactorrhea. Hyperinsulinemia because of obesity and associated reactive metabolic response of burn trauma contribute to the stimulation of prolactin secretion and sustained hyperprolactinemia. Interestingly, our patients who developed postburn galactorrhea also developed refractory hypertrophic scars not readily amenable to preventive and conservative therapeutic treatment methods. The responsible factor for its development can be a rise in prolactin levels with interplay of other hormones, such as melanocyte-stimulating hormone (MSH), from the anterior pituitary. Repeated serum prolactin measurements and early control of rising levels during the burn treatment, particularly in obese patients, are recommended. Early and vigorous measures to prevent scar hypertrophy also are advocated. In our study, we failed to correlate chest wall burns with galactorrhea.
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PMID:Postburn galactorrhea with refractory hypertrophic scars: role of obesity under scrutiny. 1461 Apr 25

Neuronal plasticity during the critical postnatal period of development seems to promote a change in the function of the hypothalamic regulatory system of body weight. Rats raised in small litters (SL) of only three pups per mother compared to ten or twelve in control litters (CL) gain significantly more weight than normal rats till weaning and are overweight also in later life. These rats are known to express hyperleptinemia, hyperglycemia and hyperinsulinemia. The review summarizes the results of action of leptin and insulin as well as of several feeding-relevant neuropeptides on neuronal activity of hypothalamic regulatory centres in overweight SL rats compared to controls. The study was performed on brain slices perfused with solution containing 10 mM glucose. Whereas a normally inhibitory action of leptin and insulin on medial arcuate neurons (ArcM) is reduced in SL rats and partly replaced by activation, the normally activating effect of these hormones on ventromedial (VMH) neurons is altered to predominant inhibition. Inhibition of ArcM neurons may decrease the release of the orexigenic neuropeptide Y (NPY) and agouti gene-related protein (AGRP). Thus, the negative feedback by leptin and insulin on food intake is replaced by diminished response and partly positive feedback processes in SL rats. The action of NPY and AGRP as well as of the orexigenic melanin-concentrating hormone on paraventricular (PVH) and VMH neurons is also shaped from activation or bimodal effects to predominant inhibition. Such inhibition of PVH and VMH might lead to reduced energy expenditure in small litter rats. Also the anorexigenic melanocortin alpha-MSH seems to contribute into increased energy storage. These altered responses of hypothalamic neurons in overweight small litter rats might reflect a general mechanism of neurochemical plasticity and "malprogramming" of hypothalamic neuropeptidergic systems leading to a permanently altered regulatory function.
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PMID:Altered neuronal responses to feeding-relevant peptides as sign of developmental plasticity in the hypothalamic regulatory system of body weight. 1465 33

We investigated the effect of daily intracerebroventricular (ICV) leptin administration (neonatal age 2-7 days) on hypothalamic neuropeptides (neuropeptide Y, alpha-melanocyte-stimulating hormone) that regulate food intake, body weight (BW) gain, and the metabolic/hormonal profile in suckling (8 and 21 days) and adult rat (35, 60, 90, and 120 days). ICV leptin (0.16 mug.g BW(-1).dose(-1); n = 70) led to a postnatal decline in BW (P = 0.0002) that persisted only in the adult females (P = 0.002). The postnatal decline in BW due to leptin was associated with a decline in food intake (P = 0.01) and hypothalamic leptin receptor (P = 0.008) and neuropeptide Y (P = 0.008) immunoreactivities and an increase in alpha-melanocyte-stimulating hormone (P = 0.008) immunoreactivity. In addition, hyperinsulinemia (P = 0.01) with hypocorticosteronemia (P = 0.007) occurred during the postnatal period with hypercorticosteronemia (P = 0.007) and hypoleptinemia (P = 0.008) and an increase in leutinizing hormone (P = 0.01) in the adult male and female progeny. Persistent hyperinsulinemia (P = 0.015) with hyperglycemia (P = 0.008) and glucose intolerance (P = 0.001) were observed only in the adult female. We conclude that postnatal leptin administration alters the adult female phenotype and speculate that this may relate to retention of leptin sensitivity resulting in a lipoatrophic state.
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PMID:Postnatal intracerebroventricular exposure to leptin causes an altered adult female phenotype. 1531 6

The Obstectrics and Gynecology Hospital attached to Fudan University has made great achievements in the clinical and experimental study of integrated traditional Chinese and western medicine in the past 45 years. Study on induction of ovulation with acupuncture revealed the relationship between circulating estrogen and central beta-endorphin, and suggested that the depletion of central beta-endorphin resulted in the release of GnRH and ovulation, and the main indication for acupuncture treatment was pubertal dysfunctional uterine bleeding. Acupuncture was also successfully used to treat anorexia nervosa. The successful treatment of polycystic ovary syndrome (PCOS) with Yu's Tonifying Recipe for tonifying the kidney and resolving phlegm was found to be related to the elevation of serum FSH which resulted in ovulation. Good result was obtained in hyperinsulinemia pattern of PCOS treated with Tiangui Recipe for replenishing the kidney and activating blood. In studies on patients and animal model, Tiangui Recipe was found to decrease peripheral androgen and insulin levels and lead to central regulation of proopiomelanocortin, neuropeptide Y and leptin receptor, as well as regulation of neuro-endocrine-metabolic network. Thus it can promote ovulation and reduce body weight. In the studies, a new way to classify PCOS was suggested. Gengnianchun Recipe for women with postmenopausal syndrome was found to be effective in increasing estrogen receptors (ERs) and ER mRNA in hypothalamus and peripheral organs and regulating neuro-endocrine-immune-metabolic network in patients and aging rats. Gongtai was effective for controlling menorrhagia under the mechanism of regulating endometrial prostaglandins. The researches mentioned above indicate that illness is the disorder of some key-links in the life network of the patient which may be affected by factors from the environment. And this idea is different from the ideas in traditional Chinese medicine and biomedicine. It indicates that woman in subclinical health state has already got something incontrollable in her life network, and it also gives a new impact on the treatment and prevention of women's diseases as well as the prevention and treatment of women's reproductive health.
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PMID:[Integrated traditional Chinese and western medicine should make new contribution to the reproductive health of women]. 1533 62

Epinephrine, norepinephrine, and corticosterone responses to hypoglycemia are impaired in diabetic rats. Recurrent hypoglycemia further diminishes epinephrine responses. This study examined the sympathoadrenal system and hypothalamo-pituitary-adrenal axis for molecular adaptations underlying these defects. Groups were normal (N) and diabetic (D) rats and diabetic rats exposed to 4 days of 2 episodes/day of hyperinsulinemic hypoglycemia (D-hypo) or hyperinsulinemic hyperglycemia (D-hyper). D-hypo and D-hyper rats differentiated effects of hypoglycemia and hyperinsulinemia. Adrenal tyrosine hydroxylase (TH) mRNA was reduced (P < 0.05 vs. N) 25% in all diabetic groups. Remarkably, mRNA for phenylethanolamine N-methyltransferase (PNMT), which converts norepinephrine to epinephrine, was reduced (P < 0.05 vs. all) 40% only in D-hypo rats. Paradoxically, dopamine beta-hydroxylase mRNA was elevated (P < 0.05 vs. D, D-hyper) in D-hypo rats. Hippocampal mineralocorticoid receptor (MR) mRNA was increased (P < 0.05 vs. N) in all diabetic groups. Hippocampal glucocorticoid receptor (GR), hypothalamic paraventricular nucleus (PVN) GR and corticotropin-releasing hormone (CRH), and pituitary GR and proopiomelanocortin (POMC) mRNA levels did not differ. We conclude that blunted corticosterone responses to hypoglycemia in diabetic rats are not due to altered basal expression of GR, CRH, and POMC in the hippocampus, PVN, and pituitary. The corticosterone defect also does not appear to be due to increased hippocampal MR, since we have reported normalized corticosterone responses in D-hypo and D-hyper rats. Furthermore, impaired epinephrine counterregulation in diabetes is associated with reduced adrenal TH mRNA, whereas the additional epinephrine defect after recurrent hypoglycemia is associated with decreases in both TH and PNMT mRNA.
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PMID:Effects of diabetes and recurrent hypoglycemia on the regulation of the sympathoadrenal system and hypothalamo-pituitary-adrenal axis. 1549 9

Neonatal manipulations (10 min of maternal separation plus s.c. sham injection, daily for the first 21 d of life) determine overweight in male adult mice. In this work, we investigated the mechanisms underlying mild obesity and the alteration of caloric balance. Neonatally manipulated mice become overweight after onset of maturity, showing increased fat tissue and hypertrophic epididymal adipocytes. Increase in body weight occurs in the presence of a small increase in daily food intake (significant only in the adult period) and the absence of a decrease in spontaneous locomotor activity, while the calculated caloric efficiency is higher in manipulated mice, especially in adulthood. Fasting adult animals show hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and hyperleptinemia. Soon after weaning and in the adulthood, plasma corticosterone and adrenocorticotropin (ACTH) are also significantly increased. Thus, neonatal manipulations in nongenetically susceptible male mice program mild obesity, with metabolic and hormonal alterations that are similar to those found in experimental models of diabetes mellitus, suggesting that this metabolic derangement may have at least part of its roots early on in life and, more interestingly, that psychological and nociceptive stimuli induce these features.
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PMID:Overweight and metabolic and hormonal parameter disruption are induced in adult male mice by manipulations during lactation period. 1632 92

Studies in our laboratory and elsewhere have demonstrated numerous abnormalities of steroid and polypeptide hormone secretion in obesity: hyperestrogenemia and hypogonadotropic hypogonadism in obese men; diminished SHBG levels in both sexes; elevated free testosterone and free estradiol in obese women; PCOS-like gonadotropin and sex-hormone abnormalities in obese women; elevated serum insulin in both sexes; blunted stimulability of prolactin, growth hormone, and vasopressin in both sexes; and elevated basal levels and blunted stimulability and suppressibility of beta-endorphin in both sexes. All of these abnormalities have been clearly shown to be partly or completely reversible with weight loss, with the exception of the endorphin abnormalities. In that area, four out of the five studies reported show no reversibility with weight loss. Reversibility of nearly all the hormonal abnormalities of obesity (i.e., all but the hyperendorphinemia) by weight loss suggests that none of them is causative of obesity. Nevertheless, some of the reversible abnormalities may secondarily amplify the morbidity associated with obesity: the hyperinsulinemia may be related to the increased risk of hypertension, hyperlipidemia, coronary disease, and Type II diabetes; the elevated levels of free estradiol in obese women may be related to their increased risk of breast and endometrial cancer. The role of hyperendorphinemia in obesity clearly requires further investigation, since it is the only observed hormonal abnormality that appears to be non-reversible by weight loss, and also since there seems to be increased sensitivity to beta-endorphin in obesity. The possibility that endorphin abnormalities may be causal in obesity cannot be ruled out.
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PMID:A perspective on the hormonal abnormalities of obesity: are they cause or effect? 1635 9

Beta-endorphin were detected in the endocrine pancreas and seem able to influence insulin and glucagon release. Hence, endogenous opioids could have a role in glucoregulation and in the pathogenesis of obesity beyond the previously detected effects on appetite. Metabolic abnormalities, such as hyperinsulinemia, insulin-resistance and obesity, are common features of polycystic ovary syndrome (PCOS), and seem to have a pathogenetic role in this disorder. A link between opioids and PCOS-related hyperinsulinism is suggested by the finding of altered central opioid tone and elevated beta-endorphins levels, directly correlated with body weight, in these patients. Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. This effect is obtained chiefly through an improvement of insulin clearance. Naltrexone is also able to ameliorate the abnormal gonadotrophins secretion and to improve the ovarian responsiveness in obese PCOS women undergoing ovulation induction with exogenous GnRH. Such effects are believed to be obtained through an amelioration of hyperinsulinemia. Gonadal steroids modulate the opioid system both centrally and in peripheral districts. Nevertheless, the decline of ovarian function does not abolish the opioidergic control of glucoregulation. Post-menopausal period is characterised by a high prevalence of hyperinsulinemia and insulin-resistance. In particular, an association between hyperinsulinemia and increased opioid activity was found in postmenopausal women showing a central body fat distribution. Both naloxone and naltrexone ameliorate the metabolic imbalance also when it appears in the climacteric period, and mainly by increasing insulin clearance. The benefits of naltrexone may represent in the future a useful tool for the treatment of women with hyperinsulinism in the clinical practice.
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PMID:Role of opioid antagonists in the treatment of women with glucoregulation abnormalities. 1653 67

Free fatty acids (FFAs) affect anterior pituitary function. However, the effect of FFAs on corticotropin (ACTH) and cortisol in humans is controversial. Thus, we assessed the effect of a pronounced increase in circulating FFA levels induced by infusion of lipid/heparin on ACTH and cortisol secretion in young men. Eight healthy male volunteers who underwent a 10-hour overnight fast were investigated. A 20% lipid/heparin or saline/heparin infusion was given at a rate of 1.5 mL/min for 6 hours. A euglycemic hyperinsulinemic clamp was performed in 6 subjects 4 hours after the start of infusion. To assess steroid metabolism, we measured ACTH, cortisol, FFAs, and urinary steroids. Lipid infusion increased FFAs (6.06 +/- 0.52 vs 0.70 +/- 0.23 mmol/L; P < .005) and induced insulin resistance (glucose infusion rate, 4.08 +/- 2.15 vs 6.02 +/- 2.60 mg/kg per minute; P < .005). Serum cortisol and plasma ACTH decreased independent of lipid/heparin or saline/heparin infusion. In addition, we found no effect of hyperinsulinemia on ACTH and cortisol levels. There were no differences in urinary free cortisol, urinary free cortisone, 5beta-tetrahydrocortisol, 5alpha-tetrahydrocortisol, and tetrahydrocortisone. In conclusion, FFAs had no effect on basal ACTH and cortisol secretion in normal-weight young men. In addition, no alterations in urinary glucocorticoid metabolites were detected, suggesting unchanged cortisol metabolism during lipid infusion.
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PMID:No effect of free fatty acids on adrenocorticotropin and cortisol secretion in healthy young men. 1683 36

We have previously shown that 7B2 null mice on the 129/SvEvTac (129) genetic background die at 5 weeks of age with hypercorticosteronemia due to a Cushing's-like disease unless they are rescued by adrenalectomy; however, 7B2 nulls on the C57BL/6NTac (B6) background remain healthy, with normal steroid levels. Since background exerts such a profound influence on the phenotype of this mutation, we have evaluated whether these two different mouse strains respond differently to high circulating steroids by chronically treating wild-type 129 and B6 mice with the synthetic steroid dexamethasone (Dex). Dex treatment decreased the dopamine content of the neurointermediate lobes (NIL) of 129 mice, leading to NIL enlargement and increased total D(2)R mRNA in the 129, but not the B6, NIL. Despite the decrease in this inhibitory transmitter, Dex-treated 129 mice exhibited reduced circulating alpha-melanocyte-stimulating hormone (alpha-MSH) along with reduced POMC-derived peptides compared with controls, possibly due to reduced POMC content in the NIL. In contrast, Dex-treated B6 mice showed lowered cellular ACTH, unchanged alpha-MSH and beta-endorphin, and increased circulating alpha-MSH, most likely due to increased cleavage of NIL ACTH by increased PC2. Dex-treated 129 mice exhibited hyperinsulinemia and lowered blood glucose, whereas Dex-treated B6 mice showed slightly increased glucose levels despite their considerably increased insulin levels. Taken together, our results suggest that the endocrinological response of 129 mice to chronic Dex treatment is very different from that of B6 mice. These strain-dependent differences in steroid sensitivity must be taken into account when comparing different lines of transgenic or knockout mice.
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PMID:Strain-specific steroidal control of pituitary function. 1733 21


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