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 concentration of corticotropin and cortisol in the blood was determined 120 patients with Itsenko-Cushing radioimmunologically after insulin hypoglycemia, after administration of insulin and thyroliberin. It was established that healthy persons and patients with Itsenko-Cushing disease showed no differences in the effect of insulin and thyroliberin as compared with insulin hypoglycemia on the state of the pituitary-adrenal system.
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PMID:[Changes in the secretion of the hormones of the hypothalamo-hypophyseo-adrenal system in Itsenko-Cushing disease under the influence of insulin-induced hypoglycemia and thyroliberin]. 216 80

We evaluated six patients in whom a diagnosis of Sheehan's syndrome had been made. The plasma levels of the following hormones were measured: basal thyroxine (T4), estradiol and cortisol; and also follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and adrenocorticotropic hormone (ACTH), basally and after acute challenge with LH releasing hormone (LHRH), GRF (1-29)NH2 or insulin hypoglycemia, TSH releasing hormone (TRH) and lysine-8-vasopressin, respectively. Two patients underwent chronic LHRH stimulation by pulsatile subcutaneous administration with infusion pump. In 4 cases, computed tomography (CT) was performed although cranial X-ray study was normal. A severe and generalized pituitary involvement was found in all patients, 3 of whom had diabetes mellitus. Probably, more insidious cases go unnoticed. The presence of asymptomatic partial empty sella (ES) in all the CTs that were carried out raises the possibility that it is another evolutive feature of SS.
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PMID:[Relations between Sheehan's syndrome and empty sella turcica. A functional study apropos of 6 cases]. 217 69

A 34-year man was admitted to the hospital with symptoms of hypoglycemia. The endocrine investigations indicated adrenocortical insufficiency secondary to isolated ACTH deficiency: low ACTH and cortisol plasma levels, significant increase of cortisol following prolonged stimulation with depot tetracosactrin, normal secretory reserve of other anterior pituitary hormones. The absence of ACTH-response after corticotropin releasing hormone and insulin tolerance tests suggested a primary impairment of corticotropin cells.
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PMID:[Isolated ACTH deficiency: description of a clinical case]. 217 82

The specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29

Recently, our laboratory has reported that central administration of beta-endorphin to rat pups decreases hepatic and renal ornithine decarboxylase activity, a sensitive biochemical index of tissue metabolic activity. Since these organs are the major sites of insulin catabolism, it seemed possible that the plasma levels of this hormone could be altered by changes in central nervous system (CNS) beta-endorphin levels. In the current study we tested this hypothesis by administering beta-endorphin to rat pups intracisternally (ic), followed by insulin sc, and then analyzing for plasma levels of insulin and glucose at various times after the second injection. We found that the apparent biological half-life of administered insulin markedly increased in 6-day-old rats pretreated with beta-endorphin ic. Similarly, this neuropeptide prolonged the half-life of endogenous insulin, as indicated by a small but significant increase in the plasma levels of this hormone in animals given only beta-endorphin. As expected, hypoglycemia in rats injected with beta-endorphin and insulin was more pronounced than in animals given insulin alone. Naloxone administered ic reversed both actions of beta-endorphin, indicating the involvement of opioid receptors in the response. beta-Endorphin also altered insulin and glucose plasma levels in 2-, 10-, and 18-day-old rats, but there were no effects in 30-day-old animals at any of the doses used in these studies. Peripheral administration of beta-endorphin had no effect, indicating that CNS beta-endorphin's influences on insulin and glucose metabolism occur through brain-based mechanisms. The results from these studies suggest that CNS beta-endorphin may be an important modulator of insulin and glucose metabolism in preweanling rats. In as much as insulin is a major regulator of somatic growth, our findings further suggest that CNS beta-endorphin may have a major role in the control of growth during early postnatal development by influencing insulin homeostasis.
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PMID:Regulation of insulin and glucose plasma levels by central nervous system beta-endorphin in preweanling rats. 252 2

The opioid polypeptide beta-endorphin is present in fetal blood but it is not clear whether its source is the fetus or the placenta. We therefore measured beta-endorphin in extracts of fetal femoral arterial and umbilical venous blood plasma in sheep by radioimmunoassay to determine whether the fetus or the placenta is the major source of beta-endorphin in the fetal circulation. Chromatographic analysis of extracts of fetal arterial plasma showed that beta-lipotropin and other precursors of beta-endorphin made only a minor contribution to the immunoreactivity detected. Concentrations of immunoreactive beta-endorphin were higher in the femoral artery than in the umbilical vein in fetal sheep between 113 and 128 days of pregnancy. Therefore the placenta removes beta-endorphin or a closely related polypeptide of fetal origin from the umbilical circulation in sheep at this stage of gestation. Acute hypoxaemia and hypoglycaemia increase the concentrations of immunoassayable beta-endorphin in blood plasma of adult and fetal sheep, but little is known about the effects of chronic hypoxaemia or hypoglycaemia on the circulating levels of beta-endorphin and related polypeptides in the fetus. Therefore we also measured immunoreactive beta-endorphin in blood plasma from fetal sheep in which growth retardation in association with restricted placental growth was produced by removal of endometrial caruncles before mating. Intra-uterine growth retardation was accompanied by chronic hypoglycaemia and chronic hypoxaemia in the fetuses. This was not associated with higher concentrations of beta-endorphin-like immunoreactivity in fetal arterial or umbilical venous plasma, but was accompanied by significantly increased placental extraction of fetal immunoreactive beta-endorphin from the umbilical circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restriction of placental growth in sheep enhances placental metabolism of fetal beta-endorphin-like immunoreactivity. 252 77

The present study was designed to examine the role played by beta-endorphin in the physiological response to the stress of insulin-induced hypoglycemia. Three groups (n = 5, each) of conscious overnight-fasted dogs, chronically fitted with catheters in the femoral artery and in the third ventricle were used for these studies. Each experiment consisted of an 80-min equilibration period (0-80 min), a 40-min basal period (80-120 min), and a 180-min (120-300 min) experimental period. One group received a 220-min intracerebroventricular (icv) infusion of naloxone (0.2 mg/h) beginning at t = 80 min. The second group received a 3-h intravenous infusion of insulin at 5.0 mU.kg-1.min-1 beginning at t = 120 min. The third group received naloxone at t = 80 min and insulin beginning at t = 120 min, and both were continued throughout the experimental period. The studies show that insulin-induced hypoglycemia was associated with a rise in plasma cortisol, beta-endorphin, epinephrine, norepinephrine, and glucagon. Pretreatment with naloxone diminished the rises in plasma beta-endorphin, epinephrine, and norepinephrine without affecting the responses of plasma glucagon and cortisol. Although the levels of hypoglycemia achieved in the two groups were identical, glucose rates of appearance into and disappearance from the plasma compartment were higher in the group pretreated with icv naloxone (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of naloxone on glucose homeostasis during insulin-induced hypoglycemia. 252 11

Adrenarche, which occurs earlier than gonadarche in normal children, is marked by increases in plasma dehydroepiandrosterone and its sulfate (DHAS). Adrenarche and gonadarche can be dissociated in various situations, e.g. central precocious puberty, indicating that they are controlled by independent mechanisms. This report concerns 2 children with central precocious puberty secondary to hypothalamic hamartoma. Their plasma basal DHAS values, compared to other cases with central precocious puberty not secondary to hamartoma, remained low for chronological age and bone age over a follow-up of 6.3 (case 1) and 9.2 9.2 years (case 2): in case 1 (boy), DHAS was 9 micrograms/dl at chronological age 7.7 and bone age 13 years; in case 2 (girl), DHAS was 11 micrograms/dl for chronological age 10.5 and bone age 13.5 years. GH secretion was normal. Basal plasma cortisol levels as the levels during hypoglycemia and after corticotropin stimulation were all normal. These data suggest that hypothalamic hamartoma may affect the central control of adrenarche. They may also contribute to the diagnosis of hypothalamic hamartoma.
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PMID:Lack of adrenarche in two children with precocious puberty secondary to hypothalamic hamartoma. 253 41

In a 49-year-old woman with empty sella syndrome, corticotropin (ACTH) deficiency and various abnormalities, including increased thyrotropin (TSH) secretion, growth hormone (GH) deficiency, and inappropriately high insulin with early phase hypoglycemia, during an oral glucose tolerance test were found. Existence of serum antipituitary antibody suggested that the empty sella and ACTH deficiency may be caused by an autoimmune destruction of the pituitary gland. All of the accompanying abnormalities except for increased TSH secretion were corrected with glucocorticoid supplement. Thyroidal responses to an increase and decrease of endogenous TSH were qualitatively normal, indicating that the patient's TSH was biologically active and the set point of hypothalamic-pituitary feedback regulation for TSH secretion was shifted.
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PMID:ACTH deficiency and TSH hypersecretion in a patient with empty sella turcica. 253 55

The human corticotropin-releasing hormone (hCRH) tests were performed in twelve normal short children, and the responses of plasma ACTH and cortisol to iv administration of 1 micrograms/kg hCRH were compared with those to insulin-induced hypoglycemia. After administration of hCRH, the mean plasma ACTH level rose from a basal value of 3.3 +/- 0.4 pmol/l (mean +/- SEM) to a peak value of 9.2 +/- 0.8 pmol/l at 30 min, and the mean plasma cortisol level rose from a basal value of 231 +/- 25 nmol/l to a peak value of 546 +/- 30 nmol/l at 30 min. The ACTH response after insulin-induced hypoglycemia was greater than that after hCRH administration; the mean peak level (P less than 0.01), the percent maximum increment (P less than 0.01), and the area under the ACTH response curve (P less than 0.01) were all significantly greater after insulin-induced hypoglycemia than those after hCRH administration. Although the mean peak cortisol level after insulin-induced hypoglycemia was about 1.3-fold higher than that after hCRH administration (P less than 0.01), neither the percent maximum increment in plasma cortisol nor the area under the cortisol response curve after insulin-induced hypoglycemia was significantly different from that after hCRH administration. Consequently, the acute increases in plasma ACTH after the administration of 1 microgram/kg hCRH stimulated the adrenal gland to almost the same cortisol response as that obtained with a much greater increase in plasma ACTH after insulin-induced hypoglycemia. These results suggest that a plasma ACTH peak of 9-11 pmol/l produces near maximum acute stimulation of adrenal steroidogenesis.
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PMID:The corticotropin-releasing hormone test in normal short children: comparison of plasma adrenocorticotropin and cortisol responses to human corticotropin-releasing hormone and insulin-induced hypoglycemia. 253 90


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