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 goal pursued has been to analyze clinical observations and hormonal studies of patients with empty sella turcica (EST), in order to review this disorder and determine if it can be considered a real syndrome. Fifteen patients with EST (3 men and 12 women) and mean age of 45.6 +/- 17.9 years have been prospectively studied. In the hypothalamus-hypophysis study, reserves of thyrotropin (TSH), prolactin (PRL), gonadotropins (FSH and LH), growth hormone (GH), adrenocorticotropin (ACTH) and cortisol were assessed. In addition, thyroid hormones and, for men, testosterone, were determined. The pathogenic mechanism was explained in two cases (13.3%). We registered headache in 10 patients, obesity in 8, arterial hypertension in 2 and diabetes mellitus in 2. Multiparity antecedent was found in 2 cases. The hormonal study was abnormal in two cases (40%). Most common abnormalities were hyperprolactinemia (3 cases), deficit of gonadotropins (3 cases), without coexisting both of them in any case, and deficit of GH (2 cases). EST is frequently associated with endocrine disfunction, although clinical implications are rare. The absence of common clinical manifestations in most cases questions the EST as a real syndrome.
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PMID:[Primary empty sella turcica: clinical aspects and hormonal study of 15 cases]. 179 Feb 77

Neuroendocrine responses to psychosocial pressures have been well characterized. The defence reaction is followed by increased activity of the sympathetic nervous system. Essential hypertension might be induced by such mechanisms. The defeat reaction is characterized by increased activity along the corticotropin releasing factor-adrenocorticotropin hormone-cortisol axis, resulting in the inhibition of gonadotropin secretion. Such endocrine disturbances are followed by metabolic aberrations, and probably also by the accumulation of visceral fat. Subjects with abdominal fat accumulation (high waist/hip circumference ratio, WHR) have recently been found to exhibit a number of psychosocial handicaps, together with endocrine aberrations characteristic of the defence and, in particular, the defeat reaction, as well as the associated circulatory and metabolic aberrations. Such abnormalities, including the WHR itself, are established risk factors for cardiovascular disease and diabetes. It is postulated that increased WHR is a symptom of chronic hypothalamic arousal as a result of a defeat reaction to psychosocial pressures. This might lead to the development of disease via circulatory and metabolic derangements.
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PMID:Visceral fat accumulation: the missing link between psychosocial factors and cardiovascular disease? 189 41

This review summarizes the recent findings on the effects of endocrine manipulation on the hypothalamic and pituitary contents of met-enkephalin and beta-endorphin. In the pituitary, gonadectomy decreases beta-endorphin content in both the anterior lobe and neuro-intermediate lobe. Orchidectomy results in a decrease while ovariectomy leads to an increase in anterior lobe met-enkephalin contents. Adrenalectomy only lead to an increase in beta-endorphin contents in the anterior pituitary lobe. Hypothyroidism induced by propylthiouracil treatment is accompanied by a decrease of beta-endorphin in the neuro-intermediate lobe and a decrease in met-enkephalin in the anterior lobe while thyroidectomy entails a decrease in met-enkephalin in the anterior lobe only. Chemically induced diabetes mellitus results in a decrease in beta-endorphin content in the hypothalamus and the neuro-intermediate lobe, and a reduction in met-enkephalin level in the anterior and neuro-intermediate lobes. All these changes are reversible with appropriate hormone treatments. These results indicate the importance of hormones in the regulation of the synthesis and/or release of the opioid peptides in the hypothalamus and the pituitary.
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PMID:Endocrine control of hypothalamic and pituitary met-enkephalin and beta-endorphin contents. 190 93

We compared insulin-requiring diabetic outpatients (n = 49) with normal controls (n = 42) for indices of hypothalamic-pituitary-adrenal (HPA) axis activity. Diabetic patients showed significantly elevated 9 a.m. plasma levels of cortisol as well as significantly elevated plasma levels of cortisol and adrenocorticotropic hormone (ACTH) at both 4 p.m. before and 4 p.m. after dexamethasone. Also, there was a significant correlation between postdexamethasone plasma levels of ACTH and duration of diabetes. These results suggest that HPA-axis dysregulation is found among diabetic outpatients. The possible psychiatric implications are discussed.
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PMID:Hypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients. 215 75

The aim of this study was to investigate the pathogenesis of hypoaldosteronism in diabetes. Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. Observations were made over 12 yr on the evolution and treatment of hyperkalemia in a diabetic subject. In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. Nine yr later, persistent hyperkalemia was documented. Upright renin activity was elevated to 5.26 ng.L-1.s-1, with concomitant elevation of 18-hydroxycorticosterone (18-OHB) and a low-normal aldosterone level. One hour after administration of 0.25 mg i.m. cosyntropin, cortisol increased normally, aldosterone increased from 220 to 360 pM, and 18-OHB increased from 3700 to 4800 pM. During treatment with fludrocortisone, fludrocortisone with furosemide, and furosemide alone, improvement of hyperkalemia was noted. Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. Evolution of hyperkalemia between 1977 and 1986 suggests this defect was acquired.
Diabetes Care 1990 Jul
PMID:Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism. 216 93

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

In this study aiming to clarify the relationships between beta-endorphin and glucose levels, beta-endorphin levels were determined in children in acute stress. The study was carried out on 32 critically ill children between 5 days and 12 years presenting with clinical symptoms of acute infectious conditions. 11 healthy children were taken as controls. The results showed that although beta-endorphin levels were elevated in all critically ill patients, these levels were significantly higher than control values in hyperglycaemic cases. The insulin levels were also elevated. A follow-up of nine of the hyperglycaemic cases showed a significant decline in beta-endorphin and insulin levels with recovery. Glucose tolerance was also normal. These results confirm the reports of many other studies on the role of beta-endorphin as a stress hormone.
Diabetes Res Clin Pract 1990 Jul
PMID:Beta-endorphin levels of children in acute stress. 222 24

The nature of the genetic defects which define the obese (ob) and diabetes (db) loci in mice remain unknown, but both produce similar syndromes when maintained in the same strain of mice. There is some evidence suggesting a lesion in the central nervous system (CNS) in db/db mice, while ob/ob mice appear to have a primary lesion outside the CNS. In a search for further evidence of a unique central lesion in db/db mice, we have examined neuropeptide content in selected, microdissected brain areas in both of these mutants and lean controls. In order to rule out possible interactions of the db mutation with the genetic background, diabetes mice of both C57BL/KsJ and C57BL/6J strains were studied. When concentrations of nine neuropeptide immunoreactivities were examined in up to seven microdissected areas of the brain, C57BL/6J ob/ob mice showed only one reproducible alteration, a lower content of beta-endorphin-like immunoreactivity (LI) in the preoptic area at both 3 and 6 weeks of age as compared with lean littermates. In contrast, db/db mice of both C57BL/6J and C57BL/KsJ strains exhibited alterations in a total of four peptides in three brain areas: lower concentration of somatostatin-LI in median eminence, higher Met-enkephalin-LI in dorsal vagal complex of the medulla oblongata, higher substance P-LI and lower vasoactive intestinal polypeptide (VIP)-LI in amygdala. The concentrations of the peptides studied in medial basal hypothalamus, lateral hypothalamus, substantia nigra, and preoptic area were not reproducibly altered in db/db mice. These data provide preliminary evidence for unique brain abnormalities in db/db mice in specific areas that are involved in processing of neural signals that can affect the islets of Langerhans, gonadotrophin secretory patterns, and many other visceral functions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unique alterations of neuropeptide content in median eminence, amygdala, and dorsal vagal complex of 3- and 6-week-old diabetes mutant mice. 223 77

The monoaminergic innervation of the central nervous system (CNS) is characterized by long and short projecting neurons. The neurological correlates of diabetes are usually referred to as processes of degenerative atrophy affecting motor and sensory peripheral nerves. We have found that the long serotoninergic axons innervating the spinal cord and the cerebral cortex are unaffected in diabetic animals and that the noradrenergic innervation of the cortex is normal as well. The serotonin content is doubled in the hypothalamus with no apparent alteration of 5-HIAA levels, suggesting a supernumerary innervation that is accompanied by a reduced release. In pons medulla oblongata, serotonin and dopamine with the relative metabolites 5-HIAA and DOPAC are significantly reduced, whereas noradrenaline is markedly increased. In the hippocampus, there is a reduction of serotonin content. The serotoninergic alterations are peculiar as suggested by the sparing of the most distal projections that is accompanied by hyperinnervation of the hypothalamus and the loss of shorter collaterals in the pons medulla oblongata. In the hypothalamus and in the striatum of diabetic rats, there are significant higher levels of substance P and met-enkephalin, respectively. The abundance of proenkephalin A mRNA is also increased in the striatum. Conversely, in the lumbar cord of diabetic animals, the levels of substance P and met-enkephalin are significantly reduced. Such alterations likely reflect retrograde degeneration of the peripheral sensory input. The CNS changes are unlikely due to vascular abnormalities in the brain of diabetic rats; rather, we suggest that the persistent lack of insulin is the major factor involved as a trigger of the monoaminergic changes in the diabetic brain.
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PMID:Denervation and hyperinnervation in the nervous system of diabetic animals. II. Monoaminergic and peptidergic alterations in the diabetic encephalopathy. 248 Apr 54

The endocrine, paracrine, and neurocrine influences of the non-glucose insulin secretion regulators on the pancreatic islets are analysed. Experiments on rats using the primary monolayer culture of isolated islet cells proved that insulin secretion is directly modulated by the growth hormone (GH), C-terminal tetrapeptide of cholecystokinin, thyroliberin, and met-enkephalin, and by certain blood plasma factors of diabetes I patients. In addition, GH is showed to stimulate the islet cell proliferation by intensifying 3H-thymidine incorporation into DNA synthesis. The blood plasma factors of IdDM patients influence the islets of Langerhans activity by either stimulating or depressing the secretory function of insulin producing cells. The aspects of functional organization of the islet cells and complex regulation of insulin secretion are discussed.
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PMID:[Mechanisms of the regulation of insulin secretion]. 250 84


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