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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. The subjects were divided according to their body weight into lean (body mass index, less than 25) and obese (body mass index, greater than 29.5) groups. In lean subjects, infusion of 0.5 mg/h beta-endorphin caused significant increases in peripheral plasma glucose and glucagon levels, but no change in plasma insulin. In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. These hormonal responses to beta-endorphin were amplified in the obese diabetic patients. There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. These results indicate that beta-endorphin may have important glucoregulatory effects in man depending on the dose administered, the presence of obesity, and the prevailing plasma glucose concentration.
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PMID:Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. 295 63

This study evaluated the effect of human beta-endorphin on pancreatic hormone levels and their responses to nutrient challenges in normal subjects. Infusion of 0.5 mg/h beta-endorphin caused a significant rise in plasma glucose concentrations preceded by a significant increase in peripheral glucagon levels. No changes occurred in the plasma concentrations of insulin and C-peptide. Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. To verify whether the modification of prestimulus glucose level could be important in these hormonal responses to beta-endorphin, basal plasma glucose concentrations were raised by a primed (0.5 g/kg) continuous (20 mg kg-1.min-1) glucose infusion. After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1988 Sep
PMID:Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. 297 Apr 11

Cold stress produced a significant reduction in the concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary of diabetic female rats. IR-BE levels in the anterior pituitary of non-diabetic female rats were not affected by exposure to the cold. The effects of cold stress on IR-BE levels in the neurointermediate lobe of the pituitary and the hypothalamus were attenuated in diabetic as compared to control animals. These data suggest that in female rats, eight weeks of diabetes produced alterations in the neuroendocrine mechanisms which modulate IR-BE levels in the pituitary and hypothalamus in response to cold stress.
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PMID:Eight weeks of streptozotocin-induced diabetes influences the effects of cold stress on immunoreactive beta-endorphin levels in female rats. 297 9

offlated hypoaldosteronism with or without hyperkalemia in patients with diabetes mellitus has been shown to exist occasionally without hyporeninemia. To assess in detail the adrenal function in this disorder, the responses of plasma aldosterone (PA) and its precursor steroids to angiotensin II (AII) infusion and adrenocorticotropic hormone (ACTH) injection were studied in seven patients with asymptomatic normoreninemic hypoaldosteronism (ANH) and 11 age-matched normal subjects. The ANH diabetic patients had, by definition, a low PA level after furosemide (80 mg orally) plus upright posture (4 hours) stimulation, low PA and high plasma renin activity (PRA) increases after the stimulation (a low delta PA/delta PRA ratio), and normokalemia. Plasma inactive renin and the inactive renin/total renin ration were similar in the ANH diabetic patients and in the normal subjects. Under the pre-AII condition, plasma DOC and corticosterone levels tended to be low, and the plasma 18-OHB and PA levels were low in the ANH diabetic patients compared with the normal subjects. The ratio of plasma 18-OHB to PA was similar in the two groups. All infusion produced no increases in plasma 18-OHB and PA in the ANH diabetic patients, whereas the infusion caused dose-dependent increases in these steroids in the normal subjects. Plasma DOC and corticosterone levels remained unchanged during AII infusion in the two groups. ACTH injection produced appropriate PA increases relative to the basal PA in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unresponsiveness of plasma mineralocorticoids to angiotensin II in diabetic patients with asymptomatic normoreninemic hypoaldosteronism. 298 80

Isolated adrenocorticotropic hormone (ACTH) deficiency was documented after cesarean delivery in a patient with type I diabetes. A preceding severe headache, subsequent declining insulin requirements, and hypotension are consistent with pituitary infarction in a patient without computed tomography evidence of a pituitary tumor. Antepartum incomplete pituitary infarction with isolated ACTH deficiency is an unusual but potentially catastrophic complication of the pregnant diabetic.
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PMID:Isolated adrenocorticotropic hormone deficiency with antepartum pituitary infarction in a type I diabetic. 298 76

Lower concentrations of immunoreactive (IR) beta-endorphin were present in the neurointermediate pituitary lobes of streptozocin-induced diabetic versus control animals at both 2 and 4 weeks after the onset of diabetes. The forms of beta-endorphin-like material present appeared to be similar in both groups when studied with cation-exchange chromatography. Insulin therapy via minipump for 2 weeks did not alter this finding of lowered beta-endorphin concentrations in diabetic animals, despite normalization of blood glucose levels and body weight gain. Lower IR beta-endorphin levels were also found in neurointermediate lobes of weight-restricted rats, but this group had increased plasma IR beta-endorphin concentrations compared to diabetic animals. Concentrations of IR beta-endorphin in microdissected brain regions and in anterior pituitaries of the diabetic animals failed to show consistent changes; in addition, ACTH concentrations in pituitary lobes and plasma did not differ among groups. Circadian rhythmicity of plasma insulin and corticosterone concentrations was absent in the diabetic animals, although food and water intake, while elevated, showed the normal nocturnal pattern of increased ingestion. Furthermore, adrenal hypertrophy was present in the diabetic animals and was accompanied by an elevation of mean plasma corticosterone levels. The present findings indicate that diabetes is associated with a decrease of neurointermediate pituitary lobe synthesis of beta-endorphin, while not affecting the processing of the peptide in this lobe, and confirm previous reports of altered adrenal function in diabetic animals.
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PMID:Streptozotocin-induced diabetes is associated with reduced immunoreactive beta-endorphin concentrations in neurointermediate pituitary lobe and with disrupted circadian periodicity of plasma corticosterone levels. 299 96

A sensitive assay method for pituitary cell antibodies (PitCA) was established by a biotin/avidin system using rat pituitary. Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. PitCA observed in the sera of insulin-dependent diabetic patients were suspected of being pituitary specific and independent with islet cell antibodies (ICA) and islet cell surface antibodies (ICSA). In the sera of ACTH deficient patients, PitCA were frequently absorbed with liver acetone powder. Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. A total of 16 cases out of 21 ACTH deficient patients were female. These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency.
Diabetes Res 1986 Mar
PMID:Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 301 44

The sand-rat (Psammomys obesus) is an animal model for the study of human maturity onset diabetes which appears to be controlled by caloric intake. In the present investigations, these animals have been studied in relation to the influence of low- and high-energy diets on body weight, plasma insulin and blood glucose levels, and on insulin secretion from the perfused pancreas and the secretion of corticotropin-like intermediate lobe peptide (CLIP, ACTH18-39) and the insulin secretagogue beta-cell-tropin (beta-CT, ACTH22-39) from the pituitary neurointermediate lobe. The sand-rats maintained on the high-energy diet all became obese. Insulin secretion from the perfused pancreas of the obese sand-rat in the presence of 5.6 mM glucose was significantly higher than in the lean controls maintained on low-energy diets. Increasing the glucose concentration to 16.7 mM only produced a small stimulation of insulin secretion in the obese animals, and the difference between the two groups was not significant. Stimulation of insulin secretion by beta-CT was variable, but the obese animals appeared to be more responsive. Pituitary neurointermediate lobes were incubated for 4 h to measure the secretion of the ACTH related peptide. These were separated by gel filtration and the concentrations measured by radioimmunoassay with a CLIP antiserum and a CLIP standard. In all experiments beta-CT was 4-6 per cent of the total CLIP immunoreactive material. In these experiments the obese animals maintained on a high-energy diet were divided into two groups, those with plasma insulin levels less than 500 mu u/ml and those with insulin levels greater than 500 mu u/ml. The latter group had a significantly higher blood glucose level, presumably due to the insulin resistance resulting from the severe hyperinsulinaemia. It was also observed that CLIP-IRM and beta-CT secretion was lower in this group than in the animals maintained on low-energy diets or those on high-energy diets with moderate hyperinsulinaemia. This suggests a possible feedback inhibition by insulin on the secretion of beta-CT.
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PMID:Studies on insulin secretion and the pituitary insulin secretagogue beta-cell-tropin in the sand-rat (Psammomys obesus). 303 19

Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. Out of 18 insulin dependent diabetic patients who were positive for antibodies to islet cell surface membrane (ICSA), 3 cases (16.7%) were positive for antibodies to GH3 cells and 12 cases (66.7%) were positive for antibodies to AtT-20 cells. Moreover, out of 18 insulin dependent diabetic patients who were negative for ICSA, 2 (11.1%) and 6 cases (33.3%) were positive for antibodies to GH3 cells and AtT-20 cells, respectively. Among 5 adrenocorticotropic hormone (ACTH) deficient patients, all of the sera were positive for antibodies to AtT-20 cells. These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency.
Diabetes Res 1987 Feb
PMID:Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 303 74

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25


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