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Biomedical subjects

W Jeske

Publications and source records attributed to W Jeske.

At least 91 records · Page 5Linked to original sources
PubMed1991

[Comparative assessment of the biological effects of semisynthetic human insulin and porcine insulin in healthy subjects].

The purpose of the study was the assessment of certain biological effects of semisynthetic human insulin compared with the presently used monocomponent preparations of porcine insulin made by the same producer. The study was carried out in a group of 10 healthy subjects (7 men and 3 women) twice: during a loading test with porcine insulin, and then during a similar test with human insulin. Both insulins were administered intravenously in doses of 0.075 units/kg body weight The physiological reactions associated with hypoglycaemia were noted, including subjective experiences and hormonal responses, among them those of glucagon, growth hormone, prolactin, adrenaline, noradrenaline and C-peptide. Semisynthetic human insulin administered intravenously was found to exert an identical hypoglycaemic effect as porcine insulin. However, it was observed that the action of porcine insulin was associated with more pronounced symptoms and more intense physiological reactions (tachycardia, body temperature fall) and a striking increase of prolactinaemia, in relation to semisynthetic human insulin.

Adult↗
PubMed1990

Enhancement of plasma corticotropin-releasing hormone in pregnancy-induced hypertension.

The role of a high CRH level in normal pregnancy remains unknown. Therefore we evaluated the concentrations of CRH and the related hormones in patients with pregnancy-induced hypertension. Fourteen women with pregnancy-induced hypertension, aged 20-39, at 30-39 gestational week, were investigated. The control group consisted of 20 healthy pregnant women matched according to gestational age. Plasma CRH beta-endorphin-like immunoreactivity, cortisol, and human placental lactogen were measured by radioimmunoassay, ACTH by an immunoradiometric method. It was found that in hypertensive patients the mean CRH concentration was significantly higher (4257 +/- 840 (SEM) ng/l) than that in healthy pregnant women (1083 +/- 227 ng/l, p less than 0.001). The concentration of ACTH, however, was only slightly higher 65.0 +/- 6.0 vs 50.7 +/- 2.5 ng/l p less than 0.025, whereas the differences in beta-endorphin, cortisol and human placental lactogen were not significant. In both groups there was no correlation between the CRH level and those of the related hormones. In healthy pregnant women the CRH level closely correlated with gestational age (r = 0.76, p less than 0.001), whereas in patients with hypertension no such correlation was present (r = 0.29). We assume that the marked enhancement of plasma CRH in pregnancy-induced hypertension is probably caused by its decreased breakdown in ischemic placental tissue, but its increased synthesis in the placenta and its indirect counterregulatory hypotensive role must also be considered.

Adult↗
PubMed1989

Plasma GHRH, CRH, ACTH, beta-endorphin, human placental lactogen, GH and cortisol concentrations at the third trimester of pregnancy.

UNLABELLED: The aim of the study was to determine the concentration of GHRH and CRH in maternal plasma during the 3rd trimester of pregnancy and to search for the possible correlations with related hormones such as ACTH, beta-endorphin, cortisol, GH and human placental lactogen. Patients consisted of 31 healthy pregnant women (20-39 years) divided according to duration of pregnancy into 2 groups: I. from 26 to 32 pregnancy week N = 13), II. from 33 to 39 week (N = 18), and of 7 women evaluated 3 days after delivery. All listed hormones except ACTH were measured by RIA (GHRH, CRH and beta-endorphin-like immunoreactivity after extraction with silic acid) and ACTH by IRMA. In the late 3rd trimester plasma levels of CRH (P less than 0.001), ACTH (P less than 0.02), beta-endorphin (P less than 0.05), cortisol (P less than 0.025), as well as GHRH (P less than 0.002) and human placental lactogen (hPL) (P less than 0.001) were increased in comparison to early 3rd trimester, whereas 3 days after delivery CRH and GHRH became undetectable and those of ACTH and cortisol decreased significantly. The CRH plasma concentrations were found to be strongly correlated with gestational age (r = 0.86, P less than 0.001) but not with ACTH and cortisol. GHRH levels correlated mainly with human placental lactogen concentrations (r = 0.64, P less than 0.001). CONCLUSION: In maternal plasma at the 3rd trimester of pregnancy, apart from the known markedly elevated CRH, the GHRH level was also raised. Strong correlations between CRH and gestational age and those between GHRH and human placental lactogen suggest that there is a relationship between these neurohormones and the placental function.

Adrenocorticotropic Hormone↗
PubMed1989

High blood pressure and hyperinsulinaemia in acromegaly and in obesity.

As previously shown, in essential hypertension postprandial plasma insulin concentrations are elevated. In order to determine a relationship of high blood pressure and plasma insulin levels in acromegaly and in obesity 59 subjects with normal glucose tolerance were studied. They were divided into three groups: (I) patients with acromegaly: 7 normotensives and 8 hypertensives, (II) 12 obese normotensives and 12 obese hypertensives and (III) 10 non-obese hypertensives, and 10 healthy subjects. Blood glucose and plasma insulin concentrations were measured in a fasting state and after an oral glucose load of 75 g. The fasting insulin concentrations in all the acromegalics and in all the obese patients were higher than those in healthy subjects. The insulin response to the glucose load was significantly enhanced in all the three groups of hypertensive patients compared with those of matched normotensive controls. The results indicate that insulin may play a role in the regulation of blood pressure in essential hypertension, and in such hyperinsulinaemic disorders as acromegaly and obesity.

Acromegaly↗
PubMed1989

[Reference values for progesterone, beta-HCG, estriol and human placental lactogen in the 10th-16th weeks of pregnancy].

Progesterone, beta-hCG, estriol and hPL in sera from 745 pregnant women have been measured in weeks 10 to 16 of pregnancy. The determined reference intervalls included the 10th and 90th percentile. All confidence intervalls have been calculated for a probability level of 10 per cent. The following levels were determined during the concerning weeks of pregnancy: progesterone 32-165 nmol/l, beta-hCG 31.5-260 micrograms/l, estriol 0.04-4.94 nmol l, and hPL 0.03-2.65 mg/l. The levels of progesterone are increasing weakly with the rising weeks of pregnancy, but the levels of beta-hCG are going down continuously. The levels estriol and hPL are showing a marked growth.

Chorionic Gonadotropin↗
PubMed1989

The effect of magnesium valproate on plasma ACTH concentrations in Nelson's syndrome.

Sodium valproate, a gamma-aminobutyric acid (GABA) agonist, was found to decrease plasma ACTH concentration in some cases of Cushing's disease and Nelson's syndrome. In this study we have investigated the influence of magnesium valproate (MV), a newly introduced salt of valproic acid, on plasma ACTH levels in 8 patients with Nelson's syndrome. The daily dose, 1200 mg of MV, significantly decreased plasma ACTH level at 10 p.m. compared with placebo. A single dose of 400 mg of MV, led to a reduction in plasma ACTH concentration only in two out of seven patients during a four-hour observation. The fall in plasma ACTH level in the same patients at 10 p.m., after the next two doses of this drug, suggests that single dose may be insufficient for introducing GABA-dependent reduction in ACTH release. During a long-term therapy with MV, in all three patients investigated a marked decrease in plasma ACTH was observed. Our results suggest that magnesium valproate may be useful during chronic therapy in some patients with ACTH hypersecretion.

Adrenocorticotropic Hormone↗
PubMed1988

Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity.

The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.

Adrenocorticotropic Hormone↗
PubMed1988

Exaggerated growth hormone response to growth hormone-releasing hormone in type I diabetes mellitus.

Excessive GH response to various stimuli has been frequently described in diabetes mellitus. We studied the GH response to a synthetic GHRH in a group of 16 non-obese Type I diabetic patients. GHRH (1-44) given as iv bolus at a dose of 50 micrograms induced a markedly greater GH response in the diabetic than in the normal subjects with peak values of 39.5 and 14.7 micrograms/l, respectively, and the differences were significant from 15 to 60 min. Peak GH level was 44.6 micrograms/l in diabetic patients without retinopathy and 34.2 micrograms/l in patients with retinopathy, but the difference was not significant. Peak GH levels did not correlate with metabolic control of disease estimated by basal glucose and HbA1 levels nor with age, weight of the patients, and duration of the disease. It is concluded that Type I diabetic patients show an exaggerated GH response to GHRH and this response does not correlate with the metabolic control of diabetes.

Adult↗
PubMed1988

The possible role of beta-endorphin in pathogenesis of obesity and essential hypertension.

In order to evaluate the role of beta-endorphin in the pathogenesis of obesity and essential hypertension 44 subjects were investigated: 12 nonobese hypertensives, 11 obese hypertensives, 11 obese normotensives and 10 normal subjects. Plasma concentrations of beta-endorphin and cortisol were measured by radioimmunological and ACTH by immunoradiometric methods. The plasma concentrations and the circadian rhythms of ACTH and cortisol secretion were normal in all groups investigated. A circadian rhythm of beta-endorphin secretion was demonstrated in nonobese hypertensives and in normal subjects. The plasma concentrations of beta-endorphin were twice higher than those in nonobese subjects. Also, in all obese patients the circadian rhythm of beta-endorphin secretion was blunted. The increased concentrations and the altered circadian rhythm of beta-endorphin in all obese subjects may point to a role of beta-endorphin in the pathogenesis of obesity rather than in that of essential hypertension.

Adrenocorticotropic Hormone↗
PubMed1988

Growth hormone (GH) secretion during nocturnal sleep and after clonidine in patients with essential hypertension.

In order to estimate the neuroendocrine function of the central nervous system eventually leading to growth hormone (GH) secretion in essential hypertension, 17 patients with mild arterial hypertension (7 obese and 10 with normal body weight) were examined. The control group consisted of 16 normotensive volunteers (7 obese and 9 with normal body weight). The GH secretion was determined by radioimmunoassay during nocturnal sleep. In all the subjects, the serum GH was also measured after placebo and after the centrally acting alpha 2-adrenergic agonist-clonidine administered i.v. in a dose of 0.15 mg. The fasting serum insulin concentration was also measured in all the subjects. Clonidine decreased the mean arterial pressure in all the subjects investigated. However, in response to clonidine an increase in GH secretion in all hypertensive and normotensive cases with normal body weight was demonstrated, whereas in all obese hypertensive and normotensive patients no significant GH rise was found. It indicates that inhibition of GH secretion in patients with essential hypertension is related to coexistent obesity rather than with that of arterial hypertension. A strong (r = 0.76) and significant (p less than 0.0005) correlation demonstrated between the maximal GH concentration during the nocturnal sleep and after clonidine suggests that the mechanism of GH inhibition in response to both these stimuli is similar and it probably is related to the inhibition of neurohormonal secretion of the growth hormone releasing factor (GRF). However, the negative correlation between the fasting insulin concentration and GH response to clonidine shown in obese subjects only, points to a more complex mechanism of GH inhibition in obesity.

Adolescent↗