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Biomedical subjects

E Jungmann

Publications and source records attributed to E Jungmann.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Somatomedin C level and stimulation of growth hormone and adrenal cortex function by administration of releasing hormones and physical exertion in patients with obesity].

In a clinical study on potential determinants underlying the impairment of growth hormone stimulation in obese human subjects, we examined in 20 otherwise healthy adult obese subjects (14 females, six males, age 18 to 40 years, body mass index greater than 29 kg/m2) the responses of growth hormone (hGH), adrenocorticotropic hormone (ACTH) and cortisol to releasing hormone stimulation (growth hormone-releasing hormone and corticotropin-releasing hormone) and the responses of hGH, ACTH, cortisol and free fatty acids (FFA) to physical exercise. Subjects with somatomedin-C levels less than or equal to 0.7 U/ml (group 1) were more obese than subjects with somatomedin-C levels greater than 0.7 U/ml (group 2) (p less than 0.01). In group 1, hGH increased by 4.3 +/- 1.2 ng/ml in response to releasing hormone administration and by 0.9 +/- 0.3 ng/ml in response to physical exercise (normal responses, increase by greater than 7 ng/ml), in group 2, hGH increased by 6.7 +/- 1.4, and 2.4 +/- 0.8 ng/ml, respectively (p less than 0.05 vs. group 1). Moreover, FFA stimulation by physical exercise was blunted in group 1 (p less than 0.05 vs. group 2). In contrast, ACTH stimulation was found increased in group 1 in comparison to group 2, particularly in response to physical exercise (p less than 0.01), and resulted in enhanced cortisol stimulation (p less than 0.05). Thus, impaired hGH stimulation in obese human subjects is not explained by an altered relationship between hGH and somatomedin-C levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[The influence of autonomic diabetic neuropathy and human atrial natriuretic peptide on adrenal gland function in postural changes].

To investigate the influence of postural changes on plasma renin activity (PRA), plasma levels of human atrial natriuretic peptide (hANP) and on aldosterone in diabetes mellitus and autonomic neuropathy, ten patients with diabetes mellitus and autonomic neuropathy and ten patients with diabetes mellitus but without autonomic neuropathy were studied. Ten healthy subjects served as controls. Patients and controls were in supine position for 60 minutes, then changed posture sequentially to sitting (90 minutes) and to upright position (15 minutes). In controls, PRA was increased upon sitting and in the upright position, while hANP was decreased. Patients with autonomic neuropathy differed from controls in impaired renin stimulation, whereas in patients without autonomic neuropathy PRA responses to postural changes were only slightly decreased. In both groups of patients, the normal hANP responsiveness to postural changes was lacking. There were no differences in aldosterone levels between patients and controls. In patients with high basal hANP levels due to elevated systolic blood pressure renin responses to postural changes were decreased in comparison to those patients with low basal hANP levels. Thus, in patients with diabetes mellitus increased hANP levels which are not decreased in response to upright standing may contribute to the development of hyporeninism and its sequelae.

Adult↗
PubMed1991

[Long-term antihypertensive treatment in diabetes mellitus. Results with the calcium antagonist felodipine].

In 17 hypertensive, insulin-treated diabetics (eight type 1 diabetics, nine type 2 diabetics) the effectiveness of 10 mg/day felodipine was investigated over a period of one year. In both groups, felodipine brought about a lasting decrease in blood pressure (p less than 0.05). After four weeks' treatment, type 1 diabetics experienced a 143% increase in albumin excretion, and an 83% increase in fractional albuminuria, as compared with the initial values (p less than 0.05). In type 2 diabetics, in contrast, albumin excretion decreased by 25%, fractional albuminuria by 48% (p less than 0.05; p less than 0.01, as compared with type 1 diabetics). After 28 weeks of treatment, the fractionale albuminuria in the two groups had decreased by 27% (p less than 0.05 compared with the short-term response) and 37%, respectively. No change in hormone or metabolic parameters was observed.

Adult↗
PubMed1991

[Comparison of ischemic pain threshold and reactive hyperemia in autonomic diabetic neuropathy and silent myocardial ischemia].

31 patients with coronary artery disease (11 patients with diabetes mellitus and autonomic neuropathy. 10 patients with diabetes without neuropathy, and 10 patients with asymptomatic myocardial ischemia) participated in a study designed to investigate whether there is a difference in forearm skeletal muscle ischemia and pain threshold. The degree of ischemia was determined by plethysmographically measured reactive hyperemia. There was no difference in maximum reactive hyperemia after passive forearm ischemia of 5-min duration in the three groups. After symptom-limited ischemic work, there was significantly more reactive hyperemia in patients with silent myocardial ischemia as compared to diabetic patients. Exercise time was longer in patients with silent myocardial ischemia (153 +/- 51 s) than in patients with diabetic neuropathy (139 +/- 45 s) and diabetics without neuropathy (120 +/- 45 s). Pain as a cause of termination of symptom-limited ischemic forearm exercise occurred less frequently in patients with diabetic neuropathy (2/11) and patients with silent myocardial ischemia (3/10) as compared to patients with diabetes without neuropathy. Patients with silent myocardial ischemia had a higher ischemic tolerance in the ischemic working forearm than did diabetic patients with and without neuropathy. In patients with neuropathy, however, ischemic pain occurred less frequently at the same ischemic work level compared to diabetics without neuropathy. Therefore, diabetic neuropathy appears to facilitate the occurrence of silent myocardial ischemia. The data presented here suggest that there is a qualitative difference in ischemic tolerance between patients with silent myocardial ischemia and patients with diabetic neuropathy.

Angina Pectoris↗
PubMed1990

[Compliance problems in therapy with levothyroxine].

In order to evaluate problems with long-term levothyroxine therapy, the course of treatment in 185 patients of an endocrinological outpatient ward (88 with euthyroid goiter, 41 with overt or latent hypothyroidism, ten with Hashimoto's thyroiditis, 46 after resection of goiter) was analyzed retrospectively. Duration of therapy ranged from one to 28 years. Suppressive therapy of euthyroid goiter was stopped by the treating physician in eleven patients (11%), in five permanently. To the contrary, 30 patients (34%) stopped medication by themselves 31 times, 29 times, however, levothyroxine was restarted again. Observations in the group with latent hypothyroidism were similar. After operation levothyroxine therapy was stopped by the physician eight times, six times only for a limited time period. Eight patients (17%) decided to stop therapy without knowledge of the treating physician, but in all it was restarted later. The presented results show that the success of levothyroxine therapy of euthyroid goiter as well as of prophylaxis of goiter relapse after operation is threatened by dyscompliance of the patients. In goiter suppression therapy compliance is further challenged by a lack of consequence in therapy planning and guidance.

Adolescent↗
PubMed1990

[Behavior of the renal functional reserve in type I diabetic patients: effect of ACE-inhibition].

Renal functional reserve capacity was evaluated in 19 normotensive type I diabetics without microalbuminuria. All patients had normal basal renal function as assessed by 24-hour creatinine clearances higher than 120 ml/min. PAH, inulin, and creatinine clearances were carried out every hour before, during, and after infusion of an amino acid (AA) solution. The same experiment was repeated after ACE inhibition with captopril (25 mg). Two groups of patients were found: Group A (responders) showed a significant rise in GFR after AA infusion (inulin clearances from 117 +/- 8 to 138 +/- 10 ml/min) (p less than 0.05), whereas in Group B (non-responders) no significant change in GFR was observed. Groups were comparable in age, duration of diabetes, metabolic control, and mean arterial blood pressure. Group B, however, had a significantly higher basal inulin clearance (167 +/- 17 ml/min) than Group A (117 +/- 8 ml/min). In Group A ACE inhibition completely blocked the AA-induced rise in GFR, while basal GFR in Group B was significantly reduced (167 +/- 17 to 148 +/- 8 ml/min) after captopril administration. In both groups renal plasma flow was enhanced by ACE inhibition. A rise in glucagon was observed in all patients during AA infusion. It is concluded that type I diabetics with normal basal renal function already have reduced (Group A) renal functional reserve capacity, which is completely abolished (Group B) when concomitant hyperfiltration occurs. ACE inhibition reduces hyperfiltration and is capable of blocking the AA-induced rise in GFR in these patients.

Adult↗
PubMed1990

[The effect of atrial natriuretic peptide on glucose tolerance and insulin level].

In previous studies, a pharmacological dose of human atrial natriuretic peptide (hANP) was found to increase serum insulin without influencing C-peptide levels. To examine whether blood glucose and insulin response to an oral or i.v. glucose load are influenced by raising hANP levels into the pathophysiological range, eight healthy, normal-weighted, male volunteers were studied. According to a randomized, double-blind study design, an oral glucose tolerance test (ogtt, 75 g) or an i.v. glucose tolerance test (ivgtt, 0.5 g/kg b.w.) were carried out. Beginning 30 minutes before glucose administration infusions of hANP 0.3 micrograms/min) or placebo were given for 180 minutes (ogtt) or 120 minutes (ivgtt). During the hANP-infusions maximal hANP levels were 72 +/- 11 pg/ml (normal less than 25 pg/ml). Responses of blood glucose and C-peptide levels to the glucose load remained unaffected by hANP in both studies. However, hANP increased mean insulin responses (given as area under the curve) by 11.5% in ogtt and by 15.9% in ivgtt (both p less than 0.05). Thus, elevated hANP levels within the pathophysiological range, as observed in chronic heart failure or in hypertension, lead to an increase in serum insulin. Unchanged C-peptide levels demonstrate that hANP does not interfere with insulin secretion, but exclusively inhibits insulin degradation in liver and/or kidney. Further studies are required to elucidate whether these findings play a part in the pathomechanisms of insulin resistance in patients with elevated hANP levels, e.g. in chronic heart failure or hypertension.

3-Hydroxybutyric Acid↗
PubMed1990

In vitro activity of biosynthetic human diarginylinsulin.

In diarginylinsulin two arginine residues are located at the C-terminal end of the B-chain (ArgB31 and ArgB32). This accounts for a shift of the isoelectric point from pH 5.4 in native insulin to pH 7.0 in diarginylinsulin leading to pharmacodynamic characteristics of an intermediate acting insulin when administered s.c. as pH 4.0-5.0 solution. We have investigated insulin receptor binding and biological activity of biosynthetic human diarginylinsulin in human adipocytes and compared to native insulin and proinsulin. Association- and dissociation studies of insulin receptor binding revealed no differences for diarginylinsulin and native insulin. In competition studies under steady-state binding conditions, half-maximal displacement of tracer occurred at 352 +/- 33 pmol/l, 337 +/- 32 pmol/l and 3640 +/- 480 pmol/l for diarginylinsulin, insulin and proinsulin, respectively. The biologic potency of human diarginylinsulin was evaluated by the ability to stimulate D-glucose transport and by the assessment of the antilipolytic activity. Activation of D-glucose transport was half-maximal at 49.6 +/- 5.4 pmol/l (diarginylinsulin), 44.8 +/- 5.8 pmol/l (insulin) and at 476.7 +/- 134.3 pmol/l (proinsulin). Half-maximal inhibition of lipolysis occurred at 13.9 +/- 3.4 pmol/l, 15.4 +/- 2.9 pmol/l and 138.4 +/- 38.6 pmol/l, respectively. In conclusion, diarginylinsulin has almost identical insulin receptor binding characteristics and full biological activity in vitro compared to native insulin. This pharmacodynamically intermediate acting insulin preparation is therefore of potential therapeutical value.

Adipose Tissue↗
PubMed1990

In vivo evidence that human atrial natriuretic factor-(99-126) (hANF) stimulates parasympathetic activity in man.

In a double-blind study 8 healthy male subjects received 100 micrograms human atrial natriuretic facotr-(99-126) (hANF) and NaCl0.9% in random order on different days. Following hANF injection a significant increase in cardiac beat-to-beat variation was observed (4.65% vs 5.95%). This shows that in vivo human atrial natriuretic factor stimulates cardiac parasympathetic activity in man.

Adult↗
PubMed1989

Effects of nifedipine on renal responses to human atrial natriuretic peptide in healthy subjects and normoglycemic patients with type 1 diabetes mellitus.

We examined renal responses to a pharmacological dosage of human atrial natriuretic peptide (hANP) and the potential interference of nifedipine administration with the effects of hANP on kidney function in healthy subjects and normoglycemic patients with type 1 diabetes mellitus. Ten healthy volunteers (age, 28 +/- 1 years) and ten patients (age, 33 +/- 2 years; diabetes duration; 14 +/- 3 years; HbAI 7.2% +/- 0.2%) were studied. According to a double-blind, randomized, placebo-controlled trial design, three experiments were performed in each subject using the double-dummy technique: placebo only, hANP only, and nifedipine + hANP. As i.v. bolus injection 100 micrograms hANP was given; nifedipine was applied buccally, at a dose of 10 mg 90 min before and at a dose of 5 mg together with hANP injection. At base-line and in the placebo only experiment, patients did not differ from controls. In the hANP only experiment, in both groups hANP resulted in increased urinary volume and both sodium and chloride excretion (P less than 0.05 vs placebo only experiment). In patients, hANP-induced increase in electrolyte excretion was greater than in controls (P less than 0.05). In the nifedipine + hANP experiment, hANP-induced changes in renal indexes were enhanced in controls (P less than 0.05 vs hANP only experiment) but not in patients. Thus, diuretic response to nifedipine + hANP in patients was decreased in comparison with controls (P less than 0.05). In patients, however, nifedipine administration decreased the hANP-induced increase in urinary albumin excretion (P less than 0.05 vs hANP only experiment). Creatinine clearance was uninfluenced throughout the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Buccal↗
PubMed1989

[Injection aids for intermediate-term acting insulin. Experiences with the OptiPen].

Twenty diabetics conventionally treated with Depot H and/or Basal H Insulin Hoechst received the OptiPen as an injection aid for the corresponding U100 insulin preparations. Seventeen patients had such a positive opinion of the pen, that they wanted to continue using it. After 15.6 +/- 5.3 weeks of "pen therapy", the mean insulin dose remained unchanged. In the 14 patients who had been treated with insulin long before the change over to the pen, the mean HbA1 level showed no change (8.8 +/- 1.2% before versus 8.7 +/- 1.5% under pen therapy). The use of an injection aid--in this case the OptiPen--facilitates insulin therapy for the usually older diabetics treated with intermediate acting or mixed insulin, too. Technical problems over the long term were not encountered and the quality of metabolic control remained unchanged.

Adult↗
PubMed1989

Effect of human atrial natriuretic peptide on blood glucose concentrations and hormone stimulation during insulin-induced hypoglycaemia in healthy man.

A double-blind placebo-controlled study using the double-dummy technique has been done to examine whether the responses of pituitary and adrenal hormones to insulin-induced hypoglycaemia were impaired by a pharmacological dose of human atrial natriuretic peptide (human ANF-(99-126),hANP). After an overnight fast eight male healthy volunteers (aged 23-40 years) received in random order i.v. bolus injections of insulin 0.125 U.kg-1 + placebo,hANP 100 micrograms + placebo,insulin + hANP, or both placebo preparations. In the insulin-only experiment, human growth hormone, adrenocorticotrophic hormone, cortisol, aldosterone, plasma renin activity, adrenaline, and noradrenaline were all stimulated by hypoglycaemia. In the hANP-only experiment there were no hormonal changes other than decreases in plasma renin activity and aldosterone concentration. In the insulin + hANP experiment the nadir of blood glucose was decreased to 1.3 from the 2.0 mmol.1-1 found in the insulin-only experiment. The exaggerated hypoglycaemia resulted in increased stimulation of human growth hormone, adrenocorticotrophic hormone and adrenaline when compared to the insulin-only experiment. The rise in the cortisol and aldosterone concentrations was only slightly increased, and the stimulation of plasma renin activity was blunted. Unexpectedly, hANP was found to enhance the hypoglycaemic action of insulin, most probably by inhibiting insulin degradation within the liver. There was no evidence of an inhibitory effect of hANP on the stimulation of pituitary or adrenal hormones during insulin-induced hypoglycaemia. The reduction in renin may indicate an inhibitory action of hANP on catecholaminergic effects within the kidney.

Adrenocorticotropic Hormone↗