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Biomedical subjects

U Adamson

Publications and source records attributed to U Adamson.

At least 91 records · Page 5Linked to original sources
PubMed1981

Neutrophil function in hypothyroid patients.

We investigated whether some in vitro polymorphonuclear (PMN) granulocyte functions were impaired in patients with hypothyroidism, since this disease has previously been associated with an increased susceptibility to infectious agents and decreased leukocyte heat production. PMNs from 9 of 17 hypothyroid patients exhibited a decreased ability to kill Staph. aureus in vitro compared with euthyroid controls (p less than 0.02). This was normalized in all patients tested after therapy with levothyroxine. In 3 patients, studied repeatedly during the initial phase of therapy, PMN bactericidal capacity was gradually normalized. In addition, PMN adherence to nylon fibres showed a transient decrease approximately 6 weeks after initiation of therapy. PMN chemiluminescence during phagocytosis of Staph. aureus and stimulated and spontaneous migration under agarose were normal and did not change during therapy. Thus, the decreased bactericidal capacity found in half of these hypothyroid patients might confer an increased susceptibility to cerain infectious agents.

Adult↗
PubMed1981

On the diabetogenic effect of growth hormone in man: effects of growth hormone of glucagon and insulin secretion.

The effects of human growth hormone (GH) on glucose homeostasis and the secretion of insulin and glucagon was investigated in eighteen healthy subjects. GH (40 microgram/kg) was given as a 30 min i.v. infusion and was followed immediately, or after 60 min, by either a glucose infusion, or an i.v. L-arginine infusion or i.v. insulin (0.05 IU/kg). An insulin-like effect of GH was seen about 15 min after the start of the GH infusion, and became a diabetogenic action 90 min later. Basal and glucose stimulated insulin secretion were suppressed 60 min after the start of the GH infusion, while insulin response to i.v. L-arginine, on the whole, was uninfluenced. Basal glucagon as well as glucagon response to arginine or hypoglycaemia were uninfluenced by GH. GH did not alter the degree of hypoglycaemia reached after i.v. insulin, whereas the rapidity of blood glucose fall was significantly decreased. The restitution of blood glucose after its nadir was not modified by the hormone. These results demonstrate that the diabetogenic action of GH is not mediated by GH effects on glucagon secretion, and that GH is of little importance in the acute counter-regulation of insulin-induced hypoglycaemia.

Adult↗
PubMed1980

Glucose tolerance, growth hormone and somatomedin levels in osteosarcoma patients.

Intravenous glucose tolerance, insulin response to glucose, the sensitivity of the periphery to insulin as well as growth hormone and somatomedin levels were determined in osteosarcoma patients and control subjects matched by age, sex, weight an length. The insulin response to glucose and the peripheral sensitivity to insulin were evaluated by using the individual blood glucose and plasma insulin curves for parameter identification in a mathematical model. The mean glucose tolerance was significantly decreased in the patients, most likely due to decreased peripheral insulin sensitivity. Plasma growth hormone levels were normal in all patients which was also the case with somatomedin levels determined by both radioreceptor- and radioimmunoassay.

Adolescent↗
PubMed1980

Longitudinal growth and dental development in osteosarcoma patients.

The body height at 8.0 years and at the time of diagnosis, as well as the dental maturity, were analysed in a sample of patients with classical and primary osteosarcoma, registered in Sweden between 1972 and 1974, in order to investigate whether these patients have an accelerated body height growth. In contrast to previous reports the height development was found to be normal. The dental maturity was also normal.

Adolescent↗
PubMed1980

Preoperative localization of aldosterone-producing adenomas. An analysis of the efficiency of different diagnostic procedures made from 11 cases and from a review of the literature.

The efficiency of six different methods available for topographical diagnosis of primary aldosteronism was analysed in retrospect from 11 surgically verified cases and by an analysis of 360 cases reported in the literature. Differentiation between hyperplasia and adenoma was most safely predicted by monitoring the diurnal rhythm of plasma aldosterone and its reaction to posture. Adrenal vein catheterization with aldosterone determinations was helpful in establishing the presence of hyperplasia in approximately 70% of these cases. Correct localization of aldosterone-producing adenomas was made in more than 90% by vein catheterization while venography and radio-cholesterol scintigraphy had lower diagnostic accuracy. It is therefore suggested that determination of plasma aldosterone both by vein catheterization and by peripheral monitoring should be used ahead of other diagnostic procedures for topographical examinations in primary aldosteronism.

Adenoma↗
PubMed1979

Glucose memory of pancreatic B and A2 cells: evidence for common time-dependent actions of glucose on insulin and glucagon secretion in the perfused rat pancreas.

The influence of previous exposure to glucose on the subsequent B- and A(2)-cell secretory responses to arginine was investigated in the perfused pancreas of the rat. Arginine (8 mM) was administered in two brief (9 min) pulses separated by a period of 66 min. In pancreata from 18-h-fasted animals the two pulses of arginine elicited biphasic glucagon secretory responses, while stimulation of insulin release was barely detectable. When 27.7 mM glucose was administered for 30 min during the intervening period up to 20 min before the second pulse of arginine, the glucagon response to arginine was diminished by 55% while the insulin release was markedly increased in comparison with the first pulse. 8.3 mM glucose, when administered before the second pulse of arginine, exerted effects that were smaller but otherwise similar to those of 27.7 mM glucose.The inclusion of 3.9 mM glucose during the stimulation periods with arginine decreased the glucagon and greatly increased the insulin secretory response. Under these conditions, previous exposure to 27.7 mM glucose inhibited the glucagon and enhanced the insulin response to the second stimulatory pulse of arginine to the same relative degree as when arginine was administered alone. Diazoxide (2 mM), when administered together with 27.7 mM glucose, almost completely inhibited insulin release induced by the presence of glucose, yet did not influence the modulation exerted by glucose on the subsequent insulin and glucagon secretory response to arginine. Conversely, these effects of the glucose pulse could not be reproduced by 1 mug/ml of porcine insulin. Previous exposure to glyceraldehyde (10 mM) mimicked the glucose effects.Also, in pancreata from fed rats, previous exposure to 27.7 mM glucose markedly inhibited subsequent arginine-induced glucagon secretion while the concomittant insulin response was enhanced.IT IS CONCLUDED THAT: (a) both A(2)- and B-cell responsiveness is modulated by a previous exposure to glucose which produces opposite effects in the two cell types, (b) this action of glucose does not depend on its insulin-releasing capacity, and (c) instead, a "memory" of glucose is induced as a consequence of the metabolism of the sugar in the A(2) and B cells.

Animals↗
PubMed1978

Immediate and time-dependent effects of glucose on insulin release from rat pancreatic tissue. Evidence for different mechanisms of action.

Glucose-induced insulin secretion is enhanced by a preceeding glucose stimulus. The characteristics of this action of glucose were investigated in perfused pancreas and collagenase-isolated islets of Langerhans. A 20- to 30-min pulse of 27.7 mM glucose enhanced both the first and second phase of insulin release in response to a second glucose stimulus by 76-201%. This enhancement was apparent as an augmented maximal insulin release response to glucose. The effect of priming with glucose was seen irrespective of whether the pancreatic tissue was obtained from fed or fasted rats. Separating the two pulses of hexose by a 60-min time interval of exposure to 3.3 mM glucose did not abolish the potentiation of the second pulse. Omission of Ca(++) as well as the inclusion of somatostatin or mannoheptulose during the first pulse abolished insulin secretion during this time period; however, only the inclusion of mannoheptulose deleted the potentiation of the second pulse. d-Glyceraldehyde, but not pyruvate, d-galactose, or 3-isobutyl-1-methylxanthine, could substitute for glucose in inducing potentiation. In islets labeled with [2-(3)H]adenine, the [(3)H]cyclic AMP response to glucose was increased by 35% when measured after 1 min, but was increased only marginally after 2-10 min of stimulation with a second pulse of glucose. The production of (3)H(2)O from glucose was not affected by glucose priming. It is concluded that (a) the induction of the glucose-induced, time-dependent potentiation described here is dependent on glucose metabolism but not on stimulation of cyclic AMP, calcium fluxes, or insulin release per se; (b) the mechanisms that mediate the pancreatic "memory" for glucose are unknown but do not seem to involve to a major extent an increased activity of the adenylate cyclase-cyclic AMP system of the beta-cell; (c) the evidence presented supports the hypothesis of a dual role of glucose for insulin release.

Animals↗
PubMed1976

Diminished sensitivity of the insulin response to glucose following growth hormone influsion in man.

The acute effect of growth hormone (GH) administration on the dose-kinetics of glucose-stimulated insulin release was investigated in eight healthy, non-obese male subjects. The glucose-insulin dose-response relationship in these subjects was established by performing glucose infusions at three different dose levels. In a second series of experiments, the glucose infusions were preceded by a 30 min infusion of GH (40 mug/kg body weight), terminated 60 min before administration of glucose. GH induced small but significant reductions in the basal levels of blood glucose and plasma insulin. The glucose tolerance (k-value) was diminished after GH at all glucose doses. Both the initial late phases of insulin response to glucose were impaired following GH treatment. This effect was most pronounced when the intermediary glucose dose (eliciting a blood glucose level around 300 mg/100 ml) was used. Thus, the insulinogenic index (whole period of stimulation) was reduced by GH to 88.9 +/- 7.6, 60.4 +/- 7.1 and 74.3 +/- 11.0% of the respective controls when the smallest, the intermediate, and the largest glucose loads, respectively, were given. The blood glucose-plasma insulin dose-response curves were shifted to the right of the control ones when glucose infusion was preceded by GH. These findings suggest that GH diminishes the sensitivity of the islet for the insulin releasing action of glucose. Some possible mechanisms by which GH may modify insulin release are discussed.

Adult↗
PubMed1975

Acute suppressive effect of human growth hormone on basal insulin secretion in man.

The acute effects of human growth hormone (GH) on the basal levels of glucose and insulin in blood were investigated in 11 healthy men. GH doses of 5, 10, 20, and 40 mug/kg body weight were given iv as a constant-rate infusion over 30 min, and resulted in peak hormone levels (30 min) of 20.5 plus or minus 1.0, 48.5 plus or minus 2.2, 108.2 plus or minus 4.5, and 229.2 plus or minus 14.6 ng/ml, respectively. There was a small (max 9.8 plus or minus 2.6%) but significant decrease in the blood glucose level, observed already at 15 min after the beginning of the GH infusion and persisting up to 90 min. The highest dose of GH induced the most marked changes, but there was otherwise no clear correlation between dose and effect. The basal plasma insulin levels showed a more marked (max 16.0 plus or minus 4.7%) decrease which was not correlated, in time or in magnitude, with the changes in blood glucose. In some subjects, in whom no significant decrease in blood glucose was observed, plasma insulin still demonstrated a similar fall (max 20.2 plus or minus 7.6%). Neither were these changes in plasma insulin correlated to the dose of GH within the range used in this study. The findings suggested that the early, insulin-like effect of GH on blood glucose is distinct from its effect on the pancreas. The latter is a suppressive one, consistent with earlier findings on glucose-induced insulin release.

Adult↗
PubMed1975

Acute effects of exogenous growth hormone in man: time- and dose-bound modification of glucose tolerance and glucose-induced insulin release.

The time and dose dependency of the effects of a 30-min long iv infusion of human growth hormone (GH) on glucose tolerance and glucose-stimulated insulin release was investigated in 19 healthy subjects. Glucose tolerance deteriorated immediately following GH, and the k-value continued to decrease up to 300 min later. A small but significant reduction of glucose tolerance persisted 24 h after GH administration. Significant deterioration of glucose tolerance was observed with the smallest GH dose used (5 mug per kg body weight), increasing the amount of the hormone having no further major influence. Glucose-stimulated insulin release was significantly inhibited 1 h after administration of a relatively high GH dose (40 mug per kg), both if expressed as mean plasma insulin levels, or as insulin release per magnitude of glucose stimulation (insulinogenic index). In the majority of subjects, insulin release was inhibited also by lower GH doses (5-20 mug GH per kg). However, the mean change with these doses was not statistically significant. The inhibitory effect of GH on insulin secretion seemed to have a duration of several hours. Five hours, but not 24 h, after GH administration (10 mug GH per kg) insulin release was still significantly suppressed. It is suggested that the initial effect of GH on pancreatic beta cells may be inhibition of insulin release, in contrast with the enhancement of insulin secretion observed during chronic administration of GH.

Adolescent↗
PubMed1975

Acute suppressive effect of human growth hormone on insulin release induced by glucagon and tolbutamide in man.

The acute effect of human growth hormone on glucagon--and tolbutamide--induced insulin release was investigated in 14 non-obese subjects with normal glucose tolerance. Sixty mn after an i.v. growth hormone infusion of 40 mug/kg per kg body weight, the insulin response to glucagon (10 subjects) as well as to tolbutamide (6 subjects) was significantly suppressed by about 35%, both if the insulin secretion was expressed as change in peak response (p less than 0.05 for both insulinogogues) or as per cent change of the integrated insulin area over 30 minutes (p less than 0.005 and p less than 0.05, respectively). A lesser reduction of glucagon-induced insulin secretion was observed also after smaller doses of growth hormone (10 and 20 mug/kg). The reduction of the insulin response was associated with a significantly smaller blood glucose fall following the glucagon and tolbutamide administration. These results support the hypothesis that growth hormone in vivo has an acute suppressive effect on insulin secretion, and show that this action is not limited to glucose-induced stimulation of the islets.

Acromegaly↗