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Biomedical subjects

N Møller

Publications and source records attributed to N Møller.

118 records · Page 7Linked to original sources
PubMed1985

Body temperature elevation, exercise and serum prolactin concentrations.

Ten young healthy normal-weight males were studied in four test situations designed to elucidate the relative role of body temperature increase vs that of exercise per se for pituitary hormone release. Tympanic temperature was recorded continuously during the tests. Elevation of body temperature at rest induced by external heating resulted in parallel changes in serum prolactin (Prl), also found when temperature spontaneously returned towards normal. In contrast, temperature elevation of the same magnitude through exercise (450 kpm/min for 40 min) induced no change in Prl secretion. It is concluded that increase in core temperature is a stimulus of Prl secretion and suggested that exercise apparently inhibits the stimulatory effect.

Adult↗
PubMed1985

A test strip method for visual and reflectometric reading of blood glucose.

A double field glucose oxidase test strip, B-M Haemoglucotest 1-44 R, was tested for stability of reaction and comparability of visual and reflectometric readings (evaluating four reflectometers) with a standard laboratory glucose oxidase analysis and showed excellent precision and accuracy within the whole range when estimated immediately. Readings after 1 and 7 days showed a systematic and increasing error with time, with spuriously high and low values in the lower (less than or equal to 4.0 mmol/l) and higher (greater than or equal to 8.1 mmol/l) part of the range, respectively. In the lower range, however, the error was in the order of 1 mmol/l only, thus stability of the reaction allows mailing the strips to the clinic for rechecking.

Blood Glucose↗
PubMed1984

Characterization of growth hormone release in response to external heating. Comparison to exercise induced release.

The effects of increases in body temperature on growth hormone (GH)-release were studied in 10 young normal males in the fasting state as well as postprandially. The temperature increase of one degree centigrade was attained by external heating using thermostatically controlled water blankets covered by heat-reflecting aluminium foil. The increase in plasma GH after heating was partially suppressed in the non-fasting state reaching a mean of 7.9 +/- 3.5 (SEM), ng/ml, range 1.0-36 ng/ml. In contrast all subjects exhibited higher increases, mean 18.3 +/- 4.0 ng/ml, range 7-44 ng/ml, in response to heating when fasting. The results were compared in the same subjects to the plasma GH-responses obtained during exercise (450 kpm/min for 40 min) inducing a similar increase in body temperature of about one degree centrigrade. Nevertheless the response in plasma GH (8.4 +/- 3.3 ng/ml, range 0.4-34 ng/ml) was smaller than obtained by the heat test despite a rate of temperature increase on exercise which was about twice as high. Furthermore, the same exercise performed in a cold room under circumstances which precluded any major rises in core temperature resulted in complete inhibition of GH-release. The results indicate that exercise per se does not stimulate GH-secretion, indeed it may inhibit the response expected to be evoked by the exercise-induced rise in temperature. Evidence is also presented that it is core and not cutaneous temperature which modulated GH release. The procedure used for inducing the rise in temperature and plasma GH may be used as a simple, acceptable and safe clinical test for GH-insufficiency.

Adult↗
PubMedDate not supplied

Diabetes-like alterations in hemostatic parameters after growth hormone administration for one week in normal man.

Excess production of growth hormone (GH) in poorly controlled diabetes is believed to be a causal factor in the development of diabetic angiopathy, the mechanism(s) of which is unknown. The present study was undertaken to determine whether exogenous growth hormone would specifically change some quantities and functional parameters known to often be abnormal in long-standing diabetes and thought to result from the development of vascular lesions in general. The authors studied capillary resistance, factor VIII coagulant antigen (F VIII:Ag), von Willebrand factor (vWf:Ag), fibronectin, fibrinogen, and tissue-type plasminogen activator (t-PA) before, during, and after 1 week's subcutaneous GH administration (6 IU per day divided into two doses). Capillary resistance decreased insignificantly, but returned to higher levels (p less than 0.05) 1 week after withdrawal. F VIII:Ag, vWf:Ag, fibronectin, and fibrinogen all increased significantly during GH treatment. Except for F VIII:Ag, these quantities returned to pre-medication levels 7 days after termination of GH administration. The present results may contribute to the clarification of the role of GH hypersecretion in diabetic microangiopathy and macroangiopathy.

Adult↗
PubMedDate not supplied

Lack of effects of angiotensin-converting enzyme (ACE)-inhibitors on glucose metabolism in type 1 diabetes.

To evaluate the impact of ACE-inhibitors on insulin-mediated glucose uptake, glucose-induced glucose uptake, and hepatic glucose production, a sequential glucose clamp was performed in eight normotensive Type 1 diabetic patients after 3 weeks of enalapril therapy 20 mg day-1 and during control conditions. The experiments were carried out in random order. Mean arterial blood pressure was significantly reduced during ACE-inhibition (95 +/- 3 (+/- SE) vs 84 +/- 3 mmHg; p less than 0.02), while blood glucose control as assessed by HbA1c was unaltered (7.9 +/- 0.5 vs 7.6 +/- 0.5%). The night prior to the study normoglycaemia was maintained by a Biostator. A two-step hyperinsulinaemic euglycaemic clamp (insulin infusion rate 0.3 and 0.8 mU kg-1 min-1) was followed by a hyperinsulinaemic and hyperglycaemic clamp (insulin infusion rate 0.8 mU kg-1 min-1, plasma glucose 11 mmol l-1). Insulin concentrations were comparable with and without enalapril treatment. During the hyperinsulinaemic clamps isotopically determined glucose disposal was unchanged (low dose 2.5 +/- 0.3, high dose 4.3 +/- 0.7 vs 2.6 +/- 0.3 and 4.3 +/- 0.7 mg kg-1 min-1, enalapril vs control). Glucose-induced glucose disposal (9.2 +/- 1.2 vs 9.1 +/- 1.2 mg kg-1 min-1) was also similar, as were non-protein respiratory exchange ratios (indirect calorimetry). Glucose production was not changed by enalapril. In conclusion, treatment with enalapril has no significant effect on glucose metabolism in Type 1 diabetes.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Glucose metabolism in chronic renal failure with reference to GH treatment of uremic children.

Growth retardation is a common feature in children with end-stage renal failure (ESRF). Medical management of renal insufficiency rarely normalizes growth and optimistic reports on the effect of rhGH treatment on growth velocity may presage more extensive use of rhGH in pediatric nephrology. Ample evidence has shown beneficial effects of GH replacement therapy in both childhood and adolescent hypopituitarism. However, the remarkably few side effects of treatment reported in these conditions cannot necessarily be extrapolated to children with ESRF. Uremia is associated with a wide range of metabolic and hormonal derangements including decreased glucose tolerance. This is mainly due to impaired insulin-stimulated glucose disposal in peripheral tissues and insufficient insulin-induced suppression of hepatic glucose production. Insulin-stimulated glucose uptake in skeletal muscle in ESRF is reduced by 30-50% as compared to that in healthy subjects, and a reduction may be detected even in subjects with a more moderate reduction in renal function (GFR around 25 ml/min). Dialysis therapy improves the disturbed insulin action significantly. The cause of the insulin resistance in ESRF is multifactorial. Impaired physical fitness, accumulation of uremic toxins, raised levels of GH and glucagon, metabolic acidosis, dyslipidemia and the medication applied may all contribute. If exogenous GH administration is added to the already marked uremic insulin resistance, insulin action may be severely disturbed and the secondary hyperinsulinism further magnified. However, frank diabetes mellitus does not develop unless the beta cells fail to meet the enhanced demands. This will probably occur only in patients with a beta-cell genotype pivotal for the phenotypic expression of non-insulin dependent diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMedDate not supplied

Contamination of tritiated glucose tracers.

In vivo studies of glucose turnover have been complicated by the occurrence of theoretically impossible negative numbers for endogenous glucose production and it has only very recently been proposed that this could be due to radiochemical contamination of the tracers employed. We have analyzed tritiated glucose infusates purchased over the past 2 years and have found a surprisingly high and variable degree of radiochemical contamination, which could explain the above paradox.

Drug Contamination↗