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Biomedical subjects

O Koldkjaer

Publications and source records attributed to O Koldkjaer.

12 recordsLinked to original sources
PubMed2001

Reference intervals for glucose, beta-cell polypeptides, and counterregulatory factors during prolonged fasting.

To establish reference intervals for the pancreatic beta-cell response and the counterregulatory hormone response to prolonged fasting, we studied 33 healthy subjects (16 males, 17 females) during a 72-h fast. Glucose, insulin, C-peptide, and proinsulin levels decreased (P < 0.001), and the levels of counterregulatory factors increased during the fast [P < 0.05; glucagon and free fatty acids (FFA) with a linear increase and epinephrine, norepinephrine, and cortisol with a clear underlying circadian rhythm]. Growth hormone secretion increased from the first to third day of fasting (P < 0.05) but actually decreased from the second to third day of fasting (P = 0.03). Males had higher glucose and glucagon levels and lower FFA levels during the fast (P < 0.05), whereas no effect of gender on beta-cell polypeptides was observed. A high body mass index resulted in higher insulin and C-peptide levels during the fast (P < 0.05). In conclusion, we have provided reference intervals for glucoregulatory factors during a 72-h fast. We observed a diminished beta-cell response concomitant with an increased secretion of counterregulatory hormones. These results should be of clinical and scientific value in the investigation of hypoglycemic disorders.

Adult↗
PubMed1999

The effects of endogenous opioids and cortisol on thyrotropin and prolactin secretion in patients with Addison's disease.

This study assessed the controversial role of endogenous opioids and cortisol in the regulation of TSH and PRL secretion in humans. Seven euthyroid male patients with Addison's disease were studied four times, with an interval of 1-3 months, as follows: 1) during normocortisolism [graduated infusion of hydrocortisone, 0.4 mg/kg, over 19.5 h]; 2) normocortisolism and coadministration of naloxone, at 25 microg/kg x h during the last 6.5 h; 3) hypocortisolism (24 h withdrawal of hydrocortisone, followed by 19.5 h saline infusion); and 4) hypocortisolism plus naloxone administration. The TSH and PRL levels were measured every 15 min, from 0800-1530 h. A TRH test was performed at 1300 h and 1400 h (10 microg and 200 microg of TRH, respectively). The mean TSH level increased significantly during hypocortisolism, compared with normocortisolism (1.78 +/- 0.04 vs. 0.84 +/- 0.02 mU/L; P < 0.001). The administration of naloxone suppressed the TSH levels during hypo- and normocortisolism (1.78 +/- 0.04 vs. 1.50 +/- 0.03 and 0.84 +/- 0.02 vs. 0.61 +/- 0.02 mU/L, respectively; P < 0.001). During hypocortisolism, the TSH responses to small and high doses of TRH were significantly higher than during normocortisolism (P < 0.02). Naloxone had no effect on the TSH responses to TRH, neither during hypo- nor during normocortisolism. The mean PRL level increased significantly during hypocortisolism, compared with normocortisolism (5.8 +/- 0.4 vs. 3.6 +/- 0.2 microg/L; P < 0.001), and naloxone induced an increase in PRL levels both during hypo- and normocortisolism (7.1 +/- 0.7 vs. 4.7 +/- 0.5 microg/L, respectively; P < 0.01). The PRL responses to TRH were similar during hypo- and normocortisolism and without any change during opioid receptor blockade. In conclusion, cortisol suppressed basal TSH and PRL secretion and reduced the sensitivity of the thyrotrophs to TRH, without affecting the PRL response to TRH. Our results suggest that endogenous opioids act at the hypothalamic level to stimulate TSH secretion and to suppress the PRL secretion, but these results argue against an essential role of endogenous opioids in the physiological regulation of TSH and PRL secretion in humans.

Addison Disease↗
PubMed1998

Lack of effect of the dopamine D1 antagonist, NNC 01-0687, on unstimulated and stimulated release of anterior pituitary hormones in males.

Dopamine in humans inhibits the secretion of luteinizing hormone (LH), follicular stimulating hormone (FSH), thyroid stimulating hormone (TSH) and prolactin (PRL), and is a stimulator of growth hormone (GH) secretion. Dopamine-D1 receptor stimulation with fenoldopam increases basal PRL levels, suppresses TSH, and increases gonadotropin releasing hormone (LHRH) induced LH release. We have investigated the effect of a dopamine D1-receptor antagonist, NNC 01-0687, on the secretion of anterior pituitary hormones. In 8 healthy males NNC 01-0687 and placebo were administered orally in a double-blind placebo controlled cross-over study for three days with a wash-out period of 14 days. Hormonal responses (PRL, LH, FSH, GH, TSH, thyroid hormones and testosterone), unstimulated and LHRH/TRH stimulated, were studied on days 1 and 3. No significant difference (p > 0.05) between placebo and active periods was found neither in unstimulated nor in stimulated hormone concentrations expressed in absolute values, percent change of before, incremental values and area under the curve. These results suggest that the neuronal DA-D1 activity is not activated during basal conditions in healthy male subjects.

Adult↗
PubMed1998

Pulsatile luteinizing hormone secretion in patients with Addison's disease. Impact of glucocorticoid substitution.

The physiological and pathophysiological role of cortisol in pulsatile LH release was investigated in 14 patients (5 men, 6 premenopausal women, and 3 postmenopausal women) with Addison's disease. The explicit effect of cortisol in relation to the effect of corticotropin-releasing factor (CRF), ACTH, and opioids was ensured by hypo-, normo-, and hypercortisolism. Hypocortisolism was obtained by 24-h discontinuation of hydrocortisone (HC) followed by 23-h saline infusion. Eucortisolism was secured by infusion of HC (0.5 mg/kg) over 23 h. Stress-appropriate hypercortisolism was obtained by infusion of HC (2.0 mg/kg) over 23 h, preceded by treatment for 5 days with dexamethasone (1.5 mg/day). To imitate the normal diurnal rhythm for serum cortisol, HC was infused in graduated doses. Blood sampling was performed every 10 min during the last 10 h of the study period, followed by a LH-releasing hormone test (5 microg, i.v.) and a TRH test (10 microg, i.v.). In pre- and postmenopausal women, the mean LH level and the LH pulsatility pattern were similar on the 3 occasions. In contrast, the mean LH level in men was significantly reduced during hypocortisolism compared to that during eucortisolism (3.26 +/- 0.68 vs. 4.49 +/- 0.83 U/L; P < 0.05) and was associated with a clear decrease in LH pulse amplitude (1.09 +/- 0.33 vs. 1.96 +/- 0.53 U/L; P < 0.05). During high doses of glucocorticoids, the mean LH level in men was significantly lower than that during eucortisolism (3.81 +/- 0.88 vs. 4.49 +/- 0.83 U/L; P < 0.05). In both men and women, the mean PRL levels increased significantly (P < 0.05) during hypocortisolism, whereas high glucocorticoid doses suppressed the mean PRL level (P < 0.05). The LH and PRL responses to LH-releasing hormone and TRH were, however, similar during low, medium, and high cortisol levels in both men and women. In conclusion, our data suggest that the attenuation of pulsatile LH secretion in men during hypo- and hypercortisolism is due to variations in the hypothalamic opioid activity secondary to alterations in serum cortisol levels. A higher level of opioid receptor activity in men than in low estrogen women may explain the gender differences.

Addison Disease↗
PubMed1996

Pulsatile thyrotropin secretion in patients with Addison's disease during variable glucocorticoid therapy.

The inhibitory action of physiological to pathophysiological serum cortisol levels on TSH secretion were investigated in 12 patients with Addison's disease on 3 occasions. 1) In continuation of the conventional hydrocortisone (HC) substitution, a medium dose of HC (0.5 mg/kg) was infused over 23 h. 2) After 24-h withdrawal of HC, the patients had placebo infusion over 23 h. 3) After 5 days of dexamethasone (1.5 mg/day), a high dose of HC (2.0 mg/kg) was infused over 23 h. Blood sampling was performed every 10 min during the last 10 h of the study period, followed by a TRH test (10 micrograms, iv), To mimic the normal diurnal rhythm for serum cortisol, HC was infused in graduated doses, and during medium dose infusion, the serum cortisol level and the TSH pulsatility pattern were similar to those seen in normal controls. The TSH mean level was 1.0 +/- 0.5 mU/L during medium doses of HC, increasing significantly (P < 0.05) to 2.0 +/- 1.6 mU/L during the low cortisol state and was significantly (P < 0.05) suppressed to 0.4 +/- 0.2 mU/L during high doses of glucocorticoids, when the pulse frequency was also significantly reduced (P < 0.01). Together with a dose-dependent inhibitory action of glucocorticoids on the TSH response to TRH, our data indicate that even physiological serum levels of cortisol have an influence on endogenous TSH secretion, probably caused by regulation of the pituitary sensitivity to TRH.

Addison Disease↗
PubMed1983

The diagnostic value of determination of intraerythrocytic sodium and potassium concentrations versus plasma digoxin concentration in digoxin intoxication.

Plasma digoxin measurements have proved unserviceable as a means of differentiating between toxic and non-toxic patients. In order to assess the value of a biological effect of digoxin in this discrimination, intraerythrocytic sodium and potassium concentrations were determined in 55 chronically digitalized patients of whom 10 were digoxin-intoxicated according to ECG criteria. Digitoxicity was associated with elevated intraerythrocytic sodium concentration (mean +/- SEM 19.3 +/- 1.2 versus 11.3 +/- 0.3 mmol/l, p less than 0.001) and reduced intraerythrocytic potassium concentration (94.6 +/- 2.3 versus 100.0 +/- 0.6 mmol/l, p less than 0.001) compared to non-toxic patients. Mean (+/- SEM) plasma digoxin concentrations in the two groups were 3.14 +/- 0.41 and 1.57 +/- 0.09 nmol/l, respectively (p less than 0.001). When diagnosing toxicity in chronically digitalized patients, plasma digoxin and intraerythrocytic sodium determinations showed sensitivities of 60 and 100%, respectively. The predictive values of a positive test were 75% for plasma digoxin and 83% for intraerythrocytic sodium.

Aged↗
PubMed1982

Immunoelectrophoretic characterization of human mitochondrial aspartate aminotransferase purified by ion exchange and affinity chromatography.

Human mitochondrial aspartate aminotransferase (m-ASAT) was prepared for use as an antigen for antibody production and as a standard, i.e. a high degree of purity was demanded. The purification was performed by three ion exchange chromatography steps followed by affinity chromatography on aspartate coupled gel. Four preparations gave specific activities of 230 to 300 U/mg at 37 degrees C. The purity of m-ASAT was assessed by crossed immunoelectrophoresis, which showed that the final preparation did not contain contaminating proteins. Immunization with the purified m-ASAT gave a good antibody response.

Aspartate Aminotransferases↗
PubMed1982

Intraerythrocytic sodium and potassium concentrations during acute and chronic digitalization.

To assess the cellular effects of digoxin, intraerythrocytic sodium and potassium concentrations were measured in 17 patients during the early phase of digitalization, in 45 patients on long-term therapy and in 64 non-digitalized control patients. Acute digitalization raised intraerythrocytic sodium from 11.6 +/- 0.4 to 16.7 +/- 1.0 mmol/l (mean +/- SEM) (p less than 0.01) and reduced intraerythrocytic potassium from 100.1 +/- 1.3 to 95.9 +/- 1.8 mmol/l (p less than 0.01). These changes were strongly correlated with the steady-state plasma digoxin concentration. During a few weeks of digoxin therapy, the intraerythrocytic cation composition normalized gradually. In patients on chronic treatment, neither intraerythrocytic sodium (11.3 +/- 0.3 mmol/l) nor potassium concentrations (100.0 +/- 0.6 mmol/l) differed significantly from the values of the control group (11.4 +/- 0.2 and 99.9 +/- 0.5 mmol/l, respectively). The changes in intraerythrocytic cation concentrations, induced by acute digitalization, seem to disappear during chronic administration of the drug.

Aged↗
PubMed1978

Cellular and humoral indices of disease activity in inflammatory bowel disease.

In 51 untreated cases of ulcerative colitis and Crohn's disease some cellular (neutrophil alkaline phosphatase activity, neutrophil NBT reducing capacity, and neutrophil and plasma lysozyme activities) and humoral (serum orosomucoid and serum haptoglobin) indices of disease activity were quantitated. The most pronounced signs of disease activity, thus, were found in severe cases of ulcerative colitis. Combining lysozyme activities with other disease activity indices seems to facilitate the distinction between severe cases of Crohn's disease and ulcerative colitis. Beyond this the addition of the humoral indices seemed not to offer substantial help.

Adolescent↗
PubMed1977

Lysozyme in plasma and neutrophilic granulocytes in ulcerative colitis and Crohn's disease.

The concentration of lysozyme in plasma (P) and in neutrophil leucocytes (N) was determined by a turbidimetric method in 32 patients with ulcerative colitis (U.C.), 11 patients with Crohn's disease (C.D.), 9 patients with haemorrhagic proctitis, and 39 healthy volunteers. In active U.C., P was significantly elevated (p less than 0.05), whereas C.D. showed normal values. Corresponding N was significantly reduced in active U.C. (p less than 0.05) but normal in C.D. In calculating the ratio N/P, highly significant lower values were found in active U.C. (p less than 0.001) compared to normal levels in C.D. The high P in active U.C. is presumed to reflect an accelerated destruction of neutrophil leucocytes as well as an intensified turnover rate. The reduced N is probably attributable to an inhibited synthesis. The findings suggest that lysozyme determinations are valuable in be differential diagnosis of active U.C. and C.D.

Adolescent↗