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Biomedical subjects

R Jorde

Publications and source records attributed to R Jorde.

At least 55 records · Page 3Linked to original sources
PubMed1996

Thyroid antibodies in northern Norway: prevalence, persistence and relevance.

OBJECTIVES: To investigate the prevalence and persistence of thyroid autoantibodies in a population sample and to assess the development of biochemical hypothyroidism (defined as an elevated serum thyrotropin [TSH] concentration) in relation to their presence. DESIGN AND SETTING: A cross-sectional and longitudinal study based on the Tromsø Study in 1979-80 and 1986-87. SUBJECTS AND MAIN OUTCOME MEASURES: From 2551 random participants in 1979-80 aged 34 +/- 8.4 (mean +/- SD) years, sera were available in 2513 and 2504 persons for determination by passive haemagglutination of the antibody to thyroid microsomal antigen (anti-Tm) and of the antibody to thyroglobulin (anti-Tg). Total thyroxine (TT4) and TSH were measured in 114 of 176 antibody-positive subjects and in 101 controls. After 7 years, anti-Tm and anti-Tg were remeasured in 1939 and 1931 subjects, and TT4 and TSH in 92 of the initially antibody-positive subjects and in 69 controls. RESULTS: Anti-Tm occurred more frequently than anti-Tg (in 6.1 vs. 2.8%; P < 0.001). Anti-Tm (P < 0.001) and anti-Tg (P = 0.027) were both more common in women than in men. The prevalence of anti-Tm (P = 0.025), but not of anti-Tg, increased with age. Changes in titre levels after 7 years were mostly small or moderate. Both in women (P = 0.005) and in men (P < 0.001) the TSH concentrations increased with increasing levels of anti-Tm, whereas in men, the concentrations also increased with increasing anti-Tg levels (P < 0.001). Biochemical hypothyroidism developed with a 2.7% yearly incidence only in antibody-positive subjects, all except one of whom had anti-Tm. CONCLUSIONS: The prevalences of thyroid antibodies were comparable to those found in similar studies in other areas. Their presence was associated with the development of biochemical hypothyroidism.

Adult↗
PubMed1996

Sex hormone responses in healthy men and male patients with chronic obstructive pulmonary disease during an oral glucose load.

The responses of serum testosterone, sex hormone-binding globulin (SHBG) and luteinizing hormone (LH) to an oral glucose tolerance test (OGTT) were investigated in 16 healthy subjects as well as in 11 normoxaemic and 10 hypoxaemic chronic obstructive pulmonary disease (COPD) patients. The latter group were investigated on two occasions, with and without oxygen therapy. Testosterone and apparent free testosterone concentration (AFTC) fell significantly in the healthy subjects as well as in the hypoxaemic patients on oxygen therapy (p < 0.01), whereas LH increased in all groups during the OGTT (p < 0.05). There were significantly higher SHBG levels (p < 0.01), and lower AFTC levels (p < 0.05) in the hypoxaemic group compared to the healthy subjects. In the hypoxaemic group short-term oxygen therapy increased basal AFTC significantly (p < 0.05). With oxygen therapy, the 120-min glucose levels fell significantly from 9.1 +/- 3.2 to 7.6 +/- 2.7 mmol l-1 (mean +/- SD) in the hypoxaemic group (p < 0.05). In conclusion, we have found the serum testosterone and AFTC levels to decrease after an oral glucose load in healthy subjects, together with a compensatory increase in LH. The same pattern is seen in COPD patients. The hypoxaemic patients have a reduced AFTC which is partly reversed by oxygen therapy.

Aged↗
PubMed1996

Impaired glucose tolerance in patients with chronic hypoxic pulmonary disease.

This study investigated glucose metabolism and glucose-mediated hormone responses in patients with chronic respiratory hypoxaemia. Glucose as well as insulin, glucagon, adrenaline, cortisol and growth hormone (GH) were measured before and at 30, 60 and 120 min during an oral glucose-tolerance test. The following chronic obstructive pulmonary disease (COPD) patients were studied: 10 normoxaemic (mean paO2 10.9 +/- 0.4 kPa), 10 hypoxaemic (mean paO2 7.6 +/- 0.2 kPa before, and 10.6 +/- 0.4 after 24-h oxygentherapy, and 6 hypoxaemic patients on long-term oxygen therapy (LTOT) (mean paO2 10.9 +/- 0.7 kPa before, and 7.1 +/- 0.3 after 4 h with less than 0.5 litre oxygen per minute). The hypoxaemic patients were tested both with and without (or reduced) oxygen therapy. Twenty healthy sex- and age-matched subjects served as controls. Plasma glucose at 120 min was significantly higher in LTOT patients than in controls (p < 0.01), normoxaemic patients (p < 0.01) or hypoxaemic patients (p < 0.01). The areas under the curve for plasma glucose and insulin were significantly higher in both the LTOT and hypoxaemic groups compared to controls (p < 0.01 and 0.05, respectively). Glucose values for normoxaemic COPD patients were similar to those for controls. Glucagon, adrenaline, cortisol and GH levels did not differ significantly between the groups. A 4-h low-dose or oxygen-free interval in the LTOT group or 24 h of oxygen supplementation in the hypoxaemic group did not affect glucose and hormone levels significantly. It is concluded that severely hypoxaemic COPD patients have altered glucose metabolism which cannot be readily explained by changes in gluco-regulatory hormones or short-term alterations in oxygenation.

Aged↗
PubMed1996

Autonomic nervous system function in rheumatoid arthritis. A controlled study.

OBJECTIVE: To study cardiovascular autonomic nervous functions in patients with rheumatoid arthritis (RA) compared with controls and to investigate fasting and meal stimulated pancreatic polypeptide (PP) in RA and its possible associations with autonomic functions and disease activity. METHODS: Forty-three women meeting the American Rheumatism Association 1987 diagnostic criteria for RA and 61 healthy controls were studied. Blood pressure recordings and cardiovascular heart rate studies were performed. PP was measured by radioimmunoassay. RESULTS: Cardiovascular reflexes were equal in the 2 groups, but the patients had significantly higher fasting plasma PP level with mean log10 value of 0.94 pmol/l (SD = 0.38) compared with 0.68 pmol/l (SD = 0.35) in the controls (p = 0.0006). Mean log10 plasma PP increase 30 min after the meal was 1.80 pmol/l (SD = 0.42) for the patient group and 1.47 pmol/l (SD = 0.40) in the controls (p = 0.0001). Feeding caused a mean PP increase of 1.85 (SD = 0.42) for the patients and 1.44 (SD = 0.42) in the controls 60 min postprandially (p = 0.0001). Multiple regression and correlation analysis showed no association between PP and disease activity. CONCLUSION: The higher basal and postprandial PP in the RA group indicates a relationship between the disease and PP by unknown mechanisms.

Adolescent↗
PubMed1995

[Osteoporosis drugs prescribed on blue forms!].

The National Insurance Administration, through the system of blue prescription forms, refunds part of the cost of drugs used to treat a number of chronic diseases. To obtain a refund, the indication for prescribing the drug must be included in the list of diagnoses which entitle a refund through the system. The list is a long one, and costs are refunded for prophylactic drugs (e.g. against hypertension and hypercholesterolemia), drugs to alleviate symptoms (e.g. for certain skin diseases and heart failure) and curative measures. The qualitative criteria for a refund, over and above the diagnosis, are not precisely defined, and doctors are free to choose the drug they prefer, regardless of price. The authors discuss whether the list of diagnoses should be extended to include osteoporosis, and recommend that doctors should be able to prescribe the relevant preventive and palliative drugs on a blue form. Many think that this refund system is a good initiative.

Aged↗
PubMed1995

Dysfunction in the beta 2-adrenergic signal pathway in patients with insulin dependent diabetes mellitus (IDDM) and unawareness of hypoglycaemia.

The majority of the impaired symptoms in hypoglycaemia unawareness, such as palpitations, tachycardia and tremor, are caused by increased release of adrenaline (ADR) and noradrenaline (NA), and induced by stimulation of beta-adrenergic receptors. Binding of ADR or NA to the beta-adrenergic receptor generates a signal, transmitted via a guanine nucleotide binding protein complex (G-protein), which in turn activates adenylate cyclase with increased production of cAMP. The aim of this study was to show whether IDDM-patients with hypoglycaemia unawareness had deficient coupling between beta2-adrenergic receptors and G-proteins compared to IDDM-patients with hypoglycaemia unawareness and healthy controls. The IDDM-patients were subgrouped as hypoglycaemia aware or unaware based on questionnaire answers, clinical information and the results of isoprenaline sensitivity tests. Mononuclear leukocytes (MNL) were isolated from venous blood. By saturation binding experiments, using [125I]-(-)-iodopindolol ((-)-IPIN), total receptor number (Bmax) and affinity (Kd) were determined. By displacement experiments the relative number of low- and high-affinity receptors for the beta-adrenergic agonist (-)-isoprenaline ((-)-ISO) were determined. We found no difference in Bmax- or Kd-values. for (-)-IPIN between the subgroups. However, there was a reduced capability to form high-affinity binding complexes with (-)-ISO in MNL from IDDM-patients with hypoglycaemia unawareness. It was concluded that hypoglycaemia unawareness in IDDM was associated with dysfunction of the proximal beta2-adrenergic signal pathway.

Adrenergic beta-Agonists↗
PubMed1995

Short-term treatment of Graves' disease with methimazole in high versus low doses.

OBJECTIVES: To compare the relapse rates in Graves' disease the first 2 years after methimazole 60 mg day-1 combined with thyroxine versus a titration regimen with methimazole alone, and to look for possible prognostic factors. DESIGN: A randomized, open, prospective study. Methimazole was given for 6 months in both groups, and thyroid status evaluated every 3rd month during the first year, and every 6th month during the second year. SETTING: The study was performed at our outpatient clinic with patients referred from primary care. SUBJECTS: Fifty-six patients were included. One became pregnant and one dropped out during the treatment period. Furthermore, nine patients in the high-dose and four in the low-dose group stopped the treatment because of side-effects. Thus, 19 patients in the high- and 22 in the low-dose group completed 6 months with methimazole. RESULTS: In those tolerating the treatment, the relapse rates in the high- and low-dose groups were 26.3 vs. 59.1% (P < 0.05), 42.1 vs. 77.3% (P < 0.02); and 57.9 vs. 77.3% (NS) after 3, 12 and 24 months, respectively. The corresponding relapse rates calculated on an 'intention to treat' basis were: 51.7 vs. 66.7%; 62.1 vs. 81.5%: 72.4 vs. 81.5% (NS). The thyroid volume was significantly (P < 0.05) larger in those that relapsed (17.8 +/- 2.9 vs. 11.6 +/- 1.2 mL; mean +/- SEM). CONCLUSIONS: In those tolerating the treatment, methimazole significantly reduced the relapse rate the 1st year when given in a high dose. However, the relapse rates in both groups, and the number of side-effects in the high-dose group, were unacceptably high.

Adult↗
PubMed1995

Reduced beta-adrenergic sensitivity in healthy volunteers induced by hypoglycemia.

A single causative mechanism for development of hypoglycemia unawareness in insulin-dependent diabetes mellitus (IDDM) is not yet apparent. Reduced adrenergic sensitivity may be part of the explanation. This study was carried out to investigate the effect of hypoglycemia on beta-adrenergic sensitivity. Ten healthy male subjects (age 19-23 years) gave informed consent to take part in the study. They were hospitalized overnight at the University Hospital of Tromsø, Department of Clinical Research, on two occasions. Isoprenaline and metoprolol sensitivity tests were performed the morning after hospitalization: once after an intravenous (iv) injection of placebo (0.9% NaCl), and once after an iv injection of insulin (0.15 IU insulin/kg body weight) to induce hypoglycemia. The dose of isoprenaline needed to increase heart rate (HR) by 25 beats per minute (bpm) (I25), and the dose of metoprolol (M-12.5) needed to inhibit I25 with 50% or 12.5 bpm, when injected simultaneously, were used as determinants of isoprenaline and metoprolol sensitivity. In this study, there was a significant (p < 0.05) increase both in I25 and M-12.5 after hypoglycemia. The dose-response curve of isoprenaline/HR was significantly shifted to the right after hypoglycemia. This study shows that acute hypoglycemia induces a reduction in beta-adrenergic sensitivity, and it supports the hypothesis of reduced beta-adrenergic sensitivity as an important pathophysiological mechanism in hypoglycemia unawareness in IDDM.

Adult↗
PubMed1995

Estimation of glucose-alanine-lactate-glutamine cycles in postabsorptive humans: role of skeletal muscle.

To evaluate transfer of carbon between plasma glucose and plasma alanine (glucose-alanine cycle) and lactate (Cori cycle), to assess the contribution of skeletal muscle to these cycles, and to determine whether a glucose-glutamine cycle exists in postabsorptive humans, we infused 11 normal overnight-fasted volunteers with [2-3H]glucose, [6-14C]glucose, and [3-13C]alanine to isotopic steady state and in 7 of these simultaneously measured forearm net balance, uptake, and release of labeled and unlabeled glucose, lactate, and alanine. We found that 40.9 +/- 3.3, 66.8 +/- 3.2, and 13.4 +/- 1.1%, respectively, of plasma alanine, lactate, and glutamine carbon came from plasma glucose. More plasma glucose was converted to plasma alanine than could be derived from plasma alanine (1.89 +/- 0.20 vs. 1.48 +/- 0.15 mumol.kg-1.min-1, P < 0.001). A similar direction of net carbon flux was found for lactate (8.5 vs. 4.2 mumol.kg-1.min-1), with only glutamine adding more carbon to plasma glucose than was received from it (1.0 vs. 0.75 mumol.kg-1.min-1). Skeletal muscle accounted for 50.2 +/- 3.9 and 45.5 +/- 5.7% of the overall appearance of alanine and lactate in plasma and 54.2 +/- 5.4 and 36.4 +/- 4.2% of their respective origins from plasma glucose. Skeletal muscle release of alanine and lactate that had been formed from plasma glucose accounted for 19.1 +/- 2.1 and 48.4 +/- 4.8%, respectively, of muscle glucose uptake and 42.4 +/- 5.5 and 49.9 +/- 5.8% of the overall release of alanine and lactate from muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of naloxone on glucagon and insulin concentrations after injection of endotoxin in rats.

OBJECTIVE: To find out how infusions of endotoxin and endotoxin plus naloxone affected glucose, glucagon, and insulin concentrations in rats. DESIGN: Random control study. SETTING: University hospital, Norway. MATERIAL: 27 Male Wistar rats. INTERVENTIONS: 8 Rats were given Escherichia coli endotoxin 0.25 mg in saline; 5 were given a naloxone infusion (0.4 ml of 0.04 mg/ml for the first half hour and continued at a rate of 0.4 ml/hour for a total of 80 minutes) starting 10 minutes before the same dose of endotoxin; 6 were given saline alone for 70 minutes, and 8 saline alone for 10 minutes. Blood was taken for analysis after 70 minutes in the first three groups and at the end of the infusion in the 10 minute group. MAIN OUTCOME MEASURES: Serum concentrations of glucose, glucagon, and insulin compared with baseline (10 min group). RESULTS: Median (interquartile) concentrations of all three substances rose significantly 70 minutes after the injection of endotoxin compared to basal values: 9.8 (8.2-10.9) compared with 6.0 (4.8-7.5) mmol/l for glucose (p < 0.01); 53.1 (44.6-56.0) compared with 3.6 (3.1-5.1) ng/l for glucagon; and 39.4 (38-50.4) compared with 16.7 (11.2-25.5) pmol/l for insulin. When naloxone was combined with endotoxin glucagon and insulin concentrations were significantly lower: 24.3 (23.9-37.5) ng/l (p < 0.01), and 30.6 (24.5-31.6 pmol/l (p < 0.05), respectively. The concentration of glucose in venous blood was unchanged. CONCLUSIONS: The rise in glucagon and insulin concentrations after endotoxin infusions may be partly mediated by opioids. Naloxone in the dose given did not abolish the increase in glucagon after endotoxin. The high glucagon:insulin ratio after both endotoxin alone and endotoxin plus naloxone may be important in the aetiology of the hyperglycaemia seen.

Animals↗
PubMed1994

Reduced sensitivity to beta-adrenoceptor stimulation and blockade in insulin dependent diabetic patients with hypoglycaemia unawareness.

Nine IDDM-patients with hypoglycaemia unawareness, seven IDDM-patients with hypoglycemia awareness and a control group of nine healthy persons were included in this study. The patients were recruited from the medical out-patients' department of the University Hospital of Tromsø. The pathophysiological changes which cause hypoglycaemia unawareness are today not clear. Reduced peripheral tissue sensitivity to catecholamines is suggested as one of several mechanisms which may contribute. For further investigation of beta-adrenergic sensitivity an isoprenaline/metoprolol sensitivity test was performed. Isoprenaline and metoprolol were administered intravenously, and the effects on heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and plasma levels of adrenaline (ADR) and noradrenaline (NA) were measured. All subjects were given the same doses of isoprenaline (0.25-8 micrograms) and metoprolol (0.5-8 mg). Metoprolol was given together with the dose of isoprenaline which increased heart rate by 25 beats min-1. The dose/response curves of both isoprenaline/HR and metoprolol/HR were significantly shifted to the right in IDDM-patients with hypoglycaemia unawareness compared with controls and IDDM-patients with hypoglycaemia awareness (P < 0.05). Reduced sensitivity of isoprenaline stimulation has also been shown before, whereas reduced sensitivity of a blocking agent has not earlier been shown. These findings support the hypothesis of reduced beta-adrenergic sensitivity as one pathophysiological component in hypoglycaemia unawareness.

Adult↗
PubMed1994

Autonomic function in systemic lupus erythematosus.

A controlled study with paired analysis of data was performed in 34 patients with systemic lupus erythematosus (SLE) and 34 age and sex-matched healthy controls. Autonomic function was not affected significantly in SLE patients as judged by standardised cardiovascular tests. Pancreatic polypeptide (PP) response to meal stimulation, which is impaired in parasympathetic failure, was for unknown reasons found to be significantly increased in SLE patients both in unstimulated and stimulated states. Neither cardiovascular nor serological tests could thus reveal significant autonomic dysfunction in SLE. Drugs with cardiovascular effects highly influenced autonomic function and could thus be misinterpreted as autonomic dysfunction caused by SLE itself.

Adolescent↗
PubMed1994

Increased plasma glucose levels after Hypnorm anaesthesia, but not after Pentobarbital anaesthesia in rats.

The effects of the fentanyl fluanisone combination (Hypnorm) and pentobarbitone sodium (Pentobarbital) anaesthesia on blood glucose, insulin and glucagon were tested in rats in the fed and fasted state. Blood glucose was measured before and at 10, 20 and 30 min after injection of the anaesthetic agents. At 30 min the rats were sacrificed, and blood was drawn for measurement of glucagon and insulin. Pre-anaesthetic values for insulin and glucagon were established in separate groups of fasted and fed rats. In fasting rats given Hypnorm, blood glucose and plasma insulin were unchanged while there was a non-significant increase in plasma glucagon. The fasted rats given Pentobarbital had unchanged blood glucose and plasma insulin and a non-significant depression of glucagon. The fed rats given Hypnorm had a significant increase in blood glucose at 10 min and nearly a doubling of glucose values at 20 and 30 min (P < 0.001). Glucagon increased far less than in the fasted group, whereas insulin was doubled from preanaesthetic values (P < 0.05). The fed rats given Pentobarbital, had unchanged blood glucose, a slight non-significant depression of glucagon and a significant increase in insulin (P < 0.01). Thus Hypnorm induced hyperglycaemia in fed but not in fasted rats, probably because more glucose was available in the fed state. Fed animals are a modification of the standard fasted animal model, and may be preferable when exploring hyperglycaemic or other reactions to anaesthetic agents.

Anesthesia↗
PubMed1994

Haemorrhage-induced increases in glucose, glucagon and insulin levels are blocked by naloxone in rats.

OBJECTIVE: To find out if the opioids that are liberated during bleeding influence the concentrations of glucagon, insulin, somatostatin, corticosterone and glucose in rats, and if naloxone has any regulatory effect. DESIGN: Laboratory study. SETTING: University hospital. MATERIAL: 56 Male Wistar rats. INTERVENTIONS: Removal of blood corresponding to 2% of body weight through a catheter in the internal jugular vein. Before bleeding (n = 8), and at 5, 15 and 30 minutes afterwards (n = 16 at each time point, half of which had received naloxone 0.04 mg/ml, 0.7 ml/hour, for 10 minutes before bleeding and up to 30 minutes afterwards) rats were killed and samples of heart blood taken. MAIN OUTCOME MEASURES: Concentrations of glucose, glucagon, insulin, somatostatin, and corticosterone in heart blood. RESULTS: In the control group (saline) concentrations of glucose, glucagon and insulin increased significantly after bleeding, and had returned to baseline concentration by 30 minutes. Naloxone blocked the increases in the treated group. CONCLUSION: Endogenous opioids, possibly endorphin, may be important in the acute regulation of blood glucose, glucagon and insulin concentrations after haemorrhage.

Animals↗
PubMed1994

Glycemic thresholds for hypoglycemic responses in obese subjects.

The objective of this study was to compare glycemic thresholds for hypoglycemic responses in obese and control subjects. A modified glucose-clamp technique was used to produce a standardized fall in plasma glucose (0.5 mmol/l per 40 min) in nine morbidly obese and ten control subjects. The release of the counter-regulatory hormones was measured and a symptom questionnaire was filled out every 10 min. The hypoglycemic thresholds (taken as the plasma glucose level where the response exceeded the basal level +2 s.d.) were practically identical in the two groups both for the hormones and the symptoms (including hunger). Our results argue against the hypothesis that an increased sensitivity to a falling plasma glucose is of importance in the pathogenesis of obesity.

Adult↗
PubMed1993

Comparison of the modifying effects of somatostatin and propranolol on morphine-induced changes in glucose, glucagon and insulin levels in fed rats.

Twenty-eight rats in four different groups were used. Catheters were implanted in the carotid artery and jugular vein one week before the experiments were performed. The rats were trained to the experimental situation daily, and allowed food and water ad libitum. One group of rats was used to establish control values; a second was injected with morphine (10 mg/ml, 1 ml/kg); a third group got morphine injection (10 mg/ml, 1 ml/kg) combined with somatostatin infusion (0.01 mg/ml, 1 ml/h); and the fourth group was injected with morphine (10 mg/ml, 1 ml/kg) combined with propranolol (0.4 ml, 1 mg/ml). Blood samples for venous glucose and arterial insulin and glucagon were drawn 15 min after start of stimulation. Glucose, insulin and glucagon levels were significantly higher in morphine treated than in control rats. When morphine was combined with somatostatin, the increase in glucose, insulin and glucagon was significantly reduced. However, after the morphine and propranolol stimulation the increase in glucose and glucagon was significantly reduced, whereas the insulin levels were as high as when morphine was given alone. The combined reduction of both glucagon and glucose after somatostatin or propranolol treatment in morphine exposed rats, points to glucagon as a potential link between opioid stimulation and hyperglycemia. Beta-receptor stimulation seems to contribute to the glucagon but not to the insulin release after morphine.

Animals↗
PubMed1993

Morphine and morphine/naloxone modification of glucose, glucagon and insulin levels in fasted and fed rats.

In rats weighing 200-250 g catheters were placed in the internal jugular vein and carotid artery. After 1 week of accommodation the training for the experimental situation, morphine (10 mg kg-1) was injected intravenously alone or in combination with naloxone (0.04 mg ml-1, 0.8 ml h-1). Otherwise no form of anaesthesia was used during the experiments. In control fed and fasted rats, there were no significant differences in blood glucose. In fed rats, morphine increased blood glucose as compared to control rats (p < 0.001). This was not seen in the fasted rats. The morphine induced increase in blood glucose in the fed rats was abolished by naloxone (p < 0.001). Glucagon was significantly higher in fasted than in fed control rats (p < 0.01). It was significantly increased after morphine in fed (p < 0.05), but not in fasted rats. The morphine induced increase in glucagon in fed rats was abolished by naloxone (p < 0.01). Insulin was significantly higher in fed than in fasted control rats (p < 0.05). Morphine increased insulin levels significantly in fed and fasted rats (p < 0.001), p < 0.01). The morphine induced increase in insulin in the fed rats was abolished by naloxone treatment. It is concluded that morphine stimulates glucose and glucagon release in fed but not fasted rats, and that these increases are caused by opioid action. Insulin increases after morphine were proved to be opioid-mediated only in the fed state.

Animals↗