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Biomedical subjects

H Orskov

Publications and source records attributed to H Orskov.

At least 235 records · Page 13Linked to original sources
PubMed1982

Acetate suppresses growth hormone secretion in uremic patients: hemodialysis and acetate infusion experiments.

Growth hormone secretion in uremic patients is completely suppressed immediately after initiation of and during hemodialysis using acetate dialysate. The present study demonstrates that growth hormone secretion stimulated by arginine is also inhibited by hemodialysis. Acetate infusion experiments proved that the high blood acetate level obtained during dialysis is at least partly responsible for this growth hormone suppression by unknown mechanisms.

Acetates↗
PubMed1982

Plasma arginine-vasopressin, renal-concentrating ability and lithium excretion in a group of patients on long-term lithium treatment.

Plasma arginine-vasopressin (AVP) was measured before and after 24 h of a 26-hour renal concentration test in 47 patients treated with lithium for 6-180 months (mean 70 months). In 34 of the patients, plasma AVP was also measured before and after a 2- to 4-hour period of water loading, and in 31 of the patients, creatinine, 125iothalamate, 131I-hippuran and lithium clearances were measured. Plasma AVP values were compared to those obtained in 8 healthy controls. Baseline AVP levels were significantly higher in the lithium-treated patients than in healthy controls. During the period of water deprivation AVP values increased significantly and during oral water loading a significant decrease took place, AVP values still being significantly higher in the lithium-treated patients than in the healthy controls. During oral water loading a slight increase in lithium clearance as well as fractional lithium excretion was seen as compared to values obtained during the last 2 h of a renal concentration test. This study demonstrates that antidiuretic hormone production is neither blocked nor inhibited during lithium treatment. The hypothalamic system reacts on water deprivation as well as on water loading. This study supports the notion that the main lithium-induced renal affection is a vasopressin-resistant impairment of renal concentrating ability.

Adult↗
PubMed1982

Low cerebrospinal fluid somatostatin in Parkinson disease: an irreversible abnormality.

In 39 parkinsonian patients, CSF somatostatin content was 88.0 +/- 4.1 pg per milliliter, which was about 40% less than in controls (147.3 +/- 5.1 pg per milliliter). Somatostatin values were unrelated to age, sex, body weight, total CSF protein, immunoglobulin, or cell count in either group. Parkinsonian values were not related to duration of disease, severity, specific signs, or treatment. In contrast to multiple sclerosis, in which CSF somatostatin is low only during relapses, the low somatostatin content of CSF in Parkinson disease seems to be irreversible, to be present at the onset of symptoms, and to imply an irreparable functional or structural alteration of somatostatin-secreting neurons.

Adult↗
PubMed1982

Acetate: inhibitor of growth hormone hypersecretion in diabetic and non-diabetic uraemic subjects.

Five diabetic and 14 non-diabetic uraemic patients on long-term haemodialysis were studied during twenty-one 24 h periods including 5 to 7 h of haemodialysis against glucose-free acetate buffered dialysis fluid. Half-hourly blood samples were collected for hormonal and metabolite analysis. In addition, blood samples were analyzed in 40 experiments covering the haemodialysis and a pre-dialysis period. Before dialysis, plasma growth hormone levels were high and fluctuating, but almost always fell to low normal values within the first 2 h of haemodialysis. In the diabetic uraemic patients, the occasional severe hypoglycaemic episodes occurring during haemodialysis did not provoke growth hormone release, and hypoglycaemic reactions were not encountered. Intravenous acetate infusion studies resulted in plasma concentrations ranging from 1.3. to 2.7 mmol, ie. about 60 per cent of the levels reached during haemodialysis and in suppression of growth hormone secretion. It is suggested that the fall in growth hormone levels and the lack of hypoglycaemic symptoms during haemodialysis is due to the use of acetate as a fuel in brain.

Acetates↗
PubMed1982

Insulin-induced choleresis in relation to insulin concentrations in plasma and bile in the cat.

In experiments on fasting, chloralose-anesthetized cats the concentrations of insulin and glucagon in arterial or portal plasma and bile were studied during insulin-induced choleresis. The administration of insulin in single doses (0.1-1.0 U x kg-1) and infusions (0.001-0.01 U x kg-1 x min-1) resulted in parallel increases in bile flow and 14C-erythritol clearances of 17%-96%, whereas the net ductular fluid transport and the biliary excretion rate of bile acids remained unchanged. Insulin therefore stimulated the bile acid-independent fraction of the canalicular bile formation. When corrected for the hepatic transit time of insulin (25 min) the initial phase of insulin choleresis was closely related in time to the plasma (30-5000 microunits x ml-1) and biliary (40-210 microunits x ml-1) concentrations of insulin. Bile flow was stimulated even at plasma insulin concentrations similar to those seen postprandially. It is concluded that insulin-induced choleresis to a great extent can be explained by direct, hepatic actions of the hormone, but a delayed release of glucagon may be of importance for the terminal phase of insulin choleresis. The results also demonstrate that insulin crosses the liver by an intercellular pathway. This mode of transport could be of importance for its action on bile production.

Animals↗
PubMed1982

Transient triiodothyronine deficiency. Absence of effect on basal or adrenaline-stimulated carbohydrate and lipid metabolism in man.

Severe stress is accompanied by a fall in circulating triiodothyronine levels as well as increases in secretion of several hormones including adrenaline. The present study was designed to test the hypothesis that the fall in triiodothyronine may counteract in part the catabolic effects of stress hormones such as adrenaline. Transient hypothyroidism was induced by administration orally of sodium ipodate (3 g). Adrenaline infusions (6 micrograms/min for 2 hours) were performed in five healthy men before and four days after ipodate was given. Circulating triiodothyronine levels decreased from 1.7 +/- 0.1 to 1.1 +/- 0.1 nmol/l (p less than 0.001), associated with a small rise in serum thyroxine, but basal circulating concentrations of glucose, the gluconeogenic precursors, NEFA and 3-hydroxybutyrate were unaltered. Circulating insulin, glucagon and growth hormone concentrations were also similar with and without prior ipodate ingestion. Adrenaline infusion produced a rise in blood glucose (4.9 +/- 0.2 to 8.5 +/- 0.4 mmol/l at 60 min), lactate, pyruvate and the lactate: pyruvate ratio, which was unaltered by ipodate. Blood glycerol (0.04 +/- 0.004 to 0.13 +/- 0.03 mmol/l at 30 min), plasma NEFA (0.52 +/- 0.05 to 1.31 +/- 0.17 mmol/l at 30 min) and blood 3-hydroxybutyrate concentrations (0.04 +/- 0.004 to 0.26 +/- 0.07 mmol/l at 50 min) were elevated by adrenaline, with similar responses obtained after ipodate. Ipodate also did not influence the circulating insulin and glucagon response to adrenaline infusion. A transient decrease in circulating triiodothyronine concentrations induced by ipodate does not modulate the hormonal and metabolic response to adrenaline in normal man.

3-Hydroxybutyric Acid↗
PubMed1982

Inhibition of arginine- and hypoglycemia- induced growth hormone release by acetate in dialyzed patients.

We have previously demonstrated that acetate suppresses the basal hypersecretion of growth hormone in diabetic and non-diabetic uremic patients. The present study was designed to clarify the potency and characteristics of the growth hormone suppressive effect of acetate by applying two powerful growth hormone stimuli: arginine infusion and insulin hypoglycemia. In four non-diabetic uremic and three diabetic uremic subjects, arginine infusion caused a rise in plasma growth hormone to 22.8 +/- 3.3 ng/ml and 22.0 +/- 5.6 ng/ml (mean +/- SEM, P less than 0.05). During hemodialysis against acetate buffered dialysis fluid and during a simultaneous acetate infusion, the response to arginine infusion was almost completely inhibited in both groups. In four uremic subjects insulin hypoglycemia elicited an increase in plasma growth hormone to 30.0 +/- 7.0 ng/ml (mean +/- SEM, P less than 0.05). During hemodialysis and acetate infusion the response to insulin hypoglycemia was again almost abolished. The glucagon and insulin responses were unaffected by hemodialysis as well as by acetate infusion. The results demonstrate the high degree of efficiency of the acetate induced growth hormone suppression comparable to that of glucose.

Acetates↗
PubMed1981

Very early changes in circulating T3 and rT3 during development of metabolic derangement in diabetic patients.

Alterations in circulating iodothyronines were studied in 15 juvenile type diabetic patients during the development of metabolic derangement after withdrawal of insulin. By means of measurements of circulating C peptide, one group of patients with and one without residual beta-cell function had been selected. In both groups there was a gradual decrease in serum T3 during the 12-hour period studied after withdrawal of insulin, while an increase in serum rT3 was observed after 4-6 hours. The alterations in serum T3 and the metabolic derangement were significantly more pronounced in patients without than with residual beta-cell function.

C-Peptide↗
PubMed1981

Dopaminergic control of ketogenesis in fasting.

The role of dopamine in starvation ketonaemia was investigated in male Wistar rats by administration of a specific dopamine receptor antagonist, metoclopramide (4 mg . kg-1 . 24h-1), or placebo, intragastrically during a 48-h fast. Starvation alone caused a fall in blood glucose and gluconeogenic precursor concentrations, which was unaffected by metoclopramide administration. Circulating 3-hydroxybutyrate and acetoacetate levels rose with fasting alone but metoclopramide impaired this ketonaemic response. After 48-h starvation, total ketone body concentrations (mean +/- SEM) were 2.28 +/- 0.19 mmol/l with metoclopramide therapy, 3.49 +/- 0.21 mmol/l with placebo, P less than 0.001. Plasma non-esterified fatty acid levels were similar in metoclopramide- and placebo-treated animals, as were circulating concentrations of insulin, glucagon and growth hormone. Metoclopramide thus decreased the ketonaemic response to starvation without an apparent change in lipolysis or circulating hormone levels, suggesting a direct role for dopamine in production of starvation ketonaemia.

Animals↗
PubMed1981

Diurnal hormone-metabolite profiles in hypothyroidism.

To investigate the influence of thyroid hormones on intermediary metabolism in man, hormone and metabolite profiles were obtained over a 12-h period of normal meals and activity in eight hypothyroid subjects before and during thyroxine replacement therapy, and in sixteen matched controls. The fasting blood glucose concentration and the mean 12-h blood glucose concentration were normal in hypothyroid subjects but the blood glucose response to breakfast was exaggerated. Fasting blood lactate and pyruvate levels were normal but post-prandial hyperlactataemia and hyperpyruvicaemia were found and mean 12 h values for lactate (hypothyroid 1.80 +/- 0.06 v. control 0.77 +/- 0.03 mmol/l, P less than 0.01) and pyruvate (0.10 +/- 0.01 v. 0.08 +/- 0.003 mmol/l, P less than 0.01) were elevated. Blood alanine concentrations were elevated only in the evening. Although plasma non-esterified fatty acid levels were normal, fasting blood glycerol levels were decreased (0.06 +/- 0.01 v 0.08 +/- 0.01 mmol/l, P less than 0.001) and this decrease persisted throughout the 12-h period. Blood total ketone body concentrations did not differ from controls, but, as for plasma NEFA and blood glycerol, the normal preprandial rise in concentration was absent. Serum insulin, glucagon and growth hormone concentrations did not differ from control values at any time. Six months of thyroxine (T4) treatment produced a rise in blood glycerol concentration (mean 12 h value during T4 therapy, 0.06 +/- 0.01; before T4 therapy, 0.04 +/- 0.005 mmol/l; P less than 0.01) but not to control values (0.08 +/- 0.01 mmol/l). Concentrations of glucose and other gluconeogenic precursors were unaltered by therapy but the insulin response to meals and the mean 12 h serum insulin concentration were increased.

Acetoacetates↗
PubMed1981

Kidney function and size in normal subjects before and during growth hormone administration for one week.

Kidney function and size were studied in seven normal male subjects before and after administration of highly purified human growth hormone for 1 week. Glomerular filtration rate, renal plasma flow (steady-state infusion technique with urinary collections using 125I-iothalamate and 131I-hippuran) kidney size (ultrasonic scanning) and urinary excretion rates of albumin and beta 2-microglobulin (radioimmunoassays) were measured. Highly purified growth hormone was injected subcutaneously, 2 IU in the morning and 4 IU in the evening. Glomerular filtration rate increased from (mean +/- SEM) 114 +/- 5 to 125 +/- 4 ml/min x 1.73 m2 (P less than 0.01) and renal plasma flow increased from 554 +/- 30 to 601 +/- 36 ml/min x 1.73 m2 (P less than 0.01). Kidney size and urinary excretion rates of albumin and beta 2-microglobulin did not change significantly. Our results show that raising plasma growth hormone into a range similar to that found in insulin-dependent diabetics enhances glomerular filtration rate and renal plasma flow, while kidney size remains unchanged. Increased renal plasma flow is the major determinant of growth hormone induced elevation in glomerular filtration rate. Growth hormone may thus contribute to the enhancement of glomerular filtration rate and renal plasma flow typically found in insulin-dependent diabetics.

Adult↗
PubMed1981

The origin of cerebrospinal fluid somatostatin: hypothalamic or disperse central nervous system secretion?

The present study deals with the origin of somatostatin in cerebrospinal fluid. Two groups of experiments were performed: (1) Diagnostic lumbar puncture was performed in 37 patients admitted for various neurological diseases. Immunological determination of albumin and gamma-globulin, and radioimmunological analysis of somatostatin in successive cerebrospinal fluid taps demonstrated that while the protein concentration was approximately 20% lower in the 11th ml compared to the 1st ml drawn, the somatostatin concentration was constant. (2) Intravenous arginine infusion (30 G/30 min) induced identical patterns of plasma growth hormone in 8 patients with multiple sclerosis in relapse, in 6 patients with multiple sclerosis in the stable phase, and in 7 patients in whom no neurological disease was eventually diagnosed. Cerebrospinal fluid somatostatin was significantly lower in the patients with multiple sclerosis in relapse than in the two other groups, while cerebrospinal fluid growth hormone concentration was identical. There was no correlation between basal or arginine provoked plasma growth hormone and the cerebrospinal fluid content of somatostatin. The results indicate that cerebrospinal fluid somatostatin is released dispersely from the central nervous system including the spinal cord - and that it offers no indication of the activity or tone of hypothalamic growth hormone release inhibiting control of the pituitary gland.

Adult↗
PubMed1981

Release of somatostatin-like immunoreactivity from the perfused canine thyroid. Selective stimulatory effect of calcium ions.

It is well accepted that the C cells of the thyroid contain somatostatin, but the role in local endocrine function has not yet been firmly established in this organ, and it has not been proved that thyroidal somatostatin is released into the circulation. We have measured the contents of somatostatin-like immunoreactivity in the effluent of canine thyroid glands perfused without recirculation with a synthetic buffer medium. During basal conditions a definite release was consistently found in the order of 10 pg/ml corresponding to 12 pg/min. The somatostatin-like immunoreactivity was studied in dilution experiments and by gel-filtration chromatography, and found to have properties identical to those of synthetic cyclic somatostatin, which was also recovered quantitatively when added to sampling tubes. Various compounds were infused in concentrations that are highly active in pancreas perfusion experiments. 14-min infusion of arginine, 5 and 11.5 mmol/liter; isoproterenol, 10 and 23.7 nmol/liter and 68.7 mumol/liter; acetylcholine, 5 mumol/liter, carbamylcholine, 10 and 100 mumol/liter; glucagon, 1 and 30 nmol/liter; and porcine calcitonin, 1 and 100 ng/ml did not affect the basal release of somatostatin-like immunoreactivity significantly. Neither did an increase from the control level of 4 mmol/liter glucose of 10 or 20 mmol/liter, nor an increase in the control level of 4.4 mmol/liter K+ to 7.5 or 14.4 mmol/liter. Each of these compounds were tested in three or four dogs. The effect of an increase in Ca++ from the control level of 1.5 mmol/liter to 2.25, 3.0, and 4.5 mmol/liter was tested in random order in five thyroid lobes. All three doses elicited an immediate increase in effluent somatostatin-like immunoreactivity. In most experiments the response was biphasic with an early spike, followed by a stable level that was maintained during prolonged Ca++ infusion. The secretory response was not diminished through a series of repeated short pulses of calcium infusion. The response to 3.0 mmol/liter Ca++ (control period 8.4 +/- 1.5, test period 337 +/- 110 pg/ml, mean +/- SE) and 4.5 mmol/liter Ca++ (control period 9.5 +/- 1.4, test period 386 +/- 125) were significantly higher than 2.25 mmol/liter Ca++ (control period 7.2 +/- 1.0 test period 140 +/- 39), while there was no significant difference between responses to the two high doses. Infusion of salmon calcitonin, 10 ng/ml and 1 microgram/ml; or porcine calcitonin, 1 microgram/ml during calcium stimulation (2.25 mmol/liter of Ca++) did not induce alterations in the release of somatostatin-like immunoreactivity. The results demonstrate that thyroidal somatostatin is mobilizable, and it appears to be selectively sensitive to calcium stimulation, indicating a possible role in calcitonin release control.

Animals↗
PubMed1980

Hyperglucagonaemia in cirrhosis. Relationship to hepatocellular damage.

Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 +/- 0.1 mmol/l VS control 3.4 +/- 0.1 mmol/l (mean +/- SEM); glucagon 57.5 +/- 9.1 pg/ml VS control 51.3 +/- 7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3 +/- 0.2 mmol/l VS control 3.4 +/- 0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3 +/- 61.1 pg/ml VS control 51.3 +/- 7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portal-systemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.

Adolescent↗
PubMed1980

The significance of the Na+/K+ pump for somatostatin release.

The influence of the Na+/K+ pump on somatostatin secretion from the isolated perfused canine pancreas was investigated. The somatostatin secretion was reversibly increased in response to addition of ouabain (10(-5) mol/l) and to omission of extracellular K+, procedures which are known to cause a blockade of the Na+/K+ pump. The stimulatory effect on somatostatin release was abolished during calcium depletion. The results suggest that the operation of the Na+/K+ pump plays an important role for the somatostatin secretion. The action of the Na+/K+ pump on the secretory function of the D-cells is dependent on the presence of extracellular calcium.

Animals↗
PubMed1980

Low somatostatin content in cerebrospinal fluid in multiple sclerosis. An indicator of disease activity?

In 27 patients with multiple sclerosis (MS), and in 10 control subjects of comparable age, percent ideal body weight and sex ratio, the cerebrospinal fluid (CSF) content of somatostatin was measured by radioimmunoassay. The results showed that the group of patients in relapse (n = 16) had significantly lower somatostatin content in CSF (95 +/- 4.1 (SEM) pg/ml) than both the control group (142 +/- 8.4 pg/ml) and the group of MS patients (n = 11), who had been in a clinical stable phase for more than 6 months (131 +/- 3.2 pg/ml). Duration of the disease and degree of neurological impairment were apparently without relation to the reduction of somatostatin content in the CSF. There was no relationship between CSF content of somatostatin and the content of total protein or IgG, neither of which showed any relationship to the activity of the disease.

Adult↗