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Biomedical subjects

O Søvik

Publications and source records attributed to O Søvik.

At least 73 records · Page 4Linked to original sources
PubMed1987

Specific insulin binding in bovine chromaffin cells; demonstration of preferential binding to adrenalin-storing cells.

Insulin binding was studied in subpopulations of bovine chromaffin cells enriched in adrenalin-producing cells (A-cells) or noradrenalin-producing cells (NA-cells). Binding of 125I-insulin was carried out at 15 degrees C for 3 hrs in the absence or presence of excess unlabelled hormone. Four fractions of cells were obtained by centrifugation on a stepwise bovine serum albumin gradient. The four fractions were all shown to bind insulin in a specific manner and the highest binding was measured in the cell layers of higher densities, containing mainly A-cells. The difference in binding of insulin to the four subpopulations of chromaffin cells seemed to be related to differences in numbers of receptors as opposed to receptor affinities. We conclude that bovine chromaffin cells possess high affinity binding sites for insulin and that these binding sites are mainly confined to A-cells.

Adrenal Medulla↗
PubMed1987

Prenatal diagnosis of glycerol-kinase deficiency associated with a DNA deletion on the short arm of the X-chromosome.

Amniocentesis was performed in a woman who previously had given birth to a boy who died at 12 months of age with a diagnosis of glyceroluria and adrenal insufficiency. A high amount of glycerol (9.0 standard deviations above mean for controls) was found in the amniotic fluid. Enzyme activity of glycerol-kinase (ATP:glycerol-3-phosphotransferase, EC 2.7.1.30) in the cultured amniotic fluid cells was very low. The pregnancy was terminated and a male fetus was aborted. Examinations of DNA isolated from the fetus did demonstrate deletions of two out of 16 DNA probes mapping to the short arm of the X-chromosome. The probes failing to hybridize to DNA from the fetus were C7 (DXS28) and L1.4 (DXS68), both mapping to Xp21.3 and located terminal to the Duchenne locus.

Abortion, Induced↗
PubMed1985

Metabolic responses to physical training in young insulin-dependent diabetics.

Insulin-dependent (type 1) diabetics, aged 14-17 years, were studied according to two protocols. During a 6-month training period of moderate intensity (six participants) the aerobic work capacity and the erythrocyte insulin binding increased by 19% and 28%, respectively. Glycosylated haemoglobin (HbA1) was not significantly reduced. A 2-week intensive physical training program (10 participants) was associated with a 50% decrease of blood glucose values, which did not last beyond the training period. Plasma ketone bodies were markedly reduced. We conclude that young type 1 diabetics may participate in strenuous, short-term physical training. The improved aerobic work capacity and increased cellular insulin binding observed during training of moderate intensity is of potential benefit in the long-term management of the patients.

Adolescent↗
PubMed1985

Metabolism of leucine in fibroblasts from patients with deficiencies in each of the major catabolic enzymes: branched-chain ketoacid dehydrogenase, isovaleryl-CoA dehydrogenase, 3-methylcrotonyl-CoA carboxylase, 3-methylglutaconyl-CoA hydratase, and 3-hydroxy-3-methylglutaryl-CoA lyase.

The metabolism of leucine was studied in cultured human fibroblasts derived from patients with defects in each of the major steps in the catabolism of the amino acid. Intact fibroblasts were incubated with [U-14C]leucine and the organic acid products were isolated by liquid partition chromatography. In control fibroblasts the major product of leucine was 3-hydroxyisovaleric acid. This was also the case for fibroblasts with deficiency of 3-hydroxy-3-methylglutaryl-CoA lyase, 3-methylcrotonyl-CoA carboxylase and 3-methylglutaconyl-CoA hydratase. There was little or no accumulation of the compound with fibroblasts from patients with maple syrup urine disease and isovaleric acidemia.

2-Oxoisovalerate Dehydrogenase (Acylating)↗
PubMed1984

A child with acute pancreatitis and recurrent hypoglycemia due to 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.

A five-year-old-girl with a history of recurrent hypoglycemia presented with acidosis, intractable vomiting, and abdominal tenderness; the diagnosis of acute pancreatitis was made by abdominal ultrasonography and supportive biochemical studies. Urinary organic acid analysis revealed metabolites suggestive of HMG-CoA lyase deficiency, and subsequent enzyme assays of lymphocytes and fibroblasts confirmed this diagnosis. Acute pancreatitis, an uncommon condition in childhood, is seen with increased frequency in patients with Reye syndrome, a metabolic disorder with which HMG-CoA lyase deficiency may be confused. The pathogenesis of pancreatitis in Reye syndrome or in HMG-CoA lyase deficiency has not been determined.

Acute Disease↗
PubMed1981

Incidence, age at onset and seasonal variation of diabetes mellitus in Norwegian children, 1973-1977.

A retrospective study was undertaken to estimate the incidence of diabetes mellitus in Norwegian children. Data were collected from all hospitals in the country and from a central insurance register. Eight hundred and forty-five new cases in the age group 0-14 years and with onset in the five-year study period 1973-1977 were detected. The calculated mean annual incidence was 17.6 per 100 000 children, with a year-to-year variation of 15.4-19.3 per 100 000. The geographic variation in incidence was considerable with the lowest rate in the North (6.8/100 000/year) and the highest rates in the South-Eastern part of the country (approx. 20/100 000/year). There was a significantly higher incidence for boys (18.8/100 000/year) than for girls (16.4/100 000/year). The age variation in the incidence rates showed rising values towards a peak at 12 years for girls and a plateau at 12-14 years for boys, with an abrupt decline after 12 and 14 years, respectively. There were more cases with onset in the winter and autumn, with significant peaks in February and October. From these data the prevalence of diabetes mellitus in the age group 0-14 years can be calculated to 1.2 per 1 000 children. In the whole of Norway, about 170 new cases of diabetes mellitus below the age of 15 years can be expected every year. Compared with previous studies, the present data suggest an increasing incidence of childhood diabetes in Norway.

Adolescent↗
PubMed1981

Metabolic responses to alanine in small-for-gestational age infants: developmental aspects.

14 small-for-gestational age (SGA) infants and 4 healthy adult volunteers were subjected to an intravenous alanine tolerance test. In normoglycemic SGA infants studied during the first 6 days of life, the apparent K value for the disappearance rate of alanine was 3%/min. In 6 hypoglycemic patients studied between day 1 and day 12 the corresponding K value was 2.2%/min. In adult volunteers a K value of 5.6%/min was obtained. Plasma pyruvate increased after alanine in both normoglycemic and hypoglycemic SGA infants. The blood glucose tended to decrease after the alanine load in the hypoglycemic infants, whereas an increase was observed in infants with normoglycemia. On reexamination of 4 hypoglycemic SGA infants after the blood glucose concentration had normalized, a blood glucose profile approaching that of normoglycemic infants was recorded.

Alanine↗
PubMed1981

Responses of plasma adenosine 3',5'-monophosphate, blood glucose and plasma insulin to glucagon in humans.

The effect of glucagon on plasma cyclic AMP (cAMP), insulin and blood glucose was examined in normal adult subjects. After an i.v. injection of glucagon there was a rapid, dose-dependent increase of plasma cAMP as well as insulin and blood glucose. Multiple injection of glucagon to the same subject with 60 min intervals gave almost identical responses of plasma cAMP and blood glucose, whereas the insulin response tended to decrease with time. Dose-dependent increases of plasma cAMP, insulin and blood glucose were also seen during a continuous i.v. infusion of glucagon. With the lowest doses of glucagon the blood glucose and plasma insulin concentrations were increased without any change of plasma cAMP. Plasma cAMP, insulin and blood glucose declined prior to the termination of glucagon infusion. During an endogenous hyperglucagonaemia, induced by alanine injection, there was no discernible change of plasma cAMP. We conclude that the early events of glucagon action may be studied in vivo by monitoring plasma cAMP. However, variations of plasma glucagon within the physiological range are not accompanied by measurable changes of cAMP in the peripheral circulation.

Adult↗
PubMed1981

Immunohistochemical, morphometric, and clinical studies of the pancreatic islets in infants with persistent neonatal hypoglycemia of familial type with hyperinsulinism and nesidioblastosis.

A new era has been started in the morphological research of the human pancreatic islet parenchyma by the introduction of immunohistochemical (IHC) and modern morphometric techniques. This statement is illustrated by a report of two infants from two families with persistent neonatal hypoglycemia with hyperinsulinism, where specimens of pancreas, obtained at subtotal pancreatectomy, were analyzed together with autopsy specimens from age-matched "controls" (cardiac malformations). It was found that a nesidioblastosis-like picture occurred in the pancreas of the "controls", at least up to 6-7 months of age, and that in IHC stained sections this was indistinguishable from that observed in the endocrine pancreas of the hypoglycemic infants. Moreover, there was no difference in the total volume density of the islet parenchyma in pancreas of controls and hypoglycemic children when analyzed by morphometry. However, an increase in the relative incidence of insulin cells was found in the hypoglycemic infants as well as a moderate reduction of glucagon cells and a marked decrease of somatostatin cells. Clinically, some alleviation of the symptoms could be obtained by administration of glucagon and somatostatin, indicating that the hypothesis is correct that a defect in the maturation of the islet parenchyma during infancy may be a main pathogenetic factor in the syndrome. The familial occurrence of the disease may be more common than previously realized.

Blood Glucose↗