Search PubMed⌕ Search

Biomedical subjects

P Lautala

Publications and source records attributed to P Lautala.

At least 37 records · Page 2Linked to original sources
PubMed1989

Nocturnal release of immunoreactive growth hormone-releasing hormone and growth hormone in normal children.

To evaluate the role of growth hormone-releasing hormone (GHRH) in the physiologic release of growth hormone (GH) we studied the nocturnal secretion of immunoreactive GHRH (ir-GHRH) and its relationship to GH release and various stages of sleep in six prepubertal (three boys) and six pubertal children (two boys) with normal stature. Their ages ranged from 8.1 to 14.9 yr and their bone ages from 6.8 to 14.8 yr. Blood was withdrawn continuously between 2200-0600 h at a constant rate of 5 mL/20 min. The EEG was simultaneously registered. The ir-GHRH and GH data were analyzed by a discrete-pulse detection algorithm (Pulsar). The number of nocturnal ir-GHRH pulses varied from 0-8 (median 7) and the number of GH peaks from 2-6 (median 3). Pubertal children had significantly more (p less than 0.05) ir-GHRH pulses and the pulse amplitude was higher (p less than 0.05) than in the prepubertal children. There were no significant differences in the GH parameters between the two groups. The ir-GHRH peaks were not significantly related to any specific sleep stage. The majority of the GH pulses (71%) were associated with slow wave sleep (p less than 0.001). Two-thirds (69%) of the GHRH peaks preceded closely or coincided with GH pulses (p less than 0.02). Pubertal subjects had more isolated ir-GHRH peaks than prepubertal children (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Cardiovascular risk in young Finns, results from the second follow-up study.

A comprehensive study of coronary heart disease (CHD) risk factors and their determinants in children and adolescents in Finland was initiated in the late 1970's. The main cross-sectional study was undertaken in 1980, with 3596 subjects aged from 3 to 18 years participating. The first follow-up study was carried out in 1983, and the second in 1986. The present report describes briefly some findings in 2746 children and young adults, aged 9, 12, 15, 18, 21 and 24 years, participating in 1986. Serum total cholesterol concentrations, mean (SD), ranged between 4.31 (0.73) and 4.91 (0.81) mmol/l in boys, and between 4.73 (0.85) and 5.09 (0.82) mmol/l in girls, respectively. Mean serum cholesterol values had fallen from 1980 to 1986 by 5.4% in such age cohorts, which had been included in all three studies. Fat content in the diet remained unchanged (38 E %), whereas the mean P/S ratio increased from 0.24 in 1980 to 0.31 in 1986. Young Finns from East Finland had a higher somatic risk index than those from West Finland (P greater than 0.001). The clustering of somatic risk factors was stable between 1980 and 1986. Further follow-up of the cohorts will, we hope, provide the tools for implementing primary prevention of CHD in Finland.

Adolescent↗
PubMed1988

Reduced insulin removal and erythrocyte insulin binding in obese children.

To study the relationship between childhood obesity, weight loss, hyperinsulinaemia and the erythrocyte insulin receptor, we measured the plasma concentrations of immunoreactive insulin (IRI) and C-peptide and the binding of 125I-insulin to erythrocytes in 12 obese children with a mean age +/- SD of 11.4 +/- 2.5 years and a mean relative weight score +/- SD of 4.8 +/- 1.4 and 12 age-matched normal-weight children. Eight obese children were re-evaluated after 1 year's participation in a weight reduction programme. The obese children had higher fasting plasma concentrations of IRI (P less than 0.01) and C-peptide (P less than 0.05) and a lower C-peptide to IRI molar ratio (P less than 0.01) than the normal-weight children. The obese children had in addition a reduced erythrocyte insulin binding (P less than 0.05 or less) over the physiological range of circulating insulin concentration. There was a negative correlation (r = -0.60; P less than 0.01) between the insulin tracer binding and the relative weight. The weight reduction programme resulted in a decrease of 1.0 SD (P less than 0.05) in the mean relative weight score. At the end of the therapy the obese children had lower fasting blood glucose levels (P less than 0.05) and lower plasma IRI concentrations at 90 min (P less than 0.05) after an oral glucose load than at the onset of therapy. There were no significant differences between the insulin binding characteristics at the commencement and at the end of the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1988

Postnatal decrease in insulin binding to erythrocytes in infants of diabetic mothers.

To clarify the role of insulin receptors in the macrosomia and the tendency to hypoglycemia in infants of mothers with insulin-treated diabetes mellitus (IDM) we studied insulin binding in erythrocytes from mixed umbilical blood and from peripheral venous blood collected when the infants were 3-14 days old. Normal infants were matched for gestational and postnatal age. The IDM infants were macrosomic, with significantly higher birth weights relative to gestational age than the control infants. Plasma free insulin concentrations in cord blood were 15-fold higher in the IDM than in the normal infants and more than 3-fold higher in the peripheral venous blood at the median age of 4 days. Hypoglycemia occurred in 12 of the 17 IDM and in none of the normal infants. In umbilical blood insulin binding to erythrocytes was similar in the IDM and normal infants. In both groups insulin binding decreased during the first postnatal weeks, but the decrease was significantly greater in the IDM than in the normal infants. The decrease in insulin binding to erythrocytes was a consequence of decreased receptor affinity as well as decreased receptor concentration in the IDM infants, but was mainly due to decreased receptor concentration in the normal infants. We conclude that insulin binding to its erythrocyte receptor in cord blood in IDM infants is similar to that in normal infants in spite of the simultaneous gross hyperinsulinemia in the IDM infants. The resulting increase in insulin action would then contribute to the tendency toward hypoglycemia and may be partly responsible for the macrosomia in IDM infants. The marked postnatal decrease in insulin binding in IDM infants is a possible explanation for their diminishing risk of hypoglycemia after the first few days of life in spite of persisting hyperinsulinemia.

Birth Weight↗
PubMed1988

Variable plasma growth hormone (GH)-releasing hormone and GH responses to clonidine, L-dopa, and insulin in normal men.

The effects of synthetic GHRH-(1-44) (1 microgram/kg, iv), clonidine (0.15 mg/m2, orally), L-dopa (0.5 g, orally), and insulin (0.1 IU/kg, iv) on plasma immunoreactive (ir) GHRH and GH levels were determined in normal men, aged 31-46 yr (n = 4-8). In addition, plasma ir-GHRH and GH concentrations were determined before and after the administration of clonidine in six younger men, aged 19-25 yr. GHRH was extracted from plasma using Sep-Pak C18 cartridges and measured with a mid-portion-specific GHRH antiserum. The mean plasma ir-GHRH and GH levels ranged from 9-11 ng/L and 0.5-1.5 microgram/L, respectively, in the older men during a 2-h control study. After GHRH administration, the mean plasma ir-GHRH concentration increased to a peak of 512.5 ng/L at 3 min and GH to a peak of 9.2 micrograms/L at 10 min. Clonidine resulted in a significant increase in mean plasma GH levels (P less than 0.05) in the younger men, but not in the older men. Plasma ir-GHRH concentrations did not change after clonidine. L-Dopa increased plasma ir-GHRH at 60 min (P less than 0.05) and GH at 60-120 min (P less than 0.05). Insulin-induced hypoglycemia increased plasma GH levels (to a mean of 23.8 micrograms/L at 60 min; P less than 0.001), whereas plasma ir-GHRH levels did not change. We conclude that the mechanisms of the various GH stimulation tests differ. Some GH responses, including those induced by insulin, do not appear to be mediated by GHRH.

Adult↗
PubMed1986

Erythrocyte insulin binding in preterm newborn infants.

To characterize the erythrocyte insulin receptor in newborn infants we studied the binding of 125I-insulin to the erythrocytes from 42 preterm infants (14 at birth, 14 aged 2-7 days, and 14 aged 8-16 days) with a mean gestational age of 34.1 wk, and from 32 term infants (16 at birth and 16 aged 2-7 days). The insulin binding to cord blood erythrocytes from preterm infants was significantly higher than that of cord blood cells from term infants and to postnatal cells from preterm as well as term infants. The erythrocytes from preterm infants aged 2-7 days bound more insulin than cells from preterm infants aged 8-16 days. The maximum insulin binding (specific insulin binding at tracer concentration of insulin) correlated negatively with the gestational age both at birth and over the 1st postnatal wk. In the preterm infants there was a strong negative correlation between the maximum insulin binding and postnatal age. The enhanced insulin binding to cord blood erythrocytes from preterm infants was due to both an increased receptor concentration and a high affinity for insulin. The increased affinity persisted over the 1st wk of life. In preterm infants older than 1 wk the insulin binding characteristics were basically similar to those in term newborn infants. In all infants studied the receptor concentration seemed to be postnatal age dependent while the receptor affinity was gestational age dependent. No correlation was found between the insulin binding data and the plasma concentrations of immunoreactive insulin or C-peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1986

Insulinotropic activity in the serum of obese and nonobese infants and children.

The ability of a serum fraction, mol wt 1000-5000, to stimulate insulin release in vitro was studied in 123 obese and normal weight children aged 0-17 yr. The sera were fractionated by serial molecular filtration after treatment with urea. Stimulation of insulin release was determined with a bioassay using isolated rat islets in perifusion. The islet-stimulating activity was found in all obese children less than the age of 10 yr and in the majority of the obese children older than 10 yr of age. In normal weight children the activity was also found in the majority of infants, but was infrequent in older children. The serum islet-stimulating activity was positively correlated with the duration and degree of obesity and with linear growth rate. The molecular structure and origin of the insulinogenic activity in the serum is still unknown. In high-performance liquid chromatography it has the same elution characteristics as the hypothalamic insulin-glucagon liberin. The present results suggest a role for the serum islet-stimulating activity in the pathogenesis of obesity.

Adolescent↗
PubMed1986

Serum insulin-releasing activity and the Prader-Willi syndrome.

Pathogenesis and etiology of the various clinical features of the Prader-Willi syndrome (PWS) are not completely understood. There is evidence suggesting a hypothalamic abnormality leading to hypogonadism in this syndrome. To test the possible hypothalamic involvement in the pathogenesis of obesity in these patients we studied the sera of 5 patients with PWS for insulin-releasing activity of possible hypothalamic origin. In addition 4 patients with a PWS-like syndrome and 6 obese patients with signs of central nervous system damage were studied. All five patients with PWS showed significant insulin-releasing activity in their sera. Of the four patients with PWS-like symptoms three showed similar activity while three of the obese patients with central nervous system damage had this activity in their sera. Serum insulin-releasing activity has been shown earlier to be associated with childhood obesity and it could play a role in the pathogenesis of obesity in PWS.

Adolescent↗
PubMed1985

Atherosclerosis precursors in Finnish children and adolescents. VII. Serum immunoreactive insulin.

In the Finnish Multicentre Study of the risk factors of coronary heart disease serum immunoreactive insulin (IRI) was measured in 3,486 children and adolescents aged 3-18 years. Serum IRI increased with age till the age of 15 years in both sexes. The increase in serum IRI levelled off with the progression of pubertal development. Serum IRI levels were higher in girls than in boys from the age of 6 years onwards. Comparison of serum IRI gave identical results from eastern and western parts of the country. Serum IRI correlated positively with skinfold thickness, weight, relative weight and body mass index in all age groups except the 3-year-old children.

Adolescent↗
PubMed1983

Partial purification of an insulin-releasing activity in human serum.

An activity that enhances insulin release from perifused rat pancreatic islets has recently been isolated from human serum fractions (molecular weight 1,000-5,000 daltons). To characterize this activity we have studied the insulin-releasing effect of serum subfractions from obese and non-obese children obtained by reversed-phase high-performance liquid chromatography (HPLC). The serum insulin-releasing activity eluted in the HPLC system at 12-13 minutes, which corresponded to the retention time of the tridecapeptide insulin-glucagon liberin isolated from bovine hypothalamus. Insulin-releasing activity was found in serum subfractions from both obese and normal-weight children. The relative insulin-releasing potency of the active subfractions was higher than that of the original total serum fractions, indicating the presence of some substance(s) which inhibit insulin secretion in the total serum fractions. Oral glucose loading increased the relative insulin-releasing activity in the HPLC subfractions from obese children. This study suggests that the insulin secretagogue in human serum might be identical to hypothalamic insulin-glucagon liberin as these substances behave similarly on reversed-phase HPLC and have parallel insulin-releasing properties.

Animals↗
PubMed1983

Relation of enteroinsular hormones at birth to macrosomia and neonatal hypoglycemia in infants of diabetic mothers.

To study the role of enteroinsular hormones in fetal macrosomia and neonatal hypoglycemia in infants of diabetic mothers, we measured plasma concentrations of free and total immunoreactive insulin, C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide at birth in 35 IDMs and 35 infants of normal mothers. Twenty fasting adults of normal weight were also studied. Sixteen IDMs were macrosomic at birth; 17 developed neonatal hypoglycemia over the first postnatal hours. The IDMs had ten times higher concentrations of free IRI than the normal infants in cord blood. Free IRI concentrations were related to the severity of maternal diabetes, with the infants of white class D to F mothers having the highest levels. The IDMs with macrosomia had a twofold increase in the concentrations of free IRI when compared with IDMs of normal weight. There was a significant correlation between the birth weight ratio and the concentrations of free IRI. The IDMs who developed neonatal hypoglycemia had considerably higher concentrations of free IRI than did normoglycemic IDMs. The decrease of blood glucose over the first postnatal hours correlated strongly with the free IRI concentrations in the cord blood. The IDMs had a threefold increase of the C-peptide concentrations over those in normal infants. Six IDMs had a molar ratio of C-peptide to free IRI of less than 1. Both the IDMs and normal infants had substantially higher concentrations of enteroglucagon and lower concentrations of GIP than did the fasting adults. Our data provide direct evidence that IDMs are markedly hyperinsulinemic at birth and that ambient hyperinsulinemia plays a crucial role in the development of fetal macrosomia and neonatal hypoglycemia. Moreover, the observed discrepancy in the relative increase of free IRI and C-peptide, combined with the low molar ratio of C-peptide to IRI, suggests a decreased metabolic clearance of insulin or transplacental passage of insulin from the maternal circulation in infants of mothers with insulin-treated diabetes.

Adult↗
PubMed1983

Ceftazidime in the treatment of chronic suppurative otitis media in children.

Seventeen children aged 5 months to 3 years with recurrent or chronic otitis media complicated by Pseudomonas aeruginosa were treated with ceftazidime. All patients had been previously treated with several antibiotics. All strains of Pseudomonas were initially sensitive to ceftazidime. In four of the six cases which failed bacteriologically, the Pseudomonas was found to be of intermediate sensitivity after treatment. In 11 patients the Pseudomonas was eradicated during treatment but reappeared in 4 during the follow-up period. All 11 patients were clinically cured or improved. Three of the six children whose Pseudomonas was not eliminated from aural discharge showed some clinical improvement whereas the remaining three showed no clinical response to treatment. The range of MIC values of ceftazidime, gentamicin and carbenicillin for the Pseudomonas isolated were respectively 0.5 to 4.0, 0.25 to 2.0 and 4.0 to 125 mg/l. The mean ceftazidime serum level at 1 h after the first injection of 50 mg/kg was 74.12 (S.D. 12.84) mg/l and at 12 h post injection 1.93 (S.D. 4.14) mg/l.

Ceftazidime↗
PubMed1983

Erythrocyte insulin binding in normal infants, children and adults.

To establish normal insulin binding criteria, we studied the binding of insulin to erythrocytes from normal subjects of different ages. Insulin binding to cord erythrocytes and to erythrocytes from infants aged 2-7 days was significantly higher at tracer and physiological insulin concentrations than was binding to cells from children aged 1-15 years and adults. In infants aged 1-12 months the maximum insulin binding to erythrocytes was significantly higher than that to erythrocytes from children, and in addition, it correlated negatively with age. An increase in receptor concentration was found in cord erythrocytes whereas an increased receptor affinity for insulin was found in erythrocytes from infants. Insulin binding characteristics in erythrocytes from prepubertal and pubertal children were basically similar to those in women. Erythrocytes from men bound significantly higher amounts of insulin than did those from women. This difference was associated with changes in receptor affinity for insulin. There was no correlation between the insulin binding characteristics and the circulating concentration of insulin or C-peptide. The increased erythrocyte insulin binding at birth persisted over the neonatal period. There was an overall negative correlation between the maximum insulin binding and age in the subjects studied, but the major decrease in erythrocytes insulin binding occurred during the first year of life past the neonatal period. These observations stress the importance of using age-matched controls in studies on erythrocyte insulin binding in disease states.

Adolescent↗
PubMed1983

Basal insulin secretion and erythrocyte insulin binding in preterm and term newborn infants.

To study the ontogeny of the insulin secretion and the erythrocyte insulin receptor we measured plasma immunoreactive insulin and C-peptide concentrations and the binding of [125I]-insulin to the erythrocytes in cord blood from 16 preterm and 16 term infants. 20 normal-weight adults were also studied. The C-peptide concentrations and the molar ratio of C-peptide to insulin were lower in the newborn infants than in the adults. The immunoreactive insulin correlated positively with birth weight in the term infants. The insulin binding to erythrocytes from the newborn infants was increased when compared to the adults. Erythrocytes from the preterm infants bound more insulin than the cells from the term infants. There was a strong negative correlation between insulin binding and gestational age. In the term infants, plasma C-peptide correlated negatively with the insulin binding. The increased binding to erythrocytes from the term infants was due to an increase in the receptor concentration. The high insulin binding in the preterm infants was a result of both an increased receptor concentration and affinity. These data suggest that the basal insulin secretion is similar in preterm and term infants and that the clearance of insulin is decreased in newborn infants. The increased insulin binding in newborn infants may be a mechanism by which the growth stimulatory effect of insulin in fetal life is mediated.

Adult↗
PubMed1983

Serum calcium and 25-OH-D3 in mothers of newborns with craniotabes.

Serum calcium and 25-OH-D3 in mothers of newborns with craniotabes. The aim of this study was to investigate whether calcium or vitamin D balance during late pregnancy have influence on the outcome of newborn craniotabes. 27 mothers and their fullterm newborns with craniotabes in two series were studied for clinical findings, course of pregnancy and calcium and vitamin D metabolism after the pregnancy. Calcium and phosphorus balance were studied in the first 16 mother-newborn pairs and were studied in the first 16 mother-newborn pairs and compared to a control group. Serum 25-OH-D3 concentrations were determined in the next 11 pairs and compared to a control group delivering in the same season and also to unpregnant women. The course of pregnancy did not show retrospectively any significant alterations and the clinical findings except craniotabes of the newborns were normal. In four cases the fetal head was engaged before 33th of gestation. In mothers serum calcium level was lower (p less than 0.05) and the excretion of phosphorus decreased (p less than 0.05) after the pregnancy as compared to controls. The values of serum 25-OH-D3 were at the same level in mothers and newborns with craniotabes as compared to controls but the values of mothers were lower (p less than 0.001) as compared to unpregnant controls In conclusion, craniotabes of the newborns seems to have no unique etiologic factor. The changes of calcium and vitamin D metabolism during pregnancy may be considered as predisposing factors in some cases and early engagement in some other. Perhaps also other reasons can be found.

Alkaline Phosphatase↗
PubMed1981

Glucose metabolism in rat hypothalamus.

In vitro glucose oxidation and glucose transport in the rat medial (MH) and lateral (LH) hypothalamic areas was measured. Glucose oxidation was calculated from the conversion of [U-14C]glucose to 14CO2 and glucose transport from 14CO2 produced from [1-14C]glucose in the presence of phenazine and methosulphate and NaF. Increasing glucose in the medium from 1 mM to 20 mM enhanced glucose oxidation two-fold in MH and 40% in LH. Addition of insulin, 100 microU/ml, to the medium decreased glucose oxidation 30% both in MH and LH at both 4 mM and 20 mM glucose. Fasting did not affect glucose oxidation in either of these hypothalamic areas. Glucose transport was not affected by insulin, but was increased significantly when glucose was raised from 0.25 mM to 1.0 mM. Fasting also increased glucose transport in both hypothalamic areas. In conclusion, extracellular glucose concentration seems to be the major regulator of glucose utilization by the rat hypothalamus. Insulin, rather than increasing, seems to decrease glucose oxidation while having no effect on glucose transport.

Animals↗