Search PubMed⌕ Search

Biomedical subjects

G Dahlquist

Publications and source records attributed to G Dahlquist.

123 records · Page 7Linked to original sources
PubMed1983

Effect of metabolic control and duration on exercise-induced albuminuria in diabetic teen-agers.

Nineteen type I diabetic teen-agers without clinical signs of nephropathy with a duration of diabetes varying from 3 to 16.8 years were examined by a standardized exercise test for analysis of urinary excretion of albumin and beta 2-microglobulin. The patients were studied both in poor and improved (but not perfect), metabolic control as defined by HbA1c and blood glucose profiles, and the values were compared to those of 14 age-matched healthy controls. The controls showed no increase in albumin excretion rate during exercise as was found in diabetic patients. The albumin excretion rate during exercise was significantly correlated (p less than 0.05) to systolic blood pressure in the diabetic patients. Blood pressure in the diabetic patients was, however, similar to that of controls both at rest and during exercise. Urinary beta 2-microglobulin did not change during exercise. The urinary albumin excretion during exercise decreased significantly with improved metabolic control in diabetic patients, but the albumin excretion rate was not correlated with either blood or urinary glucose or diuresis during the exercise test. When metabolic control was improved there was a significant correlation between the increase in albumin excretion rate during exercise and the duration of diabetes, indicating that part of the exercise-induced albumin excretion might reflect irreversible morphological changes in the diabetic kidney. This test might therefore have a predictive value for diabetic nephropathy if performed during strict metabolic control.

Adolescent↗
PubMed1983

Renal function in relation to metabolic control in children with diabetes of different duration.

To evaluate the interpretation of different kidney function tests in diabetic children and teenagers we have studied 47 children with a duration of diabetes up to 5 years, 61 children with a duration of 5.1-10 years and 49 children with a duration of greater than 10 years. Glomerular filtration rate (GFR) measured as inulin clearance or creatinine clearance, clearance PAH (CPAH), filtration fraction (FF), 24-hour urinary excretion of beta 2-microglobulin and albumin were examined and correlated with short- and longterm indices of metabolic control. In all groups of duration GFR as measured by inulin clearance was increased compared with reference values from age matched controls. In patients who had had diabetes for 0-5 years a significant positive correlation was found between inulin clearance and blood glucose during the examination. Inulin clearance was also correlated to HBA1c as well as to 24-hour urinary glucose (mean of 4-6 samples during two years). No such correlation was found in the group who had had diabetes for 5-10 years but in patients with a duration of diabetes greater than 10 years a significant inverse relation was found between GFR and HbA1c. The 24-hour urinary excretion of albumin was significantly higher in all groups of diabetics compared with controls. The urinary excretion of beta 2-microglobulin was similar in diabetics and controls. In the total material no significant correlation could be found between inulin clearance and creatinine clearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

The incidence of diabetes mellitus in Swedish children 0-14 years of age. A prospective study 1977-1980.

This is a prospective study of the incidence of insulin-dependent diabetes mellitus (IDDM) in children 0-14 years of age, including all newly diagnosed cases in the whole of Sweden from July 1, 1977 until June 30, 1980. All 45 Swedish departments of paediatrics participated. During the three-year-period studied, 1108 Swedish children, 0-14 years of age had their onset of diabetes. That means around 369 new diabetics yearly in the age groups studied. The mean yearly incidences in the years 1977-80 were 22.6, 22.8 and 22.6 per 100000 children, respectively. Mean prevalence on June 30, 1980 and 1.48 per 1000 children 0-14 years with a wide range of 0.71-2.65. The age distribution at onset showed a gradual increase and peak incidences at 11 years of age for the girls and 4 and 13 years of age for the boys. There was a consistently higher incidence for boys in the younger age groups during the three-year-period studied. Peak incidences of new cases were reached in January, March and July through October for the age groups 5-9 and 10-14 years of age. No such seasonal variation was seen for children 0-4 years of age. The cumulative incidence of IDDM at 14 years of age was 3.2 per 1000 for the boys and 2.9 per 1000 for the girls. The degree of ascertainment in this study was 93.4%.

Adolescent↗
PubMed1981

Lack of effect on body weight and content of nitrogen and fat after insulin administration to fetal rats.

The effect of fetal insulin injection on body weight and carcass lipid and nitrogen content was studied in four groups of rat fetuses. In each litter, one fetus in each horn was randomly chosen for treatment with either insulin injection, saline injection, insulin solvent injection or sham operation. Injections were given subcutaneously to the fetuses on days 18 1/2, 19 1/2, and 20 1/2 of gestation. The experimental model and the statistical evaluation took into consideration the influence of the fetal position in the uterine horn as well as the variability of fetal size between different litters. Using this experimental model we found that insulin injections to the fetal rat had no effect on body weight and body composition.

Animals↗
PubMed1979

Ketotic hypoglycemia of childhood--a clinical trial of several unifying etiological hypotheses.

We have studied 15 children referred to St. Göran's Children's Hospital because of suspected ketotic hypoglycemia. The patients were investigated according to a program designed to test several hypotheses--old and new--postulated to explain the etiology of ketotic hypoglycemia. We have used the classical ketogenic provocation with a low calorie, high fat diet and measured the blood levels of several substrates and hormones as well as the urinary excretion of certain metabolites and hormones. Out of the 15 children, 6 will fill the criteria of ketotic hypoglycemia at the time of study. The most remarkable finding in these 6 children in contrast to the other children studied was that they did not decrease their peripheral glucose utilization (measured as Kg) during starvation. These 6 children seemed to be more "advanced" in their adaptation to ketogenic diet in all other parameters studied. The children with ketotic hypoglycemia did not differ from the other children in plasma level of cortisol or urinary excretion of nitrogen, urea, 3-methylstidine and catecholamines. We favour the concept that the children with ketotic hypoglycemia represent the tail of the gaussian curve in the normal age-dependent development of the adaptation to starvation.

Alanine↗
PubMed1976

Cerebral utilization of glucose, ketone bodies and oxygen in starving infant rats and the effect of intrauterine growth retardation.

Cerebral arteriovenous differences of acetoacetate, D-beta-hydroxybutyrate, glucose, lactate and oxygen and brain DNA content was measured at 20 days of age in intrauterine growth retarded (IUGR) rats and normal littermates after 48 and 72 h of starvation. Cerebral blood flow (CBF) was measured with labeled microspheres in other comparable groups of IUGR and control rats. CBF was similar in IUGR and normal littermates (0.57+/-0.09 and 0.58+/-0.10 ml/min respectively). After 48 h of starvation, arterial glucose was significantly lower in IUGR than control animals but the arterial concentrations of ketone bodies were similar. After 48 h of starvation, cerebral arteriovenous difference of beta-hydroxybutyrate was significantly higher in control than IUGR rats also when expressed per mg brain DNA as was the fractional uptake of D-beta-hydroxybutyrate. After 72 h of starvation, arterial concentrations of ketone bodies were significantly lower in IUGR rats than controls but the fractional uptake of D-beta-hydroxybutyrate was increased compared to IUGR rats starved for 48 h. The average percentage of calculated total substrate uptake (mumol/min) accounted for by ketone bodies increased in control animals from 31.1% after 48 h of starvation to 41.0% after 72 h of starvation. In IUGR rats these percentage values were 26.5 and 25.7 respectively. After 72 h of starvation the fraction of total cerebral uptake of substrates accounted for by ketone bodies was significantly higher in control that IUGR rats. As total cerebral uptake of substrates was similar between IUGR and control animals it is concluded that IUGR rats are more dependent on glucose as a substrate for the brain during starvation.

Acetoacetates↗
PubMed1976

The rate of cerebral utilization of glucose, ketone bodies, and oxygen: a comparative in vivo study of infant and adult rats.

Cerebral blood flow (CBF) was measured by means of Celabeled microspheres in infant (20-day-old) and adult (3-month-old) rats, anesthetised with Na-5-ethyl-5-(1-methylpropyl)2-thiobarbituric acid. Cerebral arteriovenous differences of acetoacetate, D-beta-hydroxybutyrate, glucose, lactate, and oxygen and brain DNA content were determined in other groups of similarly treated infant and adult animals fed or starved for 48 or 72 hr. The mean CBF values of 0.48+/-0.04 and 0.62+/-0.07 ml/(g X min), +/- SEM, in infant and adult animals, respectively, were not significantly different. CBF was unaffected by starvation. At any given arterial concentration the cerebral arteriovenous difference of acetoacetate was significantly higher in infant than adult rats. The same was true for D-beta-hydroxybutyrate at arterial concentrations above 1 mmol/liter. There was an approximately linear relationship between arterial concentration of acetoacetate and its cerebral arteriovenous difference in both infant and adult rats. A similar relationship was found for D-beta-hydroxybutyrate only in infant animals. In the fed state, the cerebral uptake of glucose and ketone bodies (micromoles per (mg DNA X min)) was not different in infant and adult rats. During starvation, cerebral uptake of ketone bodies expressed as micromoles per (mg DNA X min) was higher in infant than adult rats, indicating a higher rate of utilization of ketone bodies per cell in these animals. For glucose, no such difference was found in either fed or starved groups (Table 3). The average percentage of the total cerebral uptake of substrates (micromoles per min) accounted for by ketone bodies increased in both infant and adult rats during starvation. This percentage value was clearly higher in infant than adult rats during starvation. After 72 hr of starvation the values were 38.8% and 15.2% in infant and adult rats, respectively (Fig. 3). Calculated cerebral metabolic rate for oxygen (CMRO2), assuming complete oxidation of glucose and ketone bodies and expressed as micromoles per (mg DNA X min), was similar in fed and starved rats of both age groups (Table 3), indicating that ketone bodies serve as an alternative substrate for glucose during starvation. Calculated CMRO2 for glucose plus ketone bodies was similar to the measured CMRO2 in adult rats both in the fed and the starved groups. For infant rats, calculated CMRO2 for glucose plus ketone bodies was higher than measured CMRO2, indicating that in this age group a portion of substrate was used for synthesis or storage rather than for complete oxidation.

Acetoacetates↗
PubMedDate not supplied

Metabolic control in 131 juvenile-onset diabetic patients as measured by HbA1c: relation to age, duration, C-peptide, insulin dose, and one or two insulin injections.

Glycosylated hemoglobin A (HbA1c), considered to reflect long-term metabolic control of diabetes, was analyzed in 131 patients, aged 2 5/12-19 6/12 yr, with juvenile-onset diabetes. Using stepwise multiple regression HbA1c, fasting blood glucose and plasma 3-hydroxybutyrate were analyzed as dependent variables versus independent variables such as age of the patients, duration of the disease, level of plasma immunoreactive C-peptide (IRCP), insulin dose, and number of insulin injections (one or two) per day. HbA1c was inversely related only to IRCP concentration. A low but significant, positive correlation was found between HbA1c and the duration of diabetes. Stepwise addition of the other independent variables did not further increase the fraction of explained variance. HbA1c was also correlated with a subjective rating score of the metabolic control performed by the treating physician. Fasting plasma glucose was significantly related to HbA1c but not to any of the independent variables. Fasting 3-hydroxybutyrate showed an inverse correlation to the age of the patient. The present study showed that in juvenile-onset diabetic patients, endogenous insulin secretion as reflected by IRCP was the factor best correlated with a low level of HbA1c. After the cessation of endogenous insulin secretion, there is a progressive deterioration of metabolic control and multiple injections of insulin rather than one or two per day may be needed to reach optimal control in the patients.

Adolescent↗
PubMedDate not supplied

Negative association between type 1 diabetes and HLA DQB1*0602-DQA1*0102 is attenuated with age at onset. Swedish Childhood Diabetes Study Group.

HLA-associated relative risks of type 1 (insulin-dependent) diabetes mellitus were analysed in population-based Swedish patients and controls aged 0-34 years. The age dependence of HLA-associated relative risks was assessed by likelihood ratio tests of regression parameters in separate logistic regression models for each HLA category. The analyses demonstrated an attenuation with increasing age at onset in the relative risk for the positively associated DQB1*0201-A1*0502/B1*0302-A1*0301 (DQ2/8) genotype (P = 0.02) and the negatively associated DQB1*0602-A1*0102 (DQ6.2) haplotype (P = 0.004). At birth, DQ6.2-positive individuals had an estimated relative risk of 0.03, but this increased to 1.1 at age 35 years. Relative risks for individuals with DQ genotype 8/8 or 8/X or DQ genotype 2/2 or 2/X, where X is any DQ haplotype other than 2, 8 or 6.2, were not significantly age-dependent. An exploratory analysis of DQ haplotypes other than 2, 8 and 6.2 suggested that the risk of type 1 diabetes increases with age for DQB1*0604-A1*0102 (DQ6.4) and that the peak risk for the negatively associated DQB1*0301-A1*0501 haplotype is at age 18 years. There was also weak evidence that the risk for DQB1*0303-A1*0301 (DQ9), which has a positive association in the Japanese population, may decrease with age. We speculate that HLA-DQ alleles have a significant effect on the rate of beta cell destruction, which is accelerated in DQ2/8-positive individuals and inhibited, but not completely blocked, in DQ6.2-positive individuals.

Adolescent↗
PubMedDate not supplied

Non-genetic risk determinants of type 1 diabetes.

A low concordance rate of Type 1 diabetes among monozygotic twins clearly indicate that genetic risk factors may be necessary but are not sufficient for the disease to occur. Descriptive epidemiological studies from all over the world have disclosed clear age, sex seasonal and geographical variability of the disease occurrence and also increasing incidence rates by time within countries and among migrant groups indicating that several different non-genetic risk factors are of importance for the etiology of Type 1 diabetes. Analytical epidemiological studies have further indicated exposures that are associated with an increased risk for the disease. Thus, early fetal events such as exposure to viruses and maternal blood-group incompatibility may be non-genetic risk factors associated with the initiation of auto-immunity in the genetically susceptible child. Further, early exposure to cow's milk protein and a high frequency of intake of nitrosamine-rich food may act as initiating events. Other risk determinants such as a high growth rate, exposure to many infectious diseases, a cold environment and stressful life events may promote an already ongoing autoimmune destructive process causing and increased work load on the beta-cell or through induction of lymphokine release. The diversity of risk determinants that are associated with Type 1 diabetes risk points at a complex interaction between the genome and environment and multivariate analyses have disclosed different risk profiles in different age groups. Further epidemiological and experimental studies are necessary to disclose the causal relationship and the mechanism of action of the non-genetic risk determinants to provide a basis for primary prevention in the general population.

Adult↗