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Biomedical subjects

D Molnár

Publications and source records attributed to D Molnár.

At least 19 recordsLinked to original sources

The effect of obesity, age, puberty and gender on resting metabolic rate in children and adolescents.

UNLABELLED: During puberty fat-free mass (FFM) and fat mass (FM) change quickly and these changes are influenced by sex and obesity. Since it is not completely known how these changes affect resting metabolic rate (RMR), the aim of the present study was to investigate the effect of body composition, age, sex and pubertal development of postabsorptive RMR in 9.5- to 16.5- year-old obese and non-obese children. Postabsorptive RMR was measured in a sample of 371 pre- and postpubertal children comprising 193 males (116 non-obese and 77 obese) and 178 females (119 non-obese and 59 obese). RMR was assessed by indirect calorimetry using a ventilated hood system for 45 min after an overnight fast. Body composition (FFM and FM) was estimated from skinfold measurements. The mean (+/- SD) RMR was significantly (P < 0.001) lower in non-obese (males: 5600 +/- 972 kJ/24 h; females: 5112 +/- 632 kJ/24 h) than in obese (males: 7223 +/- 1220 kJ/24 h; females: 6665 +/- 1106 kJ/24 h) children. This difference became non-significant when RMR was adjusted for body composition (FFM+FM). However, the difference between the genders still remained significant (control male: 6118 +/- 507, control female: 5652 +/- 507, P < 0.001; obese male: 6256 +/- 507, obese female: 5818 +/- 507 kJ/24 h, P < 0.001). The main determinant of RMR was FFM. In the whole cohort. FFM explained 79.8% of the variation in RMR, followed by age, gender and FM adding further 3.8%, 1.1% and 0.8% to the predictability of RMR, respectively. No significant contribution for study group (obese, non-obese), pubertal stage, or fat distribution was found in the regression for RMR. The adjusted value of RMR (for FFM and FM) slightly, but significantly (P < 0.01) decreased between the age of 10-16 years, demonstrating the important effect of age on RMR. CONCLUSIONS: The resting metabolic rate of obese and control children is not different when adjusted for body composition. The main determinant of RMR is the fat-free mass, however, age, gender and fat mass are also significant factors. Pubertal development and fat distribution do not influence RMR independently from the changes in body composition.

Adolescent

Reduced plasma concentrations of alpha-tocopherol and beta-carotene in obese boys.

Plasma alpha-tocopherol and beta-carotene concentrations were significantly lower in obese boys than in control subjects (medians: 3.41 versus 7.46 mg/L and 0.038 versus 0.078 mg/L, respectively, p < 0.05). The differences remained significant after correction for lipidemia. These reduced plasma concentrations of the major lipid-soluble antioxidants in obese children may add to the increased risk of cardiovascular disease in obesity.

Adolescent

Urinary sodium excretion: association with hyperinsulinaemia, hypertension and sympathetic nervous system activity in obese and control children.

UNLABELLED: The aim of the present study was to evaluate the association between 24 h urinary excretion of sodium and blood pressure, fasting plasma insulin, renin, aldosterone and serum norepinephrine concentrations in 45 obese and 15 control children. Urinary sodium excretion was significantly lower in obese subjects (1.3 +/- 0.6 mmol/kg/24 h, P < 0.01) than in controls (2.8 +/- 1.3 mmol/kg/24 h). Hyperinsulinaemia did not affect sodium excretion of obese children. Plasma renin and aldosterone levels did not correlate with sodium excretion and were significantly higher in overweight children. Serum norepinephrine levels were also significantly higher in the obese group (0.66 +/- 0.89 microgram/100 ml) as compared to the controls (0.11 +/- 0.03 microgram/100 ml, P < 0.01) and showed significant negative correlation with urinary sodium excretion (r = 0.43, P < 0.05). CONCLUSION: Hyperinsulinaemia and the consequently increased sympathetic nervous system activity might be involved in the development of high blood pressure in obese children by decreasing urinary sodium excretion.

Adolescent

Long-chain polyunsaturated fatty acids in plasma lipids of obese children.

Fatty acid composition of plasma phospholipids (PL), triglycerides (TG), and sterol esters (STE) was determined by high-resolution capillary gas-liquid chromatography in 22 obese children (age: 13.7 +/- 1.4 y, body weight relative to normal weight for height: 170 +/- 24%, mean +/- SD) and compared with data obtained in 25 age-matched healthy controls. There were no differences in the levels of linoleic acid (LA, C18:2n-6) in any of the plasma fractions from obese children and the controls. Obese children exhibited significantly higher values of arachidonic acid (AA, C20:4n-6) than controls both in PL (12.6 [2.4] vs. 8.3 [1.4], % wt/wt, [median (interquartile range)], P < 0.001) and STE (7.3 [1.8] vs. 6.0 [1.1], P < 0.05). Similarly, obese children showed higher values than controls for dihomo-gamma-linoleic acid (DHGLA, C20:3n-6) in PL (4.0 [0.5] vs. 3.0 [0.6], P < 0.001), TG (0.4 [0.1] vs. 0.2 [0.1], P < 0.001), and STE (0.9 [0.1] vs. 0.7 [0.1], P < 0.01), and for gamma-linolenic acid (C18:3n-6) in STE (1.1 [0.2] vs. 0.8 [0.2], P < 0.001). The AA/LA ratios were higher in obese children than in controls in PL (0.68 [0.16] vs. 0.42 [0.09], P < 0.0005) and STE (0.16 [0.04] vs. 0.12 [0.02], P < 0.05), whereas the AA/DHGLA ratios were lower in TG of obese children than in controls (3.40 [0.64] vs. 5.10 [1.75], P < 0.005). Plasma glucose concentrations were inversely related to AA in TG (r = 0.53, P < 0.05), and plasma TG concentrations were inversely related to AA in PL and STE (r = -0.49, P < 0.05 and r = -0.48, P < 0.05) and to the AA/DHGLA ratios in PL (r = -0.57, P < 0.01), TG (r = -0.56, P < 0.01), and STE (r = -0.56, P < 0.01). We conclude that the significantly higher values of n-6 long-chain polyunsaturated fatty acids (LCP) in plasma lipids of obese children than in age-matched controls may be caused by an enhanced activity of delta 6-desaturation, and we speculate that elevated fasting immunoreactive insulin seen in obese children (19.4 +/- 8.0 microU/mL) may stimulate synthesis of n-6 LCP fatty acids.

Adolescent

Plasma and cerebrospinal fluid hyperinsulinism in asphyxiated piglets.

Insulin (I) plays a crucial role in the maturation of the perinatal brain, and it may also be involved in the pathogenesis of neonatal brain injuries. The aim of the present study was to reveal the effect of neonatal asphyxia on the regulation of I and glucose (G) metabolism in plasma and cerebrospinal fluid (CSF) in newborn piglets. The I concentrations were measured by radioimmunoassay, while the G levels were analyzed by the G oxidase method during three phases (basal, critical, recovery) of bilateral pneumothorax in newborn piglets. We observed a significant hyperinsulinism (p < 0.001) both in plasma and CSF and a mild hypoglycemia (p < 0.05) during the recovery period. Postasphyxial G infusion (1.1 M, 10 ml.kg-1) amplified the hyperinsulinism. The ICSF/plasma ratio (mean +/- SEM; n = 16) was decreasing during cardiovascular failure (0.09 +/- 0.02; NS) as compared with the initial value (0.12 +/- 0.04), then it returned to basal values by 60 min (0.14 +/- 0.04; NS), and increased significantly 180 min (0.40 +/- 0.14; p < 0.05) after resuscitation of the piglets. There was a similar increase in GCSF/plasma ratio in asphyxiated animals at the end of experiments (0.99 +/- 0.15 vs. initial 0.76 +/- 0.05; p < 0.05). In conclusion, neonatal asphyxia resulted in plasma and CSF hyperinsulinism which may alter hypoxic-ischemic cerebral damages.

Acid-Base Equilibrium

Lipid corrected plasma alpha-tocopherol values are inversely related to fasting insulinaemia in obese children.

Plasma concentrations of alpha-tocopherol and retinol were measured in 17 obese children (10 boys and 7 girls, age: 13.9 +/- 0.3 y, mean +/- s.e.m.) and related to anthropometric indices and fasting plasma insulin concentrations. Body weight was 89.0 +/- 5.3 kg, relative body weight 165 +/- 6%, body fat content 38.9 +/- 1.2% and body mass index 32.3 +/- 1.3 kg/m2. Plasma alpha-tocopherol, retinol and insulin concentrations were 18.5 +/- 1.6 mul/l, 2.0 +/- 0.2 mu/l and 17.2 +/- 1.6 mU/l, respectively. Neither alpha-tocopherol nor retinol concentrations were related to age. Plasma retinol concentrations were positively correlated to weights (r = 0.60, P = 0.01) and heights (r = 0.65, P < 0.01), but not to body fat contents. In contrast, plasma alpha-tocopherol concentrations were not related to weights and heights, but a significant inverse relation was seen to body fat contents (r = -0.49, P = 0.04). Fasting plasma insulin concentrations did not correlate with plasma retinol values, but were inversely related to plasma alpha-tocopherol concentrations (r = -0.53, P = 0.02) and alpha-tocopherol: cholesterol+triglyceride ratios (r = -0.57, P = 0.01). These results indicate that the factors influencing the availability of retinal and alpha-tocopherol in obese children may be different.

Adolescent

[Multi-metabolic syndrome in obese children].

The occurrence of multimetabolic syndrome was studied in 114 (63 boys, 51 girls) obese children. From the blood sample taken after on overnight fast blood sugar, serum insulin, and lipid levels were determined. During oral glucose tolerance test blood sugar concentrations were followed. Body mass index, body fat (on the basis of skinfold measurements), lean body mass and waist/hip ratio were calculated and blood pressure was measured 6 times in all subjects. Multimetabolic syndrome was found in 16% of boys and 19.6% of girls. No significant sex difference in the frequency of multimetabolic syndrome was found. Patients with multimetabolic syndrome could not be characterized by high waist/hip ratio any other antropometric parameter. The duration of obesity was significantly higher in subjects with multimetabolic syndrome than in those not suffering from the syndrome. This finding supports the hypothesis that the development of the multimetabolic syndrome is a process. The authors emphasize the significance of this problem and the importance of early recognition and prevention.

Adolescent

Measured and predicted resting metabolic rate in obese and nonobese adolescents.

OBJECTIVES: The validity of equations for the calculation of resting metabolic rate (RMR) were studied and new predictive equations were developed. STUDY DESIGN: The RMR was measured in a sample of 371 10- to 16-year-old prepubertal and postpubertal children. The study group included 193 male (116 nonobese and 77 obese) and 178 female (119 nonobese and 59 obese) subjects; for each group the RMRs predicted from five equations recommended for this age group were compared. The RMR was assessed by indirect calorimetry with a ventilated hood system for 45 minutes after an overnight fast. Body composition was estimated from skin-fold measurements. RESULTS: The mean +/- SD RMR was found to be 5600 +/- 972 kJ/24 hr and 7223 +/- 1220 kJ/24 hr in nonobese and obese boys, and 5112 +/- 632 kJ/24 hr and 6665 +/- 1106 kJ/24 hr in nonobese and obese girls, respectively. All five equations applicable to 10- to 16-year-old children overestimated RMR by 7.5% to 18.1% (p < 0.001 for each equation). Stepwise regression analysis, with independent variables such as age, weight, height, and gender, allowed development of new predictive equations for the calculation of RMR in 10- to 16-year-old boys (RMR = 50.9 Weight (kg) + 25.3 Height (cm) -50.3 Age (yr) + 26.9; R2 = 0.884, p < 0.0001) and girls (RMR = 51.2 Weight (kg) + 24.5 Height (cm) - 207.5 Age (yr) + 1629.8; R2 = 0.824, p < 0.0001). These predictive equations were tested in a second, independent cohort of children (80 male and 61 female subject) and were found to give a reliable estimate of RMR in 10- to 16-year-old obese and nonobese adolescents. CONCLUSIONS: The currently used predictive equations overestimate RMR in 10- to 16-year-old children. The use of the newly developed equations is recommended.

Adolescent

Effects of ephedrine and aminophylline on resting energy expenditure in obese adolescents.

The thermogenic effect of ephedrine (E) and aminophylline (AP) was investigated in 27 and 20 obese adolescents by indirect calorimetry. Ten children receiving only water served as controls. Nine children from both groups had no thermic response to the drugs (NR). The responders (R) increased their fasting REE by 7.1+ -0.75% and 6.4+ -1.0% after E and AP administration, respectively. After one-week E treatment the thermic effect of the drug disappeared even in the R. One-week AP treatment significantly improved the thermic response in the NR and did not alter it in the R. When the combination of E and AP was given to 8 responders the thermic response was no higher than after the single drug.

Adolescent

The effect of meal frequency on postprandial thermogenesis in obese children.

The effect of meal frequency on the thermic effect of food (TEF) was studied in six obese boys and five obese girls (age: mean +/- SE, 12.7 +/- 0.6 yr). Post-absorptive and postprandial resting energy expenditure (REE) were monitored continuously by indirect calorimetry. The children consumed one large liquid meal (LM) or three consecutive small meals (SM) at 1.5 h intervals on subsequent days. The first mode of nutrient intake was determined random. The energy content of the LM and one SM was tailored to provide 30% and 10% of the 24 h postabsorptive REE, respectively. The postprandial changes in REE were monitored for 6 h. The postabsorptive REE (mean +/- SE) was 4.86 +/- 0.28 and 4.9 +/- 0.27 kJ/min before the LM and SM, respectively. REE, respiratory quotient, plasma glucose and insulin concentrations increased sooner, steeper and higher with the LM than with the SM. The magnitude of the TEF was greater (p < 0.02) after the LM (11.9 +/- 1.3%) than after the SM (8.5 +/- 0.7%). It is concluded that the frequency of food consumption influences the immediate thermogenic response as well as the changes in respiratory quotient, glycaemia and insulinaemia. However, the complex effect of different meal frequencies on the overall energy balance of obese patients cannot be answered on the basis of the present results.

Adolescent

[Lipid- and lipoprotein-cholesterol levels in the first 8 months of low-weight (less than or equal to 1500 g) premature infants].

Lipid levels were determined in 30 low birthweight (less than or equal to 1500 g) preterm infants (birthweight: 1122 +/- 192 g, gestational age: 29,0 +/- 1,7 weeks, mean +/- SD) on the 1st, 14th, 28th, 42nd and 56th days of life. Triglyceride and cholesterol were measured by a Boehringer kit, while HDL-cholesterol and its subfractions by microprecipitation methods. Both triglyceride and cholesterol levels increased significantly from the 1st to the 14th and from the 14th to the 28th days. VLDL + LDL-cholesterol level increased significantly by the 14th day, while HDL-cholesterol level by the 28th day. From the 1st to the 14th day the increment of cholesterol levels was significantly higher in breast milk-fed newborns (n = 18) than in those receiving formula (n = 12). Consequently, on the 14th, 28th and 42nd days cholesterol levels were significantly higher in breast milk-fed newborns than in those receiving formula. By the age of two months, however, the difference diminished.

Cholesterol

The glucose-induced insulin release after adrenalectomy in the rat.

Plasma glucose and insulin levels following glucose loading were investigated in adrenalectomized rats. Both oral and intravenous administration of glucose induced an elevation in plasma glucose and insulin level. The increases of plasma glucose and insulin concentrations were significantly higher in the adrenalectomized rats compared with the controls. We conclude, that corticoid hormones are capable of inhibiting glucose-induced insulin release in the rat.

Adrenalectomy

Lack of inhibitory effect of verapamil on glucose-induced insulin release in the rat.

The effect of the calcium-antagonist Verapamil was investigated on the blood glucose and insulin release in rats. Verapamil induced a significant elevation of the blood glucose and increased the insulin release too, however, it was not able to inhibit the glucose-induced insulin release. The authors suggest, that the effect of glucose is not restricted for the calcium turnover of the islets of the pancreas, and may be there are other cellular mechanisms apart from the effect on the calcium movements by which glucose induces insulin release.

Analysis of Variance

The metabolic and hormonal effects of continuous subcutaneous insulin infusion therapy in diabetic children.

To find out whether the concurrent metabolic and hormonal abnormalities are corrected when normoglycaemia is achieved, two groups of diabetic children (newly-diagnosed and chronically-treated) were treated with insulin pumps. Fasting levels of metabolites, lipids and hormones were measured before and after 8 to 10 days of pump treatment and the immediate postprandial hormonal and metabolic changes after a test-meal were also measured. Restoration of normoglycaemia was accompanied by correction of multiple metabolic abnormalities including the normalisation of fasting plasma free insulin, growth hormone, free fatty acid, triglyceride and total cholesterol levels. Plasma glucagon, however, decreased below normal, and significant hypoketonaemia developed in newly-diagnosed diabetic children. The fall in (VLDL + LDL)-cholesterol levels was accompanied by a substantial increase in HDL2-cholesterol concentration in newly-diagnosed diabetic children, whereas pump-treatment resulted in a decrease of the HDL3-cholesterol subfraction in chronically-treated diabetic children. The postprandial blood glucose and free insulin profiles were similar to that of control subjects, but there was an "abnormal" postmeal fall in plasma glucagon and free fatty acid levels. These changes together with the fasting hypoglucagonaemia and hypoketonaemia indirectly suggest that optimal glycaemic control is only achievable at the expense of "increased insulin action" despite the failure to detect peripheral hyperinsulinaemia. Furthermore, the restoration of normoglycaemia and the simultaneous normalisation of the metabolic and endocrine milieu is not entirely possible with this mode of therapy.

Adolescent