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M G Juste

Publications and source records attributed to M G Juste.

6 recordsLinked to original sources

Leptin and metabolic syndrome in obese and non-obese children.

Metabolic syndrome is characterized by a clustering of metabolic abnormalities: insulin resistance - hyperinsulinemia, dyslipidemia (high triglycerides and low HDL - cholesterol serum concentrations), impaired glucose tolerance and/or type 2 diabetes, and hypertension. The aim of this study was to analyse the role of different variables of metabolic syndrome, including leptin, in 74 non-obese children and 68 children with non-syndromal obesity. As metabolic syndrome variables, we have included body mass index, waist circumference, trunk-to-total skinfolds (%), systolic blood pressure, diastolic blood pressure, glucose, uric acid, fasting insulin, triglycerides and high-density lipoprotein-cholesterol (HDL-C). Factor analysis showed 4 factors in each group. In non-obese children, waist circumference, BMI, fasting insulin, triglycerides, trunk-to-total skinfolds (%), leptin and uric acid loaded positively on factor 1, and HDL-C loaded negatively on this factor; systolic and diastolic blood pressure had high positive loadings in factor 2; HDL-C and leptin showed positive loadings and triglycerides and uric acid, negative loadings in factor 3; and, finally, glucose and insulin showed positive loadings in factor 4. These four factors explained 72.16 % of the total variance in the non-obese group. In obese children, BMI, waist circumference, leptin, diastolic blood pressure and systolic blood pressure loaded positively on factor 1; diastolic blood pressure, trunk-to-total skinfolds (%), uric acid and systolic blood pressure showed high positive loadings in factor 2; fasting insulin, glucose and triglycerides showed positive loadings in factor 3; and, finally, triglycerides showed positive loadings and HDL-C negative loadings in factor 4. These four factors explained 74.18 % of the total variance in the obese group. Our results point to a different homeostatic control of metabolic syndrome characteristics in obese and non-obese children. Leptin seems to play a key underlying role in metabolic syndrome, especially in the obese group.

Blood Glucose↗

Serum leptin concentrations in children with Prader-Willi syndrome and non-syndromal obesity.

There is limited information on the underlying physiological mechanisms promoting obesity in patients with Prader-Willi syndrome (PWS). The aim of this study was to investigate whether body fat regulation in children with PWS is similar to that in children with non-syndromal obesity and non-obese children. We studied three groups: 1) 72 non-obese children and adolescents; 2) 68 children with non-syndromal obesity; and 3) 11 patients with PWS. Height and weight were measured and body mass index (BMI) and BMI SDS were calculated. Fasting serum leptin concentrations were determined. Median leptin serum concentrations were similar in PWS patients and children with non-syndromal obesity. Median leptin serum concentrations were higher in these two groups than in the non-obese group. Log leptin serum concentrations and BMI SDS showed significant correlations in the three groups of patients; correlation coefficients were 0.525, 0.285 and 0.854, respectively. In conclusion, median leptin serum concentrations are similar in PWS patients and children with non-syndromal obesity. The relationship between log serum leptin concentrations and BMI SDS was different in the three groups of patients studied.

Adolescent↗

[Differences of males and females regarding the binding capacity of insulin to erythrocyte receptors].

The analysis of insulin receptors in erythrocytes demands a relatively small blood sample, which justifies the interest in its use as an index of the cellular capacity for binding hormone. In order to establish criteria for normalcy, the capacity of erythrocytes for binding in vitro insulin labelled with 125I before increasing concentrations of cold insulin (from 0.5 to 10(3) ng/ml), was studied in a group of 41 healthy men and another of 35 women with normal menstrual cycles. In the female group the study was carried out in three different days of the same cycle (days 3, 12 and 21). The binding capacity in the male was higher than in the female (p less than 0.05) in the follicular phase (days 3 and 12) as well as in the luteal phase (day 21) and, among women, it was higher in the follicular phase than in the luteal one (p less than 0.05). The results indicate that progesterone, as well as prolactin and glucagon, may play an important role in the binding capacity of insulin to its receptor. To make the values comparable, it is suggested that blood extraction in women be carried out during the first five days of the cycle.

Adult↗

[Insulin receptors in intrauterine growth retardation].

This report analyses erythrocyte insulin binding and specific erythrocyte insulin receptors in the neonatal period. Authors have studied thirty normal newborns who had an adequate weight for their gestational age and another fifteen who were asymmetric intrauterine retarded growth. Cord blood samples were collected and insulin binding, insulin receptors, blood glucose concentration, serum immunoreactive insulin, serum C-peptide concentration and molar ratio of C-peptide to insulin were determined. Insulin and C-peptide sera concentrations suggest that basal insulin secretion in small for data newborns is similar to term infants. Significantly minor affinity constant (p = 0.05) and significantly major dissociation constant (p = 0.05) in small for date infants versus newborns adequately weighted for their gestational age, justify the increased sensitivity to insulin as it happens in other states of chronic undernutrition. In small for date infants, number of sites per cell correlates negatively (r = -0.57, p less than 0.05) with birth weight. Up regulation mechanism that modulates receptors concentration could explain this phenomenon.

Female↗

Urinary triiodothyronine excretion.

The purpose of this work was to estimate the 24 h urinary excretion of free and conjugated triiodotironine (T3) using a direct radioimmunoassay and enzyme hydrolysis. Mean urinary values of free and total T3 (mean +/- 1 SD) in euthyroid controls were 2074 +/- 673 and 2819 +/- 809 pmol/24 h respectively. In patients with hyperthyroidism, values of free hormone were about 4.2 times higher than the mean value of the euthyroid controls, and about one-third in patients with hypothyroidism. These results show this measurement to be useful as an indicator of thyroid function. Mean renal clearance of free T3 was 211.6 +/- 62.8 ml/min (mean +/- 1 SD) in euthyroid controls, 260.8 +/- 87.5 ml/ml in hyperthyroid patients and 229 +/- 98.7 ml/min in hypothyroid patients. The data show that T3 renal clearance is, in all cases, greater than glomerular filtration rate, suggesting tubular secretion of T3.

Adult↗

Thyroxine in unextracted urine.

The aim of this work was to estimate the daily urinary excretion of free and conjugated thyroxine using a direct radioimmunoassay and enzyme hydrolysis. The renal clearance of free T4 was also determined. The mean urinary values of free and total T4 (mean +/- 1 SD) in 112 euthyroid controls were 1353 +/- 496 and 1855 +/- 651 pmol/24 h, respectively. Urinary excretion of free hormone in 13 hyperthyroid patients was 5552 +/- 4320 pmol/24 h and total T4 was 8122 +/- 7219 pmol/24 h. Urinary free T4 excretion was 223 +/- 223 pmol/24 h in hypothyroid patients and total T4 was 542 +/- 490 pmol/24 h. These results indicate that daily urinary T4 excretion is a good indicator of thyroid function. The mean renal clearance of free T4 was 52 +/- 19 ml/min (mean +/- 1 SD) in euthyroid patients, 53.7 +/- 12.3 ml/min in hyperthyroid patients, and 67.6 +/- 13.1 ml/min in hypothyroid patients. We estimated the endogenous creatinine renal clearance as a control of the renal filtration rate. The data suggest that there is T4 filtration of unbound T4 and partial tubular reabsorption. Further experimental studies will be necessary to clarify the renal handling of thyroxine as well as the fate of reabsorbed T4.

Adult↗