Insulina, leptina y grado de resistencia a la insulina en niños escolares con y sin obesidad

Revista de Especialidades Médico-Quirúrgicas (México) Num.4 Vol.15
Source: OAI

ABSTRACT Doppler transcraneal, clipaje de aneurisma.

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    ABSTRACT: To investigate the association between plasma leptin and adiponectin and insulin sensitivity in children, 580 school children (294 boys and 286 girls) with mean age of 13.3 years (12-16 years) were randomly selected from the Taipei Children Heart Study. Baseline measurements included body weight, body mass index (BMI), plasma glucose, insulin, proinsulin, leptin and adiponectin levels. Insulin resistance and beta-cell function were assessed using the method of homeostatic model, HOMA-IR and HOMA-beta, respectively. We found that girls had higher levels of plasma leptin, adiponectin and HOMA-beta than boys. There was no significant difference in HOMA-IR between boys and girls. Plasma leptin concentrations were positively correlated with body weight, BMI, insulin and proinsulin concentrations, HOMA-IR and HOMA-beta, whereas plasma adiponectin levels were inversely associated with body weight, BMI and proinsulin levels in both sexes. In girls, adiponectin concentrations were negatively correlated with insulin concentration and HOMA-IR. In multiple regression analyses, plasma leptin was more positively associated with insulin and proinsulin levels, HOMA-IR and HOMA-beta than was adiponectin in boys. This association persisted even after adjusting for body weight, BMI and pubertal status. In conclusion, plasma leptin was more strongly associated with insulin sensitivity and beta-cell function than was adiponectin among children, particularly in boys.
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    ABSTRACT: In adults and obese children, serum leptin concentrations are closely related to body fat. To investigate whether such a relationship between leptin concentrations and body fat is also evident in children with a relatively normal body composition. The study was a cross-sectional population study in 170 Caucasian children (91 boys and 79 girls), with a mean age of 9.9+/-0.6 y (range 8.5-10.9 y) and a mean BMI of 17.4+/-2.6 (range 12.8-28.1). Serum leptin was measured and compared to total body fat as determined by dual-energy X-ray absorptiometry. In the whole population, serum leptin concentrations were highly correlated with total body fat (r=0.83, p<0.001). A stepwise forward multi-regression analysis revealed that the inclusion of other anthropometrical data did not add any significance to the model. Leptin concentrations were significantly higher in girls (5.2 ng/ml) than in boys (3.2 mg/ml; p=0.003). Gender differences still prevailed (p=0.007) after adjusting for number of kilograms of fat tissue. This study shows that, already at the young age of 9-11 y, an adult-like pattern of regulation of leptin exists. This indicates similar risk factor dependency of leptin across all age groups.
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    ABSTRACT: Skeletal muscle insulin resistance is a co-morbidity of obesity and a risk factor for the development of type 2 diabetes mellitus. Insulin resistance is associated with the accumulation of intramyocellular lipids. Intramyocellular triacylglycerols do not appear to be the cause of insulin resistance but are more likely to be a marker of other lipid intermediates such as fatty acyl-CoA, ceramides or diacylglycerols. Fatty acyl-CoA, ceramides and diacylglycerols are known to directly alter various aspects of the insulin signalling cascade. Insulin signalling is inhibited by the phosphorylation of serine and threonine residues at the levels of the insulin receptor and insulin receptor substrate 1. Protein kinase C is responsible for the phosphorylation of the serine and threonine residues. Fatty acyl-CoA and diacylglycerols are known to activate protein kinase C. The cause of the intramyocellular accumulation of fatty acyl-CoA and diacylglycerols is unclear at this time. Reduced fatty acid oxidation does not appear to be responsible, as fatty acyl-CoA accumulates in skeletal muscle with a normal fatty acid oxidative capacity. Other potential mechanisms include oversupply of lipids to muscle and/or up regulated fatty acid transport.
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