Abstract:BackgroundEpidemiological investigation of insulin resistance is difficult. Standard measures of insulin resistance require invasive investigations, which are impractical for large-scale studies. Surrogate measures using fasting blood samples have been developed, but even these are difficult to obtain in population-based studies. Measures of insulin resistance have not been validated in non-fasting blood samples. Our objective was to assess the correlations between fasting and non-fasting measures of insulin r… Show more
“…In agreement with the results from previous studies on leptin concentration and body weight, we found that serum leptin concentrations were dependent on gender and BMI (Hassink et al 1996;Blum et al 1997;Garcia-Mayor et al 1997). Our findings of a more advanced pubertal development together with higher leptin levels are also in agreement with a study showing leptin concentrations to be higher in post-pubertal girls than in prepubertal girls (Demerath et al 1999).…”
Children with peer problems have higher stress and eat more, acquire a higher body fat mass and thus, through increased leptin resistance, exhibit higher leptin levels.
“…In agreement with the results from previous studies on leptin concentration and body weight, we found that serum leptin concentrations were dependent on gender and BMI (Hassink et al 1996;Blum et al 1997;Garcia-Mayor et al 1997). Our findings of a more advanced pubertal development together with higher leptin levels are also in agreement with a study showing leptin concentrations to be higher in post-pubertal girls than in prepubertal girls (Demerath et al 1999).…”
Children with peer problems have higher stress and eat more, acquire a higher body fat mass and thus, through increased leptin resistance, exhibit higher leptin levels.
“…Such conditions can drive profound endocrine disruptions in other species, including disturbed insulin-glucose metabolism. Therefore, we assessed non-fasting insulin and glucose as measures of insulin sensitivity, as used in population-based studies of humans (Hancox and Landhuis, 2011) and for routine diagnosis of insulin resistance and metabolic syndrome in the horse (Divers, 2008;Treiber et al, 2005). The non-fasting insulin reference interval for free-ranging black rhinos of 1.8-19.4 lU/mL was similar to the 2-15 lU/mL reported for the horse (Nadeau et al, 2006;Pagan et al, 2009).…”
Section: Discussionmentioning
confidence: 95%
“…Briefly, we applied this non-parametric, robust estimation method following box-cox transformation and outlier removal. Additionally, indices of insulin secretion (insulin-to-glucose ratio, I/G) and insulin sensitivity (glucose-to-insulin ratio, G/I; quantitative insulin sensitivity check index, QUICKI; reciprocal of the square root of insulin, RISQI) validated for the human (Hancox and Landhuis, 2011;He et al, 1999;Katz et al, 2000;Kronborg et al, 2007;Sullivan et al, 2004), cat (Bjornvad et al, 2014) and horse (Frank, 2009;Kronfeld et al, 2005;Treiber et al, 2005) were calculated to allow cross-species comparisons. The insulin sensitivity index QUICKI was calculated as 1/[log(insulin)+log(glucose)], and RISQI was determined as insulin À0.5 .…”
“…While serum concentrations of insulin are markedly affected by composition and time from recent meals, serum concentrations of leptin seem less affected. However, estimates of insulin resistance measured in non-fasting blood seem to correlate well with values obtained in fasting blood samples (Hancox and Landhuis, 2011), thus suggesting that non-fasting blood samples can be used. On the other hand we cannot exclude possible bias related to taking the blood samples in the fasting state has remained.…”
Background
Several persistent organochlorine pollutants (POPs) possess endocrine disrupting abilities, thereby potentially leading to an increased risk of obesity and metabolic diseases, especially if the exposure occurs during prenatal life. We have previously found associations between prenatal POP exposures and increased BMI, waist circumference and change in BMI from 5 to 7 years of age, though only among girls with overweight mothers.
Objectives
In the same birth cohort, we investigated whether prenatal POP exposure was associated with serum concentrations of insulin and leptin among 5-year-old children, thus possibly mediating the association with overweight and obesity at 7 years of age.
Methods
The analyses were based on a prospective Faroese Birth Cohort (n=656), recruited between 1997 and 2000. Major POPs, polychlorinated biphenyls (PCBs), p,p’-dichlorodiphenyldichloroethylene (DDE) and hexachlorobenzene (HCB), were measured in maternal pregnancy serum and breast milk. Children were followed-up at the age of 5 years where a non-fasting blood sample was drawn; 520 children (273 boys and 247 girls) had adequate serum amounts available for biomarker analyses by Luminex® technology. Insulin and leptin concentrations were transformed from continuous to binary variables, using the 75th percentile as a cut-off point. Multiple logistic regression was used to investigate associations between prenatal POP exposures and non-fasting serum concentrations of insulin and leptin at age 5 while taking into account confounders.
Results
Girls with highest prenatal POP exposure were more likely to have high non-fasting insulin levels (PCBs 4th quartile: OR=3.71; 95% CI: 1.36, 10.01. DDE 4th quartile: OR=2.75; 95% CI: 1.09, 6.90. HCB 4th quartile: OR=1.98; 95% CI: 1.06, 3.69) compared to girls in the lowest quartile. No significant associations were observed with leptin, or among boys. A mediating effect of insulin or leptin on later obesity was not observed.
Conclusion
These findings suggest, that for girls, prenatal exposure to POPs may play a role for later development of metabolic diseases by affecting the level of insulin.
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