Insulin resistance markers in term, normoweight neonates. The Mérida cohort

Gesteiro, Eva; Bastida, Sara; Sánchez‐Muniz, Francisco J.

doi:10.1007/s00431-008-0750-x

Cited by 21 publications

(36 citation statements)

References 24 publications

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“…Insulin could not be measured in 7 infants due to hemolysis. The mean values of glucose, insulin, HOMA-IR, and QUICKI were within the 5th and 95th percentiles published by Gesteiro et al [14] (Fig. 1).…”

Section: Resultsmentioning

confidence: 51%

“…1 Mean homeostasis model assessment for insulin resistance (HOMA-IR) values ( a ) and quantitative insulin sensitivity check index (QUICKI) values ( b ) according to percentiles published by Gesteiro et al [14]. …”

Section: Resultsmentioning

confidence: 99%

“…The mean values of glucose, insulin, HOMA-IR, and QUICKI were then compared with the normal ranges of insulin sensitivity and resistance parameters assessed in AGA full-term newborns by Gesteiro et al [14]. …”

Section: Methodsmentioning

confidence: 99%

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Is Fat Mass Accretion of Late Preterm Infants Associated with Insulin Resistance?

et al. 2017

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Background: Late preterm infants show a major fat mass accretion from birth to term. The contribution of preterm birth to the development of the metabolic syndrome is still under investigation. Objectives: To evaluate body composition changes in late preterm infants during the first 3 months and to investigate their insulin sensitivity and resistance. Methods: We conducted an observational, longitudinal study. A total of 216 late preterm infants underwent body composition assessment using an air displacement plethysmograph at term and at 3 months of corrected age. In a subgroup of infants (n = 48) the blood glucose and insulin concentration were determined at term and insulin resistance (homeostasis model assessment for insulin resistance; HOMA-IR) and sensitivity (quantitative insulin sensitivity check index; QUICKI) were then calculated. The reference group comprised 71 healthy term infants. Results: The mean birth weight and gestational age were 2,390 ± 391 g and 35.2 ± 0.8 weeks, respectively. At term the fat mass index (kg/m²) of late preterm infants, born adequate for their gestational age and small for their gestational age, was higher than that of term infants (2.08 ± 0.82 vs. 1.62 ± 0.64 vs. 1.03 ± 0.36, p < 0.005, respectively), whereas at 3 months of corrected age no difference was found among the groups. The mean values of glucose, insulin, HOMA-IR, and QUICKI were within the 5th and 95th percentiles. Conclusions: On the basis of these preliminary findings, fat mass accretion of late preterm infants appears not to be associated with perturbation of the glucose homeostasis.

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Section: Resultsmentioning

confidence: 51%

Section: Resultsmentioning

confidence: 99%

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Is Fat Mass Accretion of Late Preterm Infants Associated with Insulin Resistance?

et al. 2017

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“…These newborns belonged to the Mérida cohort, whose characteristics have been previously defined [12]. All selected neonates were Caucasian, singleton, full-term (between 37 and <42 weeks), normoweight (between 2.5 and <4.0 kg) infants born without foetal distress (Apgar scores of ≥7 and ≥9 at 1 and 5 min, respectively).…”

Section: Sample Characteristicsmentioning

confidence: 99%

Effects of APOA5 S19W polymorphism on growth, insulin sensitivity and lipoproteins in normoweight neonates

et al. 2011

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Apolipoprotein (Apo) A5 is a protein involved in the activation of lipoprotein lipase (LPL) and the metabolism of triglyceride (TG)-rich lipoproteins. LPL plays a major role in the metabolism of TG-rich lipoproteins, and placental LPL activity is known to correlate positively with foetal fat deposition and size. We examine the association between the common APOA5 S19W polymorphism and neonatal anthropometrical measurements, lipoprotein and hormone concentrations, and insulin sensitivity in 58 normal weight Caucasian newborns from the Mérida cohort. Neonates with the W allele displayed lower BMI (P<0.001), ponderal index (P<0.001), birth weight (P< 0.01), insulin levels (P<0.05), the insulin/cortisol ratio (P< 0.05), HOMA-R (P<0.05) and Apo B values (P<0.01), but higher oxidised LDL (LDLox) values and a higher LDLox/ low-density lipoprotein (LDL) ratio (both P<0.05) than Shomozygous newborns. The APOA5 S19W polymorphism was associated with foetal growth as well as with glucose and lipoprotein metabolism in the neonates. Concurrence of the S19W polymorphism in neonates and their mothers did not affect neonatal lipid and lipoprotein concentrations but was associated with impaired foetal growth. Specifically, W allele carriers displayed a higher degree of LDL oxidation and lower body weight, plasma insulin values, insulin/ cortisol ratio and Apo B concentrations than homozygotes for the common S allele. In conclusion, these findings suggest that the W allele carriers received a less optimal nutrition during gestation and that their lipoprotein antioxidant status was inferior to that of their homozygous S allele counterparts.

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“…Hyperinsulinemia was defined as plasma IRI ≥ 2 μU/ml, as proposed by Hasegawa et al 11) The plasma cortisol level was measured by the electrochemiluminescence immunoassay method (reference value 6.2-19.4 μg/dl). Insulin resistance was also evaluated using HOMA-R (= fasting plasma glucose × fasting plasma IRI/405), QUICKI (= 1/[log (fasting plasma IRI) + log (fasting plasma glucose)]) 12,13) , plasma glucose/IRI ratio, and plasma IRI/cortisol ratio 14) . The main analyses compared insulin resistance between two groups, such as male and female neonates, preterm and full-term neonates, neonates with SGA and neonates with AGA, the presence or absence of asphyxia, and the presence or absence of hypoglycemia in hyperinsulinemia.…”

Section: Methodsmentioning

confidence: 99%

Association between Perinatal Status and Insulin Resistance in Neonates during the Birth Period

Nagano

Urakami

Fuwa

et al. 2016

Nichidai Igaku Zasshi

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The aim of this study was to assess the association between perinatal status and insulin resistance in neonates during the birth period. The subjects were 49 neonates (27 boys, 22 girls) who had been admitted to the neonatal intensive care unit at Nihon University Itabashi Hospital within 2 h after birth. We retrospectively analyzed the associations between perinatal status (Apgar score, sex, gestational age, birth weight, etc.) and insulin resistance (assessed by plasma immunoreactive insulin (IRI), plasma cortisol, homeostatic model analysis ratio (HOMA-R), quantitative insulin sensitivity check index (QUICKI), plasma glucose/IRI ratio, and plasma IRI/cortisol ratio) based on the medical records. The preterm neonates had significantly lower plasma cortisol levels (P = 0.02) and significantly higher plasma IRI/cortisol ratios (P = 0.04) compared with the full-term neonates. No significant differences were found in any of the parameters between neonates with asphyxia and those without. In cases with hyperinsulinemia, male predominance was significant (P < 0.01) in neonates with hypoglycemia; furthermore, birth weight, HOMA-R, and plasma glucose/IRI ratio tended to be lower (P = 0.07, P = 0.01 and P < 0.01, respectively), while QUICKI and plasma IRI/cortisol ratio tended to be higher (P = 0.02 and P = 0.09, respectively) in neonates with hypoglycemia compared with those without. One possible reason for these findings could be the immaturity of the hypothalamic-pituitary-adrenal axis in preterm infants. There was no significant correlation between perinatal status and the indices of insulin resistance in neonates during the birth period.

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Insulin resistance markers in term, normoweight neonates. The Mérida cohort

Cited by 21 publications

References 24 publications

Is Fat Mass Accretion of Late Preterm Infants Associated with Insulin Resistance?

Is Fat Mass Accretion of Late Preterm Infants Associated with Insulin Resistance?

Effects of APOA5 S19W polymorphism on growth, insulin sensitivity and lipoproteins in normoweight neonates

Association between Perinatal Status and Insulin Resistance in Neonates during the Birth Period

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