Cord Blood Insulin Levels Research Articles

Body Fat at Birth and Cord Blood Levels of Insulin, Adiponectin, Leptin, and Insulin-like Growth Factor-I in Small-for-Gestational-Age Infants

Low birthweight has been associated with an increased risk of obesity, insulin resistance, and diabetes in adulthood. The aim of this study was to evaluate IGF-I, adiponectin, insulin levels, and body fat in small-for-gestational-age (SGA) infants at birth. We performed a transverse comparative study in SGA and appropriate-for-gestational-age (AGA) infants. The study was conducted at the Hospital of Gynecology and Obstetrics in Leon, Mexico. Weight, length, and percent of body fat were evaluated during the first 48 h of birth. Glucose, insulin, leptin, adiponectin, and IGF-I levels in cord blood were measured. We studied 100 infants (50 SGA and 50 AGA). A history of diabetes in a second-degree relative was higher in SGA infants than in AGA infants (48.0 vs. 30.0%, respectively; p = 0.03). Glucose, adiponectin, insulin and IGF-I levels were similar between the groups. Leptin levels and percentage of body fat were lower in SGA than AGA (15.3 vs. 23.4 ng/mL; p = 0.003, 11.1 vs. 12.7%; p <0.001, respectively). Logistic regression analysis showed that length, percentage of body fat, and leptin levels were positively associated with birthweight. However, leptin levels were not independent of percentage of body fat. Low body fat and leptin levels, but no evidence of increased metabolic risk at birth, were found in SGA infants.

Perinatal Morbidity in Women with Undiagnosed Gestational Diabetes in Northern Thuringia in Germany

Undiagnosed gestational diabetes mellitus (GDM) is associated with severe perinatal complications. Out of 970 women, infant and maternal morbidity was assessed in 114 mother-children-pairs with an infant birth weight over the 90th percentile (Voigt et al., 1996). It was the aim of this retrospective study to assess the number of mothers with undiagnosed GDM, who have born a macrosomic child. The macrosomia rate in newborns was 12 % in this study excluding macrosomic infants of mothers with preexisting diabetes mellitus. Maternal data: Age 28.3 +/- 5.3 years, adipositas (body-mass-index > 30 kg/m) in 42.1 % vs. 30.4 % in the peer group (p < 0.02), increase in weight > 15 kg during pregnancy in 57.9 % of the mothers who have given birth to a macrosomic child vs. 30.9 % in the peer group (p < 0.0001), family history of diabetes mellitus (28.0 % vs. 11.3 % in the peer group, p = 0.006), preeclampsia in 8.8 % vs. 2.7 % in the peer group (p = 0.002), cervical insufficiency in 2.6 % vs. 0.4 % in the peer group (p = 0.02). After delivery HbA1c was elevated in 38.6 % of the women having born macrosomic infant (mean HbA1c: 5.0 % +/- 0.5). Infant data: neonatal jaundice 16.7 % vs. 4.5 % in the peer group, p < 0.0001. There were no statistically significant differences concerning perinatal condition and malformations. Neonatal hypoglycaemia occurred in 9.6 % of the macrosomic infants. Cord blood insulin levels were significantly elevated in comparison to the peer group of mothers without metabolic disorders and having born eutroph infants (8.4 mU/l [3.0 - 100.0] vs. 5.3 mU/l [3.0 - 30.7], p = 0.01). 11.4 % of all macrosomic infants had cord blood insulin levels above the normal range. More than one third of the mothers having born one or more macrosomic infants had an impairment of glucose metabolism immediately after birth. The elevated prevalence of preeclampsia in this group confirms the relationship of hypertension and impaired glucose metabolism during pregnancy. The detection of hyperinsulinaemia, postnatal hypoglycaemia, elevated prevalence of neonatal jaundice with need of further therapy and diabetic fetopathy in macrosomic infants of mothers, whose metabolism was not monitored during pregnancy, pinpoint the need for a diagnostic screening for GDM.

Macrosomia revisited: Ponderal index and leptin delineate subtypes of fetal overgrowth

Objectives: We sought to reanalyze the concept of fetal macrosomia with regard to the ponderal index and to investigate the role of insulin, insulinlike growth factor I, leptin, and maternal factors on birth size in a population of infants with nondiabetic mothers. Study Design: Venous cord blood levels of insulin, insulinlike growth factor I, insulinlike growth factor binding protein 3, and leptin were measured in 28 large-for-gestational-age and 21 appropriate-for-gestational-age newborns. Results: Large-for-gestational-age newborns can be divided into symmetric and asymmetric subtypes according to the ponderal index. Mean leptin concentrations in cord blood were significantly higher in asymmetric than in symmetric large-for-gestational-age newborns ( P = .01). A positive correlation was observed between leptin and the ponderal index ( r = 0.53, P = .001) and between leptin and insulin concentrations in cord blood ( r = 0.53, P = .008). Conclusion: Our results strongly suggest that macrosomia should not be classified on the basis of birth weight and gestational age alone. We also show that asymmetric macrosomic infants with nondiabetic mothers have abnormal leptin and insulin concentrations. (Am J Obstet Gynecol 1999;181:621-5.)

Cord Blood Leptin Is Associated with Size at Birth and Predicts Infancy Weight Gain in Humans

Recent discoveries of human genetic leptin deficiency have demonstrated its importance in regulating weight gain in early childhood. To investigate whether normal variation in leptin and insulin levels in cord blood could influence infancy growth, we assayed samples from 197 infants from a representative birth cohort, who were measured at birth, 4, 8, 12 and 24 months. Cord leptin levels correlated most closely with weight and ponderal index (kg/m3) at birth, but also with length and head circumference (all P<0.0005). Independent of birth size, females had higher leptin levels than males (P<0.0005). Cord levels of leptin, but not insulin, were negatively related to weight gain (P<0.005) from birth to 4 months, and accounted for 9.4% of the variance in weight gain, compared with breast/bottle feeding (3.5%) and early/late introduction of solids (1%). The effect of leptin levels on weight gain was independent of birthweight, and was still evident at 24 months. The wide variation in infancy growth (‘catch-up’ or‘ catch-down’) may be partly determined by leptin levels preset in utero. Our data support a role for leptin in the regulation of infancy weight gain, and suggest a mechanism whereby infants may ‘catch-up’ in growth postnatally following an adverse intrauterine environment.

Cord blood leptin is associated with size at birth and predicts infancy weight gain in humans. ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood.

Recent discoveries of human genetic leptin deficiency have demonstrated its importance in regulating weight gain in early childhood. To investigate whether normal variation in leptin and insulin levels in cord blood could influence infancy growth, we assayed samples from 197 infants from a representative birth cohort, who were measured at birth, 4, 8, 12 and 24 months. Cord leptin levels correlated most closely with weight and ponderal index (kg/m3) at birth, but also with length and head circumference (all p<0.0005). Independent of birth size, females had higher leptin levels than males (p<0.0005). Cord levels of leptin, but not insulin, were negatively related to weight gain (p<0.005) from birth to 4 months, and accounted for 9.4% of the variance in weight gain, compared with breast/bottle feeding (3.5%) and early/late introduction of solids (1%). The effect of leptin levels on weight gain was independent of birthweight, and was still evident at 24 months. The wide variation in infancy growth ('catch-up' or 'catch-down') may be partly determined by leptin levels preset in utero. Our data support a role for leptin in the regulation of infancy weight gain, and suggest a mechanism whereby infants may 'catch-up' in growth postnatally following an adverse intrauterine environment.

Cord blood insulin to assess the quality of treatment in diabetic pregnancies.

According to the Pedersen hypothesis, fetal hyperinsulinism is the major cause for adverse neonatal outcome. We investigated associations between insulin levels in cord blood and fetal complications. Three groups of 21 insulin-dependent diabetic patients with different insulin levels in cord blood were matched according to White Classes. Insulin levels in cord blood of < 20 microU/ml were considered normal (controls), 20-50 microU/ml intermediate group, and > 50 microU/ml high (cases). The mean (+/-S.D.) insulin level in cord blood in the three groups was 10.7+/-5.6, 28.6+/-8.1, and 104.0+/-61.0 microU/ml, respectively. Controls and cases showed significant differences in birth weight > 90th percentile (9.5% vs. 76.2%), premature birth < 37 weeks (4.8% vs. 71.4%), caesarean delivery (28.6% vs. 66.4%), hypoglycaemia of the neonate (14.3% vs. 61.9%), cushingoid appearance (4.8% vs. 42.9%) and respiratory distress syndrome (0% vs. 33.3%). The results of the intermediate group were between the controls and the cases. Insulin levels in cord blood > 20 microU/ml represent a continuum of increasing diabetogenic fetopathy. We consider neonates with insulin levels in cord blood < 20 microU/ml as metabolically healthy, those with 20-50 microU/ml as having mild fetopathy, and those with > 50 microU/ml as having marked fetopathy, respectively.

Endocrine Pancreatic Function in Fetuses of Gestational Diabetic and Nondiabetic Mothers

C-peptide, insulin, and glucagon levels were measured in the cord blood of 112 nondiabetics controls and 63 diabetic mothers. The cord blood levels of insulin and C-peptide were significantly higher in the diabetic compared to the control group. In the control group, C-peptide levels were positively correlated with fetal birthweight. In the diabetic group, there was a positive correlation between birth-weight and both C-peptide and insulin levels. Neonates were stratified into six categories of birthweight centiles. In the diabetic group, the insulin level was significantly higher than in the control group at all categories of birthweight centiles. Also, the C-peptide level was higher in the diabetic than in the control group, except at the >25 and ≥10 categories of birthweight centile. Glucagon levels were significantly higher among controls, at all categories of birthweight centiles, except in fetuses below the 10th centile of birth weight. The insulin/C-peptide ratio, a ratio that reflects hepatic insu...

Fetal growth control: the role of insulin and related peptides.

Both insulin and the related peptides, the insulin-like growth factors/somatomedins, may function as anabolic factors in the regulation of fetal body size. Infants born to women suffering from diabetes mellitus may show increased deposition of subcutaneous fat and enhanced lean body mass, findings reproduced in experimental animal fetuses with induced hyperinsulinaemia. Fetal adiposity may be associated with a life-time tendency to obesity and its associated diseases. Insulin-like growth factors I (IGFI) and II are present in the circulation of the newborn infant and animal fetus and correlate positively with birth size. The fetal tissues are biologically responsive to IGFs in vitro and are rich in specific cell membrane receptors, those predominantly recognizing IGFI being structurally and functionally similar to the insulin receptor. Insulin could theoretically influence fetal tissues by an interaction with either the insulin or IGF receptor. IGF release is a property of multiple fetal tissues in vitro, but, in contrast to postnatal life, is not dependent on growth hormone. Fetal IGF production may be influenced by placental lactogen, especially IGFII which rapidly declines in the circulation following parturition in the rat and sheep. A positive association also exists between circulating levels of insulin and IGFs when the former is experimentally manipulated in the animal fetus. Similarly the infant born with transient diabetes mellitus has low cord blood levels of insulin and IGFI. Insulin has a dual role in prenatal life. In the last trimester insulin functions as a glucoregulatory hormone, but from much earlier in gestation creates an anabolic environment in the fetus supplied with optimal nutrients. This latter mechanism of action is unclear and probably heterogeneous, but in overview is permissive rather than obligatory. In contrast the growth-promoting role of the IGFs is direct but their interaction with fetal tissues, and thus the overall emphasis of fetal growth, may be paracrine.

Transplacental Passage of Islet Cell Antibody in Infants of Diabetic Mothers

The incidence of pancreatic islet cell antibody (ICAb) was assessed in the cord blood and sera of infants of diabetic mothers (IDM). ICAb activity was detected in the cord blood of 10 of 36 (27.8%) consecutive IDM studied and in 0 of 111 (0%) cord bloods of normal control infants. In all instances, ICAb activity in the cord sera was of the immunoglobulin (IgG) class and was associated with ICAb in maternal sera at the time of delivery. No correlation was observed between the incidence of ICAb in IDM and alterations in fetal growth parameters, congenital malformation rates, cord blood insulin levels, or the incidence of neonatal complications. The evidence would support transplacental passage of ICAb from diabetic mothers to their offspring, but would not support a primary pathogenetic role for ICAb in the clinical or metabolic alterations observed in these infants.