Insulin and Leptin Levels in Appropriate-for-Gestational-Age Infants of Diabetic Mother

Objective

Intensified management of gestational diabetes mellitus can normalize birth weight. However, it is still unknown whether intrauterine exposure to maternal diabetes is a risk factor for changing hormone levels involved in the development of insulin resistance in these infants. We compared insulin and leptin levels in appropriate for gestational age (AGA) infants of diabetic and non diabetic mothers.

Methods

We performed a cross-sectional study in the department of Neonatology of the Hospital of Gynecology-Pediatrics, in Leon, Mexico. We evaluated 182 full term AGA newborns (86 infants of diabetic and 96 of non-diabetic mothers). A venous blood sample was taken from cord blood immediately after the separation of the placenta and glucose, insulin and leptin levels were measured. In all diabetic mothers HbA1c was also evaluated immediately post-partum.

Findings

Leptin, insulin and insulin resistance index were significantly higher in infants of diabetic mothers. Leptin levels were positive correlated with insulin, parents‘ body mass index and age in the entire group. In infants of diabetic mothers only insulin levels showed a significantly correlation, whereas in those of non-diabetic mothers only mothers‘ age was significantly correlated with leptin levels.

Conclusion

AGA infants of diabetic mothers showed higher leptin, insulin levels and insulin resistance index than those of non-diabetic mothers.     

Leptin and metabolic hormones in preterm newborns

AIM: To investigate the inter-relation between leptin and other metabolic hormones in preterm and term infants and to explore whether a functional "adipoinsular axis" might exist in preterm newborns. METHODS: A total of 140 preterm and term newborns were prospectively recruited and categorised according to gestation length. Blood samples were taken at 24 hours (day 1), and on day 4-5 of life. RESULTS: Serum leptin, cortisol, free thyroxine, and plasma ACTH on day 1 were significantly higher in term than in preterm infants. The relation between serum leptin and gestation followed a non-linear pattern; the slope of the curve began to increase steeply between 33 and 35 weeks gestation. Serum leptin on day 1 was significantly associated with serum insulin, insulin:glucose ratio, and plasma ACTH in infants less than 34 weeks gestation; serum leptin on day 1 and day 4-5 were significantly correlated with insulin:glucose ratio in infants 34 or more weeks gestation. Significant changes in the pattern of metabolic hormones were observed in the first week of life. Serum insulin and plasma glucose were significantly increased between day 1 and day 4-5; serum leptin was significantly decreased. CONCLUSIONS: The circulating leptin concentration increases markedly after 34 weeks gestation and bears a close temporal relation with the exponential accumulation of body fat mass during that period. The inter-relation between serum leptin and insulin or insulin:glucose ratio before and after 34 weeks gestation indicates that the "adipoinsular axis" is likely to be functional in early (<34 weeks gestation) intrauterine life. The rapid decline in the circulating concentrations of leptin after birth may be of physiological advantage to preterm and term newborns by limiting their body energy expenditure and conserving nutritional reverses for subsequent growth and development.     

Cord blood leptin levels: relationship to body weight, body mass index, sex and insulin and cortisol levels of maternal-newborn pairs at delivery

To investigate leptin and to which factors it is related during the perinatal period, we measured serum leptin levels of 46 mothers at delivery, umbilical cord blood and infants on the third day of life. Maternal leptin was higher than in cord (p < 0.001), and did not correlate with maternal age, body weight, body mass index, weight gain during pregnancy, serum glucose, cholesterol, triglycerides, CPE, cortisol or HbA1c levels, nor any biochemical values or anthropometric data of the newborns (p > 0.05). In cord blood, leptin was significantly higher than in 3 day-old infants (p < 0.05), and correlated only with maternal insulin and glucose (r = 0.5, p < 0.01 and r = 0.4, p < 0.05, respectively). In 3 day-old infants, leptin did not correlate with any clinical data (p > 0.05). Leptin was not different in the two sexes (p > 0.05). Serum leptin levels were not related to adiposity of the mother-infant pairs or neonatal growth, and were not different in the two sexes during the perinatal period.     

Postnatal changes in concentrations of free and bound leptin

AIM: To evaluate the effect of maternal diabetes on the concentrations of free and bound leptin at birth and during postnatal adaptation. METHODS: Total, bound, and free leptin concentrations and the percentage of free leptin were measured in cord plasma and plasma at 3 days of age of 13 term infants of mothers with gestational diabetes mellitus (GDM) and 13 term infants of healthy mothers. Gestational age was 40.2 (1.4) weeks, and birth weight was 3693 (549) g (means (SD)). RESULTS: At birth, infants of mothers with GDM had significantly higher concentrations of total, bound, and free leptin and a higher percentage of free leptin (all p < 0.05). In all infants, these concentrations were significantly lower at 3 days of age than at birth (all p < 0.003), and the differences in concentrations of total, bound, and free leptin between the two groups were no longer significant. In infants of mothers with GDM, the percentage of free leptin remained unchanged, and was higher (p<0.05) than in infants of healthy mothers; in the latter group the percentage of free leptin significantly declined (p = 0.02). CONCLUSIONS: GDM appears to influence fetoplacental leptin metabolism. This effect may be mediated through altered maternal glucose metabolism, or insulinaemia, or both.     

新生儿血清瘦素、生长激素、胰岛素样生长因子-1、胰岛素样生长因子结合蛋白-3水平与宫内发育的关系

目的 探讨瘦素(leptin)、生长激素(GH)、胰岛素样生长因子-1(IGF-1)、胰岛素样生长因子结合蛋白-3(IGFBP-3)在不同宫内发育状况胎儿中的变化,及对胎儿生长发育调控的作用.方法 2004年1月-2006年6月出生早产小于胎龄儿(A组)30例,早产适于胎龄儿(B组)36例,足月小于胎龄儿(C组)32例,足月适于胎龄儿(D组)37例.生后24 h内抽取患儿静脉血,用放射免疫法(RIA)检测其血清leptin、GH、IGF-1、IGFBP-3水平,组间比较采用及多元回归相关分析.结果 各组新生儿血清leptin、GH、IGF-1、IGFBP-3水平均存在明显差异(Pa<0.05,0.01),各指标基本呈C、A、B、D组次序由低到高,但A组IGF-1与C组差异无统计学意义(P>0.05);在A、B和C组,出生体质量与leptin、IGF-1、IGFBP-3呈正相关(Pa<0.01),而D组出生体质量与IGF-1呈正相关(P<0.01),与其他激素无相关性.结论 leptin、IGF-1、IGFBP-3参与宫内发育迟缓儿和早产儿宫内生长发育的调控.IGF-1在早产适于胎龄儿的宫内生长发育中也起调控作用,而leptin、GH、IGFBP-3均不是足月适于胎龄儿生长发育的主要调节因素.     

妊娠期合并糖代谢异常对新生儿胰岛素敏感性的影响

目的探讨妊娠期合并糖代谢异常对子代新生儿期胰岛素敏感性的影响。方法选择2009年12月至2010年11月本院产科出生的新生儿,根据母亲妊娠期是否合并糖代谢异常分为糖代谢异常母亲的新生儿和糖代谢正常母亲的新生儿。所有研究对象均进行出生体格测量,并于生后 3 天内测定空腹血糖( FPG) 和空腹血清胰岛素( FINS) ,计算胰岛素敏感指数( ISI) ,采用胰岛素稳态模型( HOMA) 计算胰岛素抵抗指数( IR) ,即 HOMA-IR,其中 FINS、ISI 和 HOMA-IR 值为胰岛素敏感性的评价指标。以性别、胎龄、出生体重为协变量,分别在早产儿和足月儿中进行胰岛素敏感性的协方差分析。结果 89 例早产新生儿和 96 例足月新生儿纳入分析。糖代谢异常母亲新生儿的出生体重、出生身长和重量指数( PI) 与糖代谢正常母亲的新生儿相比,差异无统计学意义( P >0. 05) 。与糖代谢正常母亲的早产儿相比,糖代谢异常母亲的早产儿 FPG 降低、FINS 升高,差异有统计学意义[FPG( mmol/L) : ( 4. 00 ±0. 25) 比( 4. 82 ±0. 18) ,FINS( 经对数 Lg 转换) : ( 0. 69± 0. 06) 比( 0. 54 ± 0. 04) ,P < 0. 05],ISI 值降低、HOMA-IR 值升高,但差异无统计学意义[ISI( 经对数 Ln 转换) : ( -2. 89 ±0. 15) 比( -2. 78 ±0. 11) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 10 ±0. 06)比( -0. 15 ±0. 05) ,P >0. 05]; 足月儿中糖代谢异常母亲的新生儿 FPG、FINS 和 HOMA-IR 值低,ISI 值高,但差异均无统计学意义[FPG( mmol / L) : ( 4. 68 ± 0. 23) 比( 5. 17 ± 0. 13) ,FINS( 经对数 Lg转换) : ( 0. 56 ±0. 06) 比( 0. 61 ±0. 03) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 14 ±0. 06) 比( -0. 03± 0. 03) ,ISI( 经对数 Ln 转换) : ( - 2. 79 ± 0. 14) 比( - 3. 04 ± 0. 08) ,P > 0. 05]。结论母亲妊娠期合并糖代谢异常虽然对新生儿的出生体重没有影响,但血糖仍然呈现低水平趋势,且对早产儿胰岛素敏感性可能有一定的影响。     

Changes in serum leptin concentration after corticosteroid treatment in preterm infants

The aim of this study was to investigate the effect of postnatal systemic dexamethasone on serum leptin, insulin and hormones of the hypothalamic-pituitary-adrenal (HPA) axis in preterm, very low birthweight (VLBW) infants. Nineteen VLBW infants who received a 3 wk dose tapering course of dexamethasone for treatment of bronchopulmonary dysplasia were prospectively enrolled. Blood for hormone assays was collected immediately before the start of the dexamethasone course (T(d-per)), 3 wk after commencement of the drug (T(d-end)) and 2 wk after dexamethasone treatment had been stopped (T(d-post)). In addition, 28 VLBW infants who participated in a concurrent longitudinal leptin study within the same period but did not receive corticosteroid had their serum leptin and insulin concentrations serially monitored. Blood specimens for the latter group of infants were obtained at 2 (T(wk-2)), 5 (T(wk-5)) and 7 (T(wk-7)) wk of postnatal age. Serum leptin and insulin at T(d-end) were significantly increased, whereas plasma ACTH and serum cortisol were significantly suppressed compared with the pretreatment (T(d-pre)) levels in the corticosteroid group (p < 0.0001 for leptin and insulin; p < 0.05 and p < 0.001 for ACTH and cortisol, respectively). In contrast, serum leptin and insulin at weeks 5 (T(wk-5)) and 7 (T(wk-7)) did not differ significantly from their respective levels at week 2 (T(wk-2)) in the non-treatment group. CONCLUSION: The administration of systemic corticosteroid resulted in significant increases in serum leptin and insulin, but marked suppression of hormones of the HPA axis. The effect of dexamethasone on the "adipoinsular" and HPA axes was transient and reversible. The adipoinsular axis in preterm infants is likely to be functional and active at an early stage of human development, and leptin may regulate energy balance in VLBW infants in the early postnatal period. Corticosteroids may, through the adipoinsular axis or its associated pathways, mediate in the regulation of body weight in preterm neonates.     

Immature sucking patterns in infants of mothers with diabetes

OBJECTIVE: To evaluate immaturity of sucking patterns of infants of mothers with diabetes. STUDY DESIGN: Term infants born to mothers with gestational diabetes mellitus (16 mothers managed with insulin and 31 with diet alone) were compared with 55 matched healthy infants (control group). Sucking patterns were recorded and analyzed for number of sucks and bursts and averages maximum suck pressure, number of sucks per burst, suck width, and time between bursts. The measurements were made for feedings of 5 minutes duration with Kron's Nutritive Sucking Apparatus on the third day of life. RESULTS: Relative to the control group, newborns of the insulin-treated mothers averaged 5.2 fewer bursts and 42 fewer sucks (P = .013 and P = .04, respectively). No differences were noted for other variables tested. There were no differences in sucking patterns between newborns of diet-managed mothers and control newborns. CONCLUSION: Poorer sucking patterns were found among infants of insulin-managed mothers with diabetes. The present findings indicate some degree of neurologic immaturity during the early neonatal period.     

Erythrocyte indicators of oxidative stress in gestational diabetes

Foetuses born to mothers with gestational diabetes are at increased risk of developing respiratory distress, foetal macrosomia, foetal anomalies and platelet hyperaggregability. High blood glucose level induces oxidative stress and decreases antioxidant defences. The present study discusses the possibility of lipid peroxidation and protein oxidation in both maternal and foetal erythrocytes as an indicator of oxygen radical activity. The level of lipid peroxidation and protein oxidation in erythrocytes was estimated in 20 mothers with gestational diabetes and their newborns. The maternal age varied between 19 and 42 y and foetal age ranged between 34 and 39 weeks. The proteolytic activities in the erythrocyte lysates obtained from mothers with gestational diabetes and their newborns were significantly greater [(mean ± SD) 24.41 ± 9.05 and 16.70 ± 3.36μM of amino groups/g haemoglobin, n = 20, respectively] than those from control group (10.18 ± 4.84 and 14.64 ± 6.21 μM amino groups/g haemoglobin, n = 15, respectively; p < 0:05 in both cases). Similarly erythrocyte malondialdehyde levels were significantly elevated in babies born to mothers with gestational diabetes (10.11 ±2.21 nM/g haemoglobin) when compared to controls (6.8 ± 3.75 nM/g haemoglobin) (p < 0:05). In the erythrocytes of mothers with gestational diabetes, malondialdehyde levels correlated significantly with glycated haemoglobin levels (p < 0:01). The results of this study indicate that the oxidative stress induced by gestational diabetes manifests as increased lipid peroxidation and protein oxidative damage in the erythrocytes of both mothers with gestational diabetes and their newborn infants.     

Maternal type 1 and gestational diabetes: postnatal differences in insulin secretion in offspring at preschool age

Background: It is well known that children born to mothers with diabetes in pregnancy are more likely to develop metabolic abnormalities in later life. Most prior studies have not differentiated between offspring of mothers with type 1 diabetes (T1DM) and gestational diabetes (GDM) or lack a control group of non‐exposed offspring. Subjects: Offspring of T1DM (n = 16), GDM (n = 22) and mothers without diabetes (n = 25) born at Oulu University Hospital. Aim: To assess insulin secretion and insulin resistance in the offspring of T1DM and GDM at preschool age in comparison with offspring of non‐diabetic mothers. Methods: Anthropometric measurements and intravenous glucose tolerance testing were performed. First‐phase insulin response (FPIR) and homoeostasis model assessment (HOMA) values were calculated. Pregnancy and birth data were analysed in relation to later metabolic parameters in all three groups using one‐way analysis of variance (anova ) and analysis of covariance (ancova ). Results: At a mean age of 4.9 yr, offspring of T1DM had increased fasting serum insulin concentrations (p = 0.044), FPIR (p = 0.034) and HOMA‐B values (p = 0.008) compared with offspring of GDM or with offspring of healthy controls (statistically non‐significant). The GDM gained least weight during pregnancy, and when adjusted for maternal weight gain during pregnancy, there were no statistically significant differences between study groups. Conclusions: Prenatal exposures to maternal type 1 and gestational diabetes may have different effects on postnatal glucose metabolism in the offspring assessed at a mean age close to 5 yr. Maternal weight gain in pregnancy may affect the postnatal glucose metabolism in the offspring.     

Plasma leptin levels in infants of diabetic mothers in fasting and satiety states

Infants born to diabetic mothers have elevated cord blood leptin levels. The aim of this study was to investigate whether the situation persists at the 2nd postnatal day, taking the fasting and satiety states into account and the influence of fetal exposure to hyperinsulinemia, which are proven important contributing factors to plasma leptin levels. Twenty infants born to mothers with gestational diabetes (Group I) and 20 controls (Group II) were included in the study. Groups were similar for sex and anthropometric measurements. Group I had higher leptin concentrations compared to Group II in fasting and satiety states (p < 0.01). Fasting state leptin levels were significantly lower than seen in satiety in both groups (p < 0.01). There was a positive and significant correlation between leptin concentrations and body mass index of infants. Leptin concentrations were positively correlated with plasma insulin levels in Group I. These findings suggest that plasma leptin levels are high in both fasting and satiety states on the 2nd postnatal day in infants born to mothers with gestational diabetes. The possible mechanism underlying this condition is fetal exposure to hyperinsulinemia due to hyperglycemia. The uniqueness of this report are that fasting and satiety states were taken into account and that the data was collected from the samples taken on the 2nd postnatal day, thus reflecting the exact milieu of the infant excluding the effects of the mother and the placenta.     

Brainstem auditory evoked responses in term small for gestational age newborn infants born to undernourished mothers.

Our aim was to assess the effect of intrauterine growth retardation on neurosensory development by evaluating brainstem auditory evoked responses (BAER) in term small for gestational age (SGA) newborn infants born to undernourished mothers. This prospective clinical study included 25 singleton healthy SGA newborn infants born between 38 and 41 weeks to undernourished mothers (weight <45kg, height <145cm, haemoglobin <8g/dl, and serum albumin <2.5g/dl). An equal number of age- and sex-matched appropriate for gestational age newborn infants born to healthy mothers served as controls. Mothers with other risk factors and newborns with complications during delivery or immediate newborn period were excluded. BAER was recorded within first 3 days of life. Interpeak latency (IPL), absolute peak latency (APL) and amplitudes of various waveforms were determined and compared between the groups.No statistically significant differences were observed for the mean interpeak and absolute latencies between term SGA and AGA infants (p>0.05). The absolute peak latency (wave V) and central conduction time (I-V interval) were borderline prolonged in the study group compared with controls (p=0.051 and 0.088 respectively). Using multiple regression analysis, maternal haemoglobin was identified to be the only parameter having a negative correlation with both IPL (waves I-V) (F[1,46]=4.12, p=0.048) and APL (wave V) (F[1,46]=5.80, p=0.02). Maternal undernourishment may have a minor effect on intrauterine development of the auditory brainstem. Maternal haemoglobin is the only factor significantly associated with these changes.     

Increased leptin concentration in preterm infants of pre-eclamptic mothers

AIM: To study the effect of maternal pre-eclampsia on cord plasma leptin concentrations in preterm infants. METHODS: Leptin concentration was analysed in cord plasma of 74 preterm infants, gestational age 24 to 32 weeks. Of these, 14 were born to pre-eclamptic mothers, in 10 intrauterine growth retardation (IUGR) was present, and 59 had been exposed antenatally to corticosteroids. RESULTS: The mean (SD) concentration of cord plasma leptin was 1.31 (0.88) microg/l. A significant correlation was found between leptin concentration and gestational age (r = 0.336; p = 0.0037). Leptin levels were higher in infants of pre-eclamptic mothers (p = 0.0007), in those with IUGR (p = 0.0005), and in infants exposed antenatally to corticosteroids (p = 0.02). In multiple regression analysis, leptin was associated with gestational age and maternal pre-eclampsia (both p < 0.05), but not with antenatal corticosteroids. CONCLUSIONS: Increased fetal leptin in maternal pre-eclampsia may reflect a physiological adaptation to fetal stress such as hypoxia.     

Circulating levels of adiponectin in preterm infants

OBJECTIVE: To determine circulating levels of adiponectin in preterm infants and examine possible associations with anthropometric measurements, weight gain, and leptin and insulin levels. DESIGN: Prospective study. SETTING: A university hospital neonatal care unit. Study population: 62 preterm (mean (SD) gestational age 32.0 (2.1) weeks) and 15 full-term infants (reference group). INTERVENTIONS: Blood samples taken at discharge (40.9 (14.8) days of life) from the preterm infants and at a comparable postnatal age in full-term infants. All infants were fed the same commercial formula, but in nine preterms the formula contained long-chain polyunsaturated fatty acids (LCPUFAs). MAIN OUTCOME MEASURES: Serum levels of adiponectin, leptin and insulin. Associations of adiponectin levels were tested only in the preterm group. RESULTS: Serum levels of adiponectin were lower in preterm (40.9 (14.8) microg/ml) than full-term infants (53.1 (16.0) microg/ml, p<0.01). However, after adjustment for body weight, the influence of prematurity on adiponectin levels was no longer significant. In preterm infants, adiponectin levels independently correlated with being born small for gestational age (SGA) (beta=-0.35, p=0.01), weight gain (beta=0.28, p=0.03) and LCPUFA-supplemented formula (beta=0.34, p=0.009). Serum adiponectin levels did not correlate with insulin or leptin levels. However, insulin levels were higher in preterm than in full-term infants after adjustment for body weight. CONCLUSIONS: Adiponectin levels are lower in preterm infants at discharge than full-term infants probably due to decreased adiposity. The levels are influenced by being born SGA, weight gain and, possibly, by dietary LCPUFAs. The importance of these findings in the development of insulin or leptin resistance in children born prematurely needs to be further studied.     

Neonatal Jaundice in Infants of Diabetic Mothers

Jährig, D., Jährig, K., Stiete, S., Beyersdorff, E., Poser, H. and Hopp, H. (Department of Paediatrics, the Data Centre of the Ernst Moritz Arndt University of Greifswald, Greifswald, and the'Gerhard Katsch'Central Research Institute for Diabetes, Karlsburg, G.D.R.). Neonatal jaundice in infants of diabetic mothers. Acta Paediatr Scand Suppl 360: 101, 1989.
357 IDMs and 20 healthy newborns of non-diabetic mothers were examined at term for body measurements, red blood cell count, serum bilirubin, cord blood insulin and blood glucose during the first postnatal week. The stage of maternal diabetes did not influence the course of neonatal bilirubin levels, but the IDMs had prolonged and higher bilirubinaemia compared with the controls. Hyperbilirubinaemia was found to be most prominent in newborns with an increased birthweightllength ratio and was not simply related to macrosomia (LGA). These infants had significantly lower blood glucose concentrations immediately after birth, whereas cord blood insulin was found to be identical between the IDM sub-groups. Bilirubinaemia in heavy for length infants was slightly correlated to haematocrit. For the pathogenesis of hyperbilirubinaemia in IDMs induction of heme oxygenase (due to a lack of energy provision following a phosphory lation disorder) is discussed. Nutritional support (early feeding, glucose infusions) does not affect the course of bilirubinaemia.     

Resistin in preterm and term newborns: relation to anthropometry, leptin, and insulin

This study aimed to investigate 1) the plasma resistin concentration at birth, 2) the relationship of resistin with leptin and insulin, and 3) the association of resistin with anthropometric indexes in newborn infants. Blood samples for hormonal assay were obtained from preterm and term newborns within the first 2 h of life and before milk feeding or energy intake. Although these infants required blood sampling for clinical reasons, all were proved to be noninfected. Plasma resistin was significantly higher in term than in preterm infants. It was also significantly correlated with serum leptin, and both hormones were significantly associated with gestational age and anthropometric indexes. Infants who were born vaginally were found to have significantly higher plasma resistin levels compared with those who were born by cesarean section. In the multivariate forward stepwise regression models, resistin was found to be significantly associated with the mode of delivery and gestational age or birth weight. The association among resistin, leptin, and anthropometric indexes suggested that both hormones might be gestation related. A high circulating resistin level at term gestation could be advantageous to the infant by promoting hepatic glucose production and preventing hypoglycemia after birth. Infants who were born vaginally had significantly higher plasma resistin levels, suggesting that this hormone might also be associated with stress or inflammation induced by the birth process.     

Leptin, insulin, and glucose serum levels in large-for-gestational-age infants of diabetic and non-diabetic mothers

BACKGROUND: It has been suggested that hyperleptinemia could be caused by hyperinsulinemia in infants of diabetic mothers (IDMs). AIM: To compare leptin, insulin, and glucose levels in large-for-gestational-age (LGA) and appropriate-for-gestational-age (AGA) infants. Methods: A cross-sectional study was conducted in IDMs, infants of non-diabetic mothers (INDM) and AGA infants. RESULTS: Seventy-seven newborns were studied (11 IDM, 16 INDM, and 50 AGA infants). Leptin levels were significantly higher in LGA infants than in the AGA group and a trend for higher levels in IDM than NIDM was observed. Insulin levels and insulin resistance were significantly higher in IDMs. Glucose levels were lower in both groups of LGA infants. CONCLUSIONS: We found insulin resistance, hyperinsulinism and hyperleptinemia in IDMs, and the trend of higher leptin levels in IDMs than INDMs shows that leptin could be related to insulin resistance in these infants.     

Early post-natal growth of large-for-dates babies of non-diabetic mothers is influenced by maternal glucose metabolism

Growth of weight, length, head circumference and skinfold thickness (subscapular and triceps) from birth to 6 months in 53 large-for-dates (LFD) Chinese babies weighing greater than 4.0 kg at term and born to non-diabetic mothers was investigated and correlated with biochemical indices of maternal glucose tolerance at birth: glycosylated haemoglobin (HbA1), serum corrected fructosamine and the area under the oral glucose (50 g) tolerance (OGTT) curve. Growth in all physical dimensions, especially weight, showed a downward shift towards a reference mean. These changes in relative size were caused by slower growth velocities. None of the mothers had abnormally high concentrations of HbA1 or fructosamine nor an abnormal OGTT. However, weight velocities did show small but significant correlations with fructosamine (r = -0.42), and OGTT area units (r = 0.39) but not with HbA1. For some macrosomic babies born to apparently normal mothers, birth is seen to interrupt a process operating in prenatal life that accelerates growth. Covert abnormalities of maternal glucose homeostasis could explain this. Abnormal glucose tolerance during pregnancy might therefore be viewed as a continuum extending from (i) its maximum expression, the frankly diabetic state, through (ii) gestational diabetes to (iii) the mother who has no biochemically evident abnormality of glucose homeostasis but who has sufficient alteration to modify fetal growth. Post-natal growth of LFD babies is additional information which, when taken along with other markers of maternal glucose tolerance, might help to identify the mother at later perinatal risk.     

极早产儿产房复苏插管影响因素分析

目的 探讨极早产儿产房复苏插管影响因素以降低插管风险.方法 回顾性分析2017年1月至2019年12月入住新生儿重症监护病房的极早产儿455例,依据复苏时是否插管分为插管组(79例)和非插管组(376例),分析复苏插管的影响因素.结果 极早产儿中复苏时插管发生率为17.4％(79/455).非插管组胎龄、出生体重及剖宫...     

Retinol concentration in maternal and cord serum: its relation to birth weight in healthy mother-infant pairs

BACKGROUND: Vitamin A is an essential micronutrient for the development and growth of the fetus. The objective of this study was to identify a possible association between low serum retinol and birth weight in healthy mother-infant pairs in Southern Israel. A secondary objective was to examine ethnic differences in maternal and cord serum retinol. METHODS: Serum retinol was measured at delivery from pairs of healthy mothers and healthy mature newborns. RESULTS: Of the 313 mother-infant pairs studied, 56% were Jews and 44% Bedouins. The proportion of infants with birth weight of 2500-2999 g was greater among mothers with lower serum retinol (<0.7 micromol/l) compared to mothers with normal serum retinol (> or =0.7 micromol/l) (p<0.001). Cord retinol <0.7 micromol/l was more frequent in infants with birth weight 2500-2990 g compared to infants with birth weight > or =3000 g (p=0.006). Using a split model and stepwise multiple regression analysis, infant's birth weight was significantly influenced by cord retinol concentration in infants born to mothers with low serum retinol; gestational age and cord retinol alone explained 27% of the variability of birth weight in this group. A higher proportion of Bedouin than Jewish infants had serum retinol <0.7 and <0.35 micromol/l (both p<0.001). CONCLUSION: Low cord and maternal serum retinol may reflect poor vitamin A status of the newborn and the mother, which in turn may affect fetal growth.