Hyperinsulinemia in Macrosomic Infants of Nondiabetic Mothers

Hoegsberg, Bente; Gruppuso, Philip A.; Coustan, Donald R.

doi:10.2337/diacare.16.1.32

Cited by 71 publications

(44 citation statements)

References 8 publications

(8 reference statements)

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“…Obesity is associated with maternal insulin resistance and foetal hyperinsulinaemia even in the absence of maternal diabetes. 18 Insulin resistant individuals have higher fasting plasma triglyceride levels and greater leucine turnover. 19,20 Amino acids are insulin secretagogues and an increased flux on amino acids could stimulate foetal hyperinsulinaemia.…”

Section: Discussionmentioning

confidence: 99%

Maternal obesity and pregnancy outcome: a study of 287 213 pregnancies in London

et al. 2001

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OBJECTIVE:To examine the maternal and foetal risks of adverse pregnancy outcome in relation to maternal obesity, expressed as body mass index (BMI, kg=m 2 ) in a large unselected geographical population. DESIGN: Retrospective analysis of data from a validated maternity database system which includes all but one of the maternity units in the North West Thames Region. A comparison of pregnancy outcomes was made on the basis of maternal BMI at booking. SUBJECTS: A total of 287 213 completed singleton pregnancies were studied including 176 923 (61.6%) normal weight (BMI 20 -24.9), 79 014 (27.5%) moderately obese ) and 31 276 (10.9%) very obese (BMI ! 30) women. MEASUREMENTS: Ante-natal complications, intervention in labour, maternal morbidity and neonatal outcome were examined and data presented as raw frequencies and adjusted odds ratios with 99% confidence intervals following logistic regression analysis to account for confounding variables. RESULTS: Compared to women with normal BMI, the following outcomes were significantly more common in obese pregnant women (odds ratio (99% confidence interval) for BMI 25 -30 and BMI ! 30 respectively): gestational diabetes mellitus (1.68 (1.53 -1.84), 3.6 (3.25 -3.98)); proteinuric pre-eclampsia (1.44 (1.28 -1.62), 2.14 (1.85 -2.47)); induction of labour (2.14 (1.85 -2.47), 1.70 (1.64 -1.76)); delivery by emergency caesarian section (1.30 (1.25 -1.34), 1.83 (1.74 -1.93)); postpartum haemorrhage (1.16 (1.12 -1.21), 1.39 (1.32 -1.46)); genital tract infection (1.24 (1.09 -1.41), 1.30 (1.07 -1.56)); urinary tract infection (1.17 (1.04 -1.33), 1.39 (1.18 -1.63)); wound infection (1.27 (1.09 -1.48), 2.24 (1.91 -2.64)); birthweight above the 90th centile (1.57 (1.50 -1.64), 2.36 (2.23 -2.50)), and intrauterine death (1.10 (0.94 -1.28), 1.40 (1.14 -1.71)). However, delivery before 32 weeks' gestation (0.73 (0.65 -0.82), 0.81 (0.69 -0.95)) and breastfeeding at discharge (0.86 (0.84 -0.88), 0.58 (0.56 -0.60)) were significantly less likely in the overweight groups. In all cases, increasing maternal BMI was associated with increased magnitude of risk. CONCLUSION: Maternal obesity carries significant risks for the mother and foetus. The risk increases with the degree of obesity and persists after accounting for other confounding demographic factors. The basis of many of the complications is likely to be related to the altered metabolic state associated with morbid obesity.

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Section: Discussionmentioning

confidence: 99%

Maternal obesity and pregnancy outcome: a study of 287 213 pregnancies in London

et al. 2001

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“…During diabetic pregnancy, fetal macrosomia is related to maternal postprandial glucose control between the 29th and 32nd week of gestation [3]. Furthermore, it has recently been shown that a subset of macrosomic infants born to non-diabetic mothers have higher insulin levels in cord blood [4]. Thus, it is possible that even subtle hyperglycaemia during pregnancy may lead to fetal hyperinsulinaemia and macrosomia, perhaps in conjunction with other factors (fetal beta-cell hypersensitivity, maternal amino adds, paternal glucose intolerance).…”

Section: Discussionmentioning

confidence: 99%

Relation of birthweight to maternal plasma glucose and insulin concentrations during normal pregnancy

et al. 1993

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Summary.Maternal diabetes mellitus is complicated by fetal macrosomia and predisposes the offspring to diabetes, but recent evidence indicates that a low, not high, birthweight is associated with a higher incidence of Type 2 (non-insulin dependent) diabetes in adult life. To clarify the relationships between maternal glucose and insulin levels and birthweight, we measured oral glucose tolerance and neonatal weight in a large group (n = 529) of women during the 26th week of pregnancy. Women with gestational diabetes (n = 17) had more familial diabetes, higher pre-pregnancy body weight, and tended to have large-for-gestational-age babies. In contrast, women with essential hypertension (n = 10) gave birth to significantly (p < 0.01) smaller babies. In the normal group (without gestational diabetes or hypertension, n --503), maternal body weight before pregnancy and at term, maternal height, week of delivery, gender of the newborn, and parity were all significant, independent predictors of birthweight, together explaining 23 % of the variability of neonatal weight. In addition, both fasting (p < 0.006) and 2-h post-glucose (p = 0.03) maternal plasma glucose concentrations were positively associated with birthweight independent of the other physiological determinants, accounting, however, for only 10% of the explained variability. In a subgroup of 134 normal mothers with prepregnancy body mass index of less than 25 kg. m 2, in whom plasma insulin measurements were available, the insulin area-under-curve was inversely related to birthweight (p < 0.02) after simultaneously adjusting for physiological factors and glucose area. When glucose and insulin measurements were combined in the I/G ratio (ratio of insulin to glucose area), this was still inversely related to birthweight. Furthermore, maternal insulinaemia was directly related to blood pressure levels (p <0.001) independently of body weight. We conclude that in normal pregnancy, whereas physiological factors account for most of the explainable variability of infant weight, the influence of the maternal metabolic milieu is dual, positive for glucose levels but negative for insulin concentrations. Maternal hyperinsulinaemia during pregnancy may be one trait linking low birthweight with predisposition to diabetes in adult life.

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“…In the literature, the lowest cutoff is Ն25 years, as recommended by the American Diabetes Association (1), but there are little data to support this recommendation. To determine the age threshold for increased risk of GDM, we have reviewed the prevalence of GDM, diagnosed by the World Health Organization criteria (2), in the singleton pregnancies managed in our department from 1998 to 2001. Data on maternal anthropometric parameters, parity status, and risk factors for GDM such as booking weight Ն70 kg, BMI Ն25 kg/m 2 , chronic hypertension, significant medical history, and smoking, as well as risk factors identified in our population that included carrier of thalassemia trait (3) and HBsAg (4) and presence of iron deficiency anemia, which reduces the risk of GDM (5), were retrieved from a computerized database.…”

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confidence: 99%

“…Diabetes during pregnancy has been associated with cord blood insulin and with insulin concentrations in adolescence (1), and in nondiabetic pregnancies, maternal weight gain was related to cord blood insulin in macrosomic neonates (2). Currently, a weight gain of 6.8 -11.5 kg is recommended for overweight women, and obese women are advised to gain a minimum of 6.8 kg.…”

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Maternal Age and Prevalence of Gestational Diabetes Mellitus

et al. 2006

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We report a boy with relapse of diabetes after 82 months (6.8 years). This boy was hospitalized with severe DϩHUS when he was 6 years old. During his stay in the intensive care unit, he developed hyperglycemia and was treated with insulin during 21 days. Eighty months later he presented with nose obstruction and headache and was diagnosed with sinusitis and polyposis nasi. He was treated with antibiotics, but the complaints persisted. Two months later, he was operated on (functional endoscopic sinus surgery), and postoperatively he received 2 mg betamethason for 5 days. On the 5th day, he presented in the emergency department with polyuria, polydipsia, and lethargy. His glycemia was 1,500 mg/dl, and his blood pH was 7.33. He was intravenously treated with insulin, and the corticosteroids were ceased.To differentiate between type 1 diabetes, glucocorticoid-induced diabetes, and post-HUS diabetes, some additional blood tests were done. Pancreatic autoantibodies, including islet cell, insulin, GAD65, and insulinoma-associated protein 2 antibodies were all negative. Insulin was 4 mU/l for a glycemia of 1,453 mg/dl. After normalization of the glycemia, the boy was started on a basal-bolus regimen with insulin aspart and insulin glargine. Twenty months later, he still requires insulin (0.5 units ⅐ kg Ϫ1 ⅐ day Ϫ1 ) and has an HbA 1c of 6.8%.Our report in which we describe a relapse of diabetes after 82 months confirms the conclusion of Suri et al. that survivors of DϩHUS should have aggressive surveillance and treatment of hyperglycemia, not only in the acute phase but also in the long run.

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Hyperinsulinemia in Macrosomic Infants of Nondiabetic Mothers

Abstract: A subset of macrosomic infants have hyperinsulinemia. Maternal anthropometric factors as well as hyperinsulinemia are correlated with macrosomia. The macrosomia may be causally related to the high insulin levels.

Cited by 71 publications

References 8 publications

Maternal obesity and pregnancy outcome: a study of 287 213 pregnancies in London

Maternal obesity and pregnancy outcome: a study of 287 213 pregnancies in London

Relation of birthweight to maternal plasma glucose and insulin concentrations during normal pregnancy

Maternal Age and Prevalence of Gestational Diabetes Mellitus

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