Leptin concentrations in maternal serum and cord blood in diabetic and nondiabetic pregnancy

Manderson, John G.; Patterson, Christopher; Hadden, David R.; Traub, A. I.; Leslie, Hilary; McCance, David R.

doi:10.1067/mob.2003.276

Cited by 48 publications

(37 citation statements)

References 22 publications

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“…Leptin measured at birth was positively related to birth weight (24,29,30) and with the amount of fetal adipose tissue (31). In both animals and humans, inefficient leptin action leads to hyperphagia, decreased fat oxidation, increased tissue triglyceride levels, insulin resistance, and obesity (32)(33)(34).…”

Section: Adipoinsular Axismentioning

confidence: 97%

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The Predisposition to Obesity and Diabetes in Offspring of Diabetic Mothers

2007

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Section: Adipoinsular Axismentioning

confidence: 97%

“…Exposure to maternal diabetes is associated with excess fetal growth in utero (23), possibly mainly due to an increase in fetal fat mass (7), and alterations of fetal hormones. Concentrations of insulin are raised (1) and, more recently, increases in fetal leptin levels have been reported (24,25).…”

Section: Adipoinsular Axismentioning

confidence: 99%

The Predisposition to Obesity and Diabetes in Offspring of Diabetic Mothers

2007

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“…The subjects were recruited between October 1997-February 2000 [23]. All participants had a single pregnancy during the study period and all had live births and singleton pregnancies [23].…”

Section: Settings and Participantsmentioning

confidence: 99%

Maternal vitamin D status in Type 1 diabetic pregnancy: Impact on neonatal vitamin D status and association with maternal glycaemic control

Bennett

McPeake

McCance

et al. 2014

Pregnancy Hypertension: An International Journal of Women's Car

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Objective: The first aim of this study was to assess 25-hydroxy vitamin D (25OHD) concentrations in women with type 1 diabetes (T1DM) during pregnancy, post-delivery and also foetal (cord blood) 25OHD concentrations and to examine relationships between these. The second aim of the study was to investigate potential interactions between maternal body mass index (BMI) and foetal vitamin D status. A further study aim was to examine potential relationships between maternal 25OHD and glycosylated haemoglobin (HbA 1c ) throughout pregnancy. Research Design and Methods:This was an observational study of 52 pregnant controls without diabetes and 65 pregnant women with T1DM in a university teaching hospital. Maternal serum 25OHD was measured serially throughout the pregnancy and post-delivery. Cord blood 25OHD was measured at delivery. 25OHD was measured by liquid chromatography tandem mass spectrometry (LC-MS/MS).Results: Vitamin D deficiency (25OHD ,25 nmol/L) was apparent in both the T1DM subjects and controls at all 3 pregnancy trimesters. Vitamin D levels in all cord blood were ,50 nmol/L. Maternal 25OHD correlated positively with cord 25OHD at all 3 trimesters in the T1DM group (p = 0.02; p,0.001; p,0.001). 25OHD levels within cord blood were significantly lower for women with diabetes classified as obese vs. normal weight at booking [normal weight BMI ,25 kg/m 2 vs. obese BMI .30 kg/m 2 (nmol/L6SD); 19.93611.15 vs. 13.7364.74, p = 0.026]. In the T1DM group, HbA 1c at booking was significantly negatively correlated with maternal 25OHD at all 3 trimesters (p = 0.004; p = 0.001; p = 0.05). Conclusion:In T1DM pregnancy, low vitamin D levels persist throughout gestation and post-delivery. Cord blood vitamin D levels correlate with those of the mother, and are significantly lower in obese women than in their normal weight counterparts. Maternal vitamin D levels exhibit a significant negative relationship with HbA 1c levels, supporting a potential role for this vitamin in maintaining glycaemic control.

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“…Cord leptin correlates with measures of adiposity at birth (2)(3)(4) and is also raised in offspring of mothers with diabetes (3,4). Assessment of insulin and leptin at birth may be a particularly useful way of monitoring whether the fetus has been exposed to abnormally high levels of glucose in utero.…”

mentioning

confidence: 99%

Hyperinsulinemia in Cord Blood in Mothers With Type 2 Diabetes and Gestational Diabetes Mellitus in New Zealand

et al. 2006

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OBJECTIVE -In genetically diabetes-prone populations, maternal diabetes during pregnancy increases the risk of their children developing diabetes and obesity (the vicious cycle of type 2 diabetes). Fetal hyperinsulinemia at birth acts as a marker of this risk. We therefore examined whether cord insulin and leptin concentrations are increased in offspring of Maori and Pacific Island mothers with type 2 and gestational diabetes mellitus (GDM) and varying degrees of glycemic control (HbA 1c ). RESEARCH DESIGNS AND METHODS -Maori and PacificIsland mothers were prospectively recruited at Middlemore Hospital, South Auckland. Cord blood was taken from umbilical vein at birth from singleton babies born after 32 weeks of gestation to 138 mothers with GDM, 39 mothers with type 2 diabetes, and 95 control mothers. , and control subjects 13 ng/ml [8 -22]; P Ͻ 0.001) in cord blood. Cord insulin concentrations Ͼ120 pmol/l were found in 29% of offspring of mothers with GDM and 31% of mothers with type 2 diabetes. Many mothers with GDM had abnormalities of glucose tolerance postpartum (20% type 2 diabetes, 34% impaired glucose tolerance or impaired fasting glucose). Higher cord insulin (57 pmol/l [40 -94]) and leptin (26 ng/ml [17-39]) concentrations were found even in offspring of GDM mothers with normal glucose tolerance postpartum. RESULTSCONCLUSIONS -Raised cord insulin and leptin concentrations are a common finding in offspring of mothers with type 2 diabetes and GDM in this population. Diabetes Care 29:1345-1350, 2006F etal hyperinsulinemia is characteristic of pregnancy complicated by maternal diabetes and underpins complications such as macrosomia (1). Cord leptin correlates with measures of adiposity at birth (2-4) and is also raised in offspring of mothers with diabetes (3,4). Assessment of insulin and leptin at birth may be a particularly useful way of monitoring whether the fetus has been exposed to abnormally high levels of glucose in utero. Fetal hyperinsulinism may also have potential prognostic implications. Several studies have suggested that the maternal intrauterine environment might result in "programming" of later disease. An increased risk of obesity (5-8) and abnormal glucose tolerance (9 -12) are observed when offspring have been exposed to maternal diabetes in utero. Fetal hyperinsulinemia acts as a marker of this increased risk, offspring of diabetic mothers with higher insulin levels in utero being at a higher risk of later metabolic complications (7,8,10).The Pacific Island and Maori peoples of New Zealand are populations at high risk of both type 2 and gestational diabetes during pregnancy. We measured concentrations of fetal insulin, insulin propeptides, and leptin, together with weight and skinfold thickness at birth, with the following hypotheses: where the mother has type 2 diabetes and gestational diabetes mellitus (GDM), fetal hyperinsulinism is common despite treatment of disease, and fetal leptin and fat mass are similarly increased; and in subgroup analysis, these effects are most pronounce...

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Leptin concentrations in maternal serum and cord blood in diabetic and nondiabetic pregnancy

Cited by 48 publications

References 22 publications

The Predisposition to Obesity and Diabetes in Offspring of Diabetic Mothers

The Predisposition to Obesity and Diabetes in Offspring of Diabetic Mothers

Maternal vitamin D status in Type 1 diabetic pregnancy: Impact on neonatal vitamin D status and association with maternal glycaemic control

Hyperinsulinemia in Cord Blood in Mothers With Type 2 Diabetes and Gestational Diabetes Mellitus in New Zealand

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