Perinatal programming of obesity

Simmons, Rebecca A.

doi:10.1016/j.exger.2005.09.007

Cited by 51 publications

(59 citation statements)

References 34 publications

(36 reference statements)

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“…35 Fetal leptin regulatory programming may be the link between the exposure to maternal diabetes and obesity in childhood. 34 Leptin levels are positively correlated with hyperinsulemia, birth weight and adiposity, with LGA infants having higher cord leptin concentrations than normal controls. 18,33,34 As leptin and insulin are intimately involved in normal metabolic homeostasis, the elevated birth levels of infants born to obese and diabetic women may indicate an acquired hypothalamic resistance that is associated with the later development of childhood obesity.…”

Section: Obesity and Inflammationmentioning

confidence: 99%

“…34 Leptin levels are positively correlated with hyperinsulemia, birth weight and adiposity, with LGA infants having higher cord leptin concentrations than normal controls. 18,33,34 As leptin and insulin are intimately involved in normal metabolic homeostasis, the elevated birth levels of infants born to obese and diabetic women may indicate an acquired hypothalamic resistance that is associated with the later development of childhood obesity. 33 Controversy continues regarding whether obesity is a significant risk factor for congenital structural abnormalities such as neural tube defects.…”

Section: Obesity and Inflammationmentioning

confidence: 99%

“…19,32 -34 In this environment, the fetal pancreas secretes an excessive amount of insulin leading to macrosomia with increased adipose tissue and glycogen deposition. 34 Excess adiposity at birth has been implicated in the later development of childhood obesity; an increase of 1 kg in birth weight of a full-term infant confers a 50% heightened risk of becoming overweight between the ages of 9 and 14. 8,34 Large for gestational age (LGA) infants of diabetic mothers are also at heightened risk of developing metabolic syndrome, diabetes and cardiovascular insults later in life.…”

Section: Obesity and Inflammationmentioning

confidence: 99%

“…34 Excess adiposity at birth has been implicated in the later development of childhood obesity; an increase of 1 kg in birth weight of a full-term infant confers a 50% heightened risk of becoming overweight between the ages of 9 and 14. 8,34 Large for gestational age (LGA) infants of diabetic mothers are also at heightened risk of developing metabolic syndrome, diabetes and cardiovascular insults later in life. 35 Children exposed to the intrauterine environment of an obese mother have an increased risk of developing metabolic syndrome, similar to children of diabetic mothers.…”

Section: Obesity and Inflammationmentioning

confidence: 99%

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Maternal obesity: the interplay between inflammation, mother and fetus

et al. 2009

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Obesity has reached epidemic proportions in our patients who are of childbearing age, with pregnant patients of normal weight being in the minority. The pregnancy-related complications attributable to obesity affect not only the pregnant women, but also her fetus and potentially both mother and child for their lifetimes. Pregnancy is associated with altered immunity. The physiologic state of chronic inflammation in obesity affects systemic immunity and metabolism, and may be associated with several of the complications associated with maternal obesity. The interplay between pregnancy, obesity and inflammation may have far-reaching implications for fertility, pregnancy, the fetus and neonate.

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Section: Obesity and Inflammationmentioning

confidence: 99%

Section: Obesity and Inflammationmentioning

confidence: 99%

Section: Obesity and Inflammationmentioning

confidence: 99%

Section: Obesity and Inflammationmentioning

confidence: 99%

See 2 more Smart Citations

Maternal obesity: the interplay between inflammation, mother and fetus

et al. 2009

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“…Accordingly, there is increasing evidence supporting the developmental origins of a health and disease hypothesis that suggests a prenatal programming towards later childhood obesity and metabolic dysregulation through the intrauterine environment (2,3). Consequently, infants that are born large for gestational age (LGA) are more likely to be obese in childhood and adolescence (4)(5)(6) and are at risk of cardiovascular and metabolic obesity-related complications later in life (7).…”

Section: Introductionmentioning

confidence: 99%

Adipokines in umbilical cord blood from children born large for gestational age

Lausten-Thomsen¹,

Christiansen

Hedley

et al. 2016

Journal of Pediatric Endocrinology and Metabolism

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Background: The etiology of childhood obesity and the associated morbidity is multifactorial. Recently, data suggesting a prenatal programming towards later childhood obesity and metabolic deregulation through the intrauterine environment has emerged. This study explored the concentrations of adipokines and their mutual relationship at birth in children born to non-diabetic mothers. Methods: Adiponectin, leptin and sOB-R were measured using ELISA-based commercial kits in umbilical cord blood from 60 neonates (30 born large for gestational age [LGA] and 30 born appropriate for gestational age [AGA]). Children exposed to maternal diabetes, chronic disease and preeclampsia were excluded. Results: The LGA group exhibited significantly elevated concentrations of leptin (p < 0.001) and of free leptin index (p < 0.001) and decreased sOB-R concentrations (p = 0.005) when compared to the AGA group, which persisted in multiple regression analysis after taking the gestational age into account (p = 0.048, p < 0.001 and p < 0.001, respectively). Only a trend towards a difference in adiponectin was demonstrated (p = 0.057) regardless of adjustment (p = 0.150). However, the leptin/adiponectin ratio was

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