Intrauterine growth and postnatal fasting metabolism in infants of obese mothers

Kliegman, Robert M.; Gross, Thomas L.; Morton, S; Dunnington, R.

doi:10.1016/s0022-3476(84)80561-2

Cited by 28 publications

(10 citation statements)

References 13 publications

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“…This phenomenon of neonatal hypoglycemia associated with increased body size is similar to the unexplained increased incidence of hypoglycemia that occurs in large for gestational age human neonates who are not infants of diabetic mothers (7,29). Neonatal hypoglycemia has also been observed in another model of accelerated fetal growth in the rat.…”

Section: Gestation (Days)supporting

confidence: 52%

Selective Ligation of Uterine Artery Branches Accelerates Fetal Growth in the Rat

Ogata

Finley

1988

Pediatr Res

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Section: Gestation (Days)supporting

confidence: 52%

Selective Ligation of Uterine Artery Branches Accelerates Fetal Growth in the Rat

Ogata

Finley

1988

Pediatr Res

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“…Thus, increased serum levels of maternal fatty acids and triglycerides may increase fatty acid transfer to the fetus. Triglyceride levels are elevated in newborn infants of obese, nondiabetic mothers, in comparison with control subjects [33]. Fatty acids are known to have detrimental effects on the adult beta cell [29,34] and they may effect beta cell development as well.…”

Section: Discussionmentioning

confidence: 99%

Long-term effect of maternal obesity on pancreatic beta cells of offspring: reduced beta cell adaptation to high glucose and high-fat diet challenges in adult female mouse offspring

Han

Epstein

et al. 2005

Diabetologia

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Aim/hypothesis: Obesity is a global problem with high risks of cardiovascular diseases, stroke and type 2 diabetes. It is well known that maternal obesity affects offspring by inducing malformation, functional abnormalities in many organs and cells, and by increased risk of obesity and type 2 diabetes. However, little is known about abnormalities induced by maternal obesity in pancreatic beta cells of offspring. Methods: We used mouse mothers with the Agouti yellow modification on a C57BL/6 background as a maternal model of normoglycaemic obesity, and produced Agouti-negative offspring. Half of the offspring were fed a high-fat diet. Offspring glucose tolerance was tested at different ages, and animals were killed at 50 weeks of age for islet function analysis. Results: Maternal obesity impaired glucose tolerance in female offspring fed a high-fat diet, and significantly reduced insulin secretion at 50 weeks of age in female offspring that had been fed a normal diet and high-fat diet. Insulin secretion and glucose potentiation from these islets were significantly reduced. Islet protein, DNA and insulin contents were increased while glyceraldehyde-3-phosphate dehydrogenase and transketolase activities were reduced in female offspring. Conclusions/interpretation: Our results indicate that maternal obesity has a long-term effect on the beta cells of female, but not of male, offspring, and leads to increased risk of gestational diabetes and type 2 diabetes in the offspring's later lives.

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“…The evidence from several anthropometric studies [15][16][17][18][19] suggests that infants of obese women are larger at birth because they are fat. However, anthropometric measurements (i.e., skinfolds) of body fat are among the least accurate methods for estimating total body fat [20,21].…”

mentioning

confidence: 99%

Maternal Obesity and Body Composition of the Neonate

Silliman

Kretchmer²

1995

Neonatology

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Obese women generally deliver heavier infants, but the body composition of these infants is unknown. The principal objective of this study was to determine if neonates of obese women have more adipose tissue. At 35–36 weeks of gestation, a fasting blood sample was collected from 37 pregnant women. Shortly after birth, the body fat of the neonates was measured with an infant total-body electrical conductivity (TOBEC) instrument using a prediction equation derived from 10 miniature pigs. At 6 weeks post partum, the infant body fat was measured a second time, and the body fat of each mother was measured using an adult TOBEC instrument. We found no differences between the obese (n = 16) and lean subjects (n = 21) in the concentrations of glycerol, β-hydroxybutyrate, triglyceride, total cholesterol, high-density lipoprotein cholesterol, or glucose in the blood. However, the insulin concentration was elevated in the obese women (199 ± 57 pmol/l) as compared with the lean women (128 ± 68 pmol/l, p < 0.01). At birth, maternal adiposity (% body fat) was significantly associated with infant adiposity (r = 0.37, p < 0.05). However, by 6 weeks post partum the association no longer existed. Multiple regression analysis showed that maternal adiposity, fasting glucose level, and gestational age are independently associated at birth with infant adiposity.

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Intrauterine growth and postnatal fasting metabolism in infants of obese mothers

Cited by 28 publications

References 13 publications

Selective Ligation of Uterine Artery Branches Accelerates Fetal Growth in the Rat

Selective Ligation of Uterine Artery Branches Accelerates Fetal Growth in the Rat

Long-term effect of maternal obesity on pancreatic beta cells of offspring: reduced beta cell adaptation to high glucose and high-fat diet challenges in adult female mouse offspring

Maternal Obesity and Body Composition of the Neonate

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