Risk of low birth weight and micronutrient deficiencies in neonates from mothers after gastric bypass: a case control study

Gascoin, Géraldine; Gerard, Maxime; Sallé, Agnès; Bécouarn, Guillaume; Rouleau, Stéphanie; Sentilhes, Loïc; Coutant, Régis

doi:10.1016/j.soard.2017.03.017

Cited by 59 publications

(48 citation statements)

References 35 publications

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“…While neonatal growth restriction after maternal GB surgery is a well described phenomenon [4,6], the underlying pathophysiol-ogy for these observation remains elusive. In a recent study on cord blood samples in neonates of gastric bypass patients, insulin and IGF-1 deviations, but no other micronutrient deficiencies were associated with growth restriction at birth [5]. This is comparable to studies on undernourished non-human primates, where caloric restriction was shown to affect fetal growth directly through placental inhibition of insulin and IGF-1 pathways, decreasing mTOR activity and resulting in downregulation of placental protein and glucose transporters.…”

Section: Discussionsupporting

confidence: 64%

“…Likewise, distinct metabolic and neurologic long-term consequences of children born SGA have been described, such as impaired glucose tolerance [26], impaired cognitive scores in school age children, as well as reduced academic achievement and professional attainment in adulthood [27]. Even though micronutrient deficiencies in GB did not correlate with fetal growth restriction, they might impact long-term neurological and cognitive outcome [5]. Investigations on long-term effects of gastric bypass-related growth restriction on children's health and metabolism are scarce.…”

Section: Discussionmentioning

confidence: 99%

“…Potential causative factors include maternal chronic undernutrition leading to micronutrient deficits and metabolic changes affecting glucose metabolism. In one study, neonates from patients after gastric bypass (GB) presented with significantly lower micronutrient cord blood-concentrations such as calcium, zinc and iron compared to non-obese healthy mothers [5]. In our recently published study, pregnant GB patients had significantly lower fasting blood glucose compared to BMI-matched, obese and non-obese patients and birthweight was positively associated with fasting glucose [6].…”

Section: Introductionmentioning

confidence: 99%

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Intrauterine Fetal Growth Delay During Late Pregnancy After Maternal Gastric Bypass Surgery

et al. 2018

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Purpose To investigate intrauterine fetal growth development and birth anthropometry of fetuses conceived after maternal gastric bypass surgery. Materials and Methods Longitudinal cohort study describing longitudinal growth estimated by ultrasound on 43 singleton pregnancies after gastric bypass compared to 43 BMI-matched controls. Results In fetuses after maternal gastric bypass surgery, growth percentiles decreased markedly from the beginning of the second trimester until the end of the third trimester (decrease of 3.1 fetal abdomen circumference percentiles (95 %CI 0.9–5.3, p = 0.007) per four gestational weeks). While in the second trimester, fetal anthropometric measures did not differ between the groups, the mean abdomen circumference percentiles appeared significantly smaller during the third trimester in offspring of mothers after gastric bypass (mean difference 25.1 percentiles, p < 0.001). Similar tendencies have been observed in estimated fetal weight resulting in significantly more SGA offspring at delivery in the gastric bypass group. In children born after maternal gastric bypass surgery, weight percentiles (32.12th vs. 55.86th percentile, p < 0.001) as well as placental weight (525.2 g vs. 635.7 g, p < 0.001) were significantly reduced compared to controls. Conclusion In fetuses conceived after maternal gastric bypass, intrauterine fetal growth distinctively declined in the second and third trimester, most prominently observed in fetal abdomen circumferences. Birth weight and placental weight at birth was significantly lower compared to BMI-matched controls, possibly due to altered maternal metabolic factors and comparable to mothers experiencing chronic hunger episodes.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Intrauterine Fetal Growth Delay During Late Pregnancy After Maternal Gastric Bypass Surgery

et al. 2018

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“…Impaired serum retinol levels were also observed in neonates from mothers who underwent RYGB 11–69 months before the onset of pregnancy, which may cause irreversible eye problems in the child [ 99 ]. In contrast to retinol, circulating levels of vitamin D and E were higher in neonates of mothers who had undergone bariatric surgery as compared to neonates from healthy mothers [ 100 ]. This argues against a general deficiency in fat-soluble vitamins in these children.…”

Section: Vitamin a And Rbp4 In The Clinical Course Of Nafld And Mementioning

confidence: 99%

Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD)

et al. 2017

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Vitamin A is required for important physiological processes, including embryogenesis, vision, cell proliferation and differentiation, immune regulation, and glucose and lipid metabolism. Many of vitamin A’s functions are executed through retinoic acids that activate transcriptional networks controlled by retinoic acid receptors (RARs) and retinoid X receptors (RXRs).The liver plays a central role in vitamin A metabolism: (1) it produces bile supporting efficient intestinal absorption of fat-soluble nutrients like vitamin A; (2) it produces retinol binding protein 4 (RBP4) that distributes vitamin A, as retinol, to peripheral tissues; and (3) it harbors the largest body supply of vitamin A, mostly as retinyl esters, in hepatic stellate cells (HSCs). In times of inadequate dietary intake, the liver maintains stable circulating retinol levels of approximately 2 μmol/L, sufficient to provide the body with this vitamin for months. Liver diseases, in particular those leading to fibrosis and cirrhosis, are associated with impaired vitamin A homeostasis and may lead to vitamin A deficiency. Liver injury triggers HSCs to transdifferentiate to myofibroblasts that produce excessive amounts of extracellular matrix, leading to fibrosis. HSCs lose the retinyl ester stores in this process, ultimately leading to vitamin A deficiency. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is a spectrum of conditions ranging from benign hepatic steatosis to non-alcoholic steatohepatitis (NASH); it may progress to cirrhosis and liver cancer. NASH is projected to be the main cause of liver failure in the near future. Retinoic acids are key regulators of glucose and lipid metabolism in the liver and adipose tissue, but it is unknown whether impaired vitamin A homeostasis contributes to or suppresses the development of NAFLD. A genetic variant of patatin-like phospholipase domain-containing 3 (PNPLA3-I148M) is the most prominent heritable factor associated with NAFLD. Interestingly, PNPLA3 harbors retinyl ester hydrolase activity and PNPLA3-I148M is associated with low serum retinol level, but enhanced retinyl esters in the liver of NAFLD patients. Low circulating retinol in NAFLD may therefore not reflect true “vitamin A deficiency”, but rather disturbed vitamin A metabolism. Here, we summarize current knowledge about vitamin A metabolism in NAFLD and its putative role in the progression of liver disease, as well as the therapeutic potential of vitamin A metabolites.

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“…Vitamin B12 (B12) is an essential coenzyme important for fetal development. Maternal B12 deficiency during pregnancy has been associated with poor fetal outcomes such as intrauterine growth retardation, recurrent fetal loss, low birth weight, and neural tube defects [ 1 , 2 , 3 , 4 , 5 ]. Yet, a rare group of patients presents a paradox.…”

Section: Introductionmentioning

confidence: 99%

Nutritional 1C Imbalance, B12 Tissue Accumulation, and Pregnancy Outcomes: An Experimental Study in Rats

2018

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Vitamin B12 deficiency during pregnancy has been associated with poor fetal outcome. Here we investigate the influence of a one-carbon (1C) imbalanced diet (low B12, high folate, high methionine) on maternal B12 status, fetal outcome, B12 distribution, and on the 24-h distribution of synthetic cyano-B12 (CN-B12) and natural hydroxo-B12 (HO-B12). Female Wistar rats were mated while on a 1C balanced (n = 12) or imbalanced diet starting two weeks (n = 10) or four weeks (n = 9) prior to pregnancy and continuing throughout pregnancy. At gestation day 18 (out of 21), all rats received an oral dose of labeled CN-B12 or HO-B12. After 24 h, the rats were sacrificed. Fetuses were inspected, and maternal tissues and fetuses were measured for endogenous and labeled B12. Pregnancy caused a redistribution of B12 from the kidneys to the liver and fetal compartment (uterus, placenta, fetuses). The 1C imbalanced diet reduced maternal kidney B12 and gave rise to lower-weight fetuses with visual malformations. In contrast, fetal B12 did not reflect fetal outcome. This suggests that maternal B12 is more important for fetal outcome than fetal B12. The 24-h distribution of labeled B12 in the rats on the 1C imbalanced diet showed a higher fetal accumulation of CN-B12 than HO-B12, while the opposite was seen in the maternal tissues.

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Risk of low birth weight and micronutrient deficiencies in neonates from mothers after gastric bypass: a case control study

Cited by 59 publications

References 35 publications

Intrauterine Fetal Growth Delay During Late Pregnancy After Maternal Gastric Bypass Surgery

Intrauterine Fetal Growth Delay During Late Pregnancy After Maternal Gastric Bypass Surgery

Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD)

Nutritional 1C Imbalance, B12 Tissue Accumulation, and Pregnancy Outcomes: An Experimental Study in Rats

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