Association of Maternal Roux-en-Y Gastric Bypass with Obstetric Outcomes and Fluid Intelligence in Offspring

Blume, Carina Andriatta; Machado, Brenda Moretto; Rosa, Raíssa Ramos da; Rigoni, Maísa dos Santos; Casagrande, Daniela Schaan; Mottin, Cláudio Corá; Schaan, Beatriz D.

doi:10.1007/s11695-018-3407-5

Cited by 7 publications

(1 citation statement)

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“…S1). Reduced birth weight, 46,47 as well other gestational complications such as preterm birth, neonatal hypocalcemia, rickets, and fetal mental retardation, can potentially damage offspring as the result of reductions in iron, vitamin B12, and folic acid absorption in pregnant women that have been submitted to RYGB. 46 Importantly, lower BW at birth is also observed in obese mothers with NAFLD during gestation.…”

Section: Discussionmentioning

confidence: 99%

Pregnancy and lactation after Roux-en-Y gastric bypass worsen nonalcoholic fatty liver disease in obese rats and lead to differential programming of hepatic de novo lipogenesis in offspring

Bertasso

Pietrobon

Ribeiro

et al. 2021

J Dev Orig Health Dis

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Maternal obesity increases the risk of nonalcoholic fatty liver disease (NAFLD) in offspring. The Roux-en-Y gastric bypass (RYBG) is effective for achieving weight loss and ameliorates NAFLD. To determine whether these benefits are maintained after pregnancy and/or lactation, and whether they modulate hepatic morphofunction in the next generation, we evaluated hepatic lipid metabolism in Western diet (WD)-obese female rats that underwent RYGB and in their F1 offspring at adulthood. Female Wistar rats consumed a WD from 21 to 130 days of age, before being submitted to RYGB (WD-RYGB-F0) or SHAM (WD-SHAM-F0) operations. After 5 weeks, these females were mated with control male breeders, and the male and female F1 offspring were identified as WD-RYGB-F1 and WD-SHAM-F1. WD-RYGB-F0 dams exhibited lower serum lipids levels, but severe hepatic steatosis and pathological features of advanced liver injury. The hepatic proteins involved in lipogenesis were reduced in WD-RYGB-F0, as were the genes related to β-oxidation and bile acids (BAs). Although the female and male WD-RYGB-F1 groups did not exhibit hepatic steatosis, the livers of female WD-RYGB-F1 demonstrated higher amounts of lipogenic genes and proteins, while male WD-RYGB-F1 presented a similar downregulation of lipogenic factors to that seen in WD-RYGB-F0 dams. In contrast, maternal and offspring groups of both sexes displayed reductions in the expressions of genes involved in BAs physiology and gluconeogenesis. As such, RYGB aggravates NAFLD after pregnancy and lactation and induces a gender-dependent differential expression of the hepatic lipogenesis pathway in offspring, indicating that female WD-RYGB-F1 may be an increased risk of developing NAFLD.

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Section: Discussionmentioning

confidence: 99%