Zhao Grace, Chondon Sarah, Gray Clint, Gentili Sheridan, Stanley Meagan, Regnault Timothy Rh
Department of Obstetrics and Gynaecology, Western University, London, ON, Canada.
Department of Obstetrics and Gynaecology, Schulich School of Medicine, Western University, London, ON, Canada.
Curr Dev Nutr. 2024 Nov 27;9(1):104510. doi: 10.1016/j.cdnut.2024.104510. eCollection 2025 Jan.
Excess fructose consumption has been linked to adverse metabolic health, including impaired hepatic function and increased adiposity. The early life period, including preconception, pregnancy, and the newborn period, are critical periods in determining later metabolic health. However, the impact of excess fructose intake during this time on maternal, fetal, and offspring hepatic and whole-body adiposity, is not well defined.
To understand the effects of maternal fructose consumption pre- and during pregnancy on maternal, fetal, and offspring hepatic and whole-body adiposity.
A systematic search of MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials was performed up to October 4, 2024, to identify animal and human studies that focused on maternal fructose consumption pre- and during pregnancy on hepatic and whole-body adiposity in the mother, fetus, and offspring. Citations, abstracts, and full texts were screened in duplicate. Hepatic adiposity was defined as elevated hepatic triglycerides or overall hepatic lipid accumulation. Whole-body adiposity was defined as increased adipose tissue, serum lipids, or adipocyte hypertrophy.
After screening 2538 citations, 37 experimental rodent studies reporting maternal fructose consumption pre- and during pregnancy in rodents were included. No human studies met the inclusion criteria. Prenatal fructose exposure was associated with maternal (9 of 12) and offspring (7 of 11) whole-body adiposity. A high proportion of studies (13 of 14) supported the association between fructose during pregnancy and increased maternal hepatic adiposity. Fetal hepatic adiposity and elevated expression of hepatic lipogenic proteins were noted in 4 studies. Offspring hepatic adiposity was supported in 16 of the 20 articles that discussed hepatic results, with 5 studies demonstrating more severe effects in female offspring.
Fructose consumption during pregnancy in rodent models is associated with maternal, fetal, and offspring hepatic and whole-body adiposity with underlying sex-specific effects. No human studies met the inclusion criteria.
H8F26 on Open Science Framework (https://doi.org/10.17605/OSF.IO/H8F26).
过量摄入果糖与不良代谢健康有关，包括肝功能受损和肥胖增加。生命早期阶段，包括孕前、孕期和新生儿期，是决定后期代谢健康的关键时期。然而，在此期间过量摄入果糖对母体、胎儿以及子代肝脏和全身肥胖的影响尚不明确。
了解孕期及孕前母体摄入果糖对母体、胎儿以及子代肝脏和全身肥胖的影响。
截至2024年10月4日，对MEDLINE、EMBASE和Cochrane对照试验中心注册库进行了系统检索，以识别关注孕期及孕前母体摄入果糖对母体、胎儿以及子代肝脏和全身肥胖影响的动物和人体研究。对文献引用、摘要和全文进行了双人筛选。肝脏肥胖定义为肝脏甘油三酯升高或肝脏脂质总体蓄积。全身肥胖定义为脂肪组织增加、血脂升高或脂肪细胞肥大。
在筛选了2538篇文献引用后，纳入了37项关于孕期及孕前啮齿动物母体摄入果糖的实验性啮齿动物研究。没有人体研究符合纳入标准。产前果糖暴露与母体（12项研究中的9项）和子代（11项研究中的7项）全身肥胖有关。高比例的研究（14项研究中的13项）支持孕期果糖摄入与母体肝脏肥胖增加之间的关联。4项研究中观察到胎儿肝脏肥胖以及肝脏脂肪生成蛋白表达升高。在20篇讨论肝脏结果的文章中，16篇支持子代肝脏肥胖，5项研究表明雌性子代的影响更严重。
啮齿动物模型中孕期摄入果糖与母体、胎儿以及子代肝脏和全身肥胖有关，且存在性别特异性影响。没有人体研究符合纳入标准。
开放科学框架上的H8F26（https://doi.org/10.17605/OSF.IO/H8F26）
