Maternal exposure to sucrose and maltodextrin alters metabolism and genotoxicity in mice offspring

IF 2.4 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2026-01-01 Epub Date: 2026-03-09 DOI:10.1016/j.mrfmmm.2026.111933

Marina Lummertz Magenis , Whayne Alves Alecrim , Otávio Lúcio Possamai , Isadora de Oliveira Monteiro , Nicollas dos Santos da Silva , Carolina Giassi Alano , Adriani Paganini Damiani , Helen Barbosa Vicente , Isadora Luciano Machado , Rafaela Cristina Silva de Almeida , Isabela da Silva Lemos , Emílio Luiz Streck , Vanessa Moraes de Andrade

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引用次数: 0

Abstract

Early metabolic events during the intrauterine period can increase susceptibility to chronic diseases in adulthood. Fetal and neonatal nutrition rich in sugars may lead to disorders such as obesity, insulin resistance, and diabetes. This study evaluated the effects of maltodextrin and sucrose intake in Swiss female mice treated during gestation and lactation, as well as in their offspring. Sixty-day-old mating pairs were used, receiving nutritional interventions (maltodextrin 10%/L, sucrose 10%/L, or water) during mating, gestation, and lactation (7, 21, and 21 days, respectively), totaling 49 days. Genetic (comet assay, micronucleus test) and biochemical (glycemia and electron transport chain) analyses were performed in dams and in offspring of both sexes at postnatal days (PND) 21 and 30. In dams, food intake and body weight were monitored, whereas in offspring, anthropometric parameters were assessed. Results showed that both carbohydrates increased fluid and calorie intake without affecting maternal body weight. Sucrose raised fasting glucose significantly. Comet assay revealed increased DNA damage after gestation and lactation, especially in the cortex for maltodextrin (p < 0.05), with no changes in liver or hippocampus. The micronucleus test showed increased PCE micronuclei in the maltodextrin group (p < 0.05). Complex I activity increased in the liver with both carbohydrates, while Complex II–III decreased with sucrose. In the cortex, both carbohydrates increased Complex II and reduced Complex IV; in the hippocampus, Complex I increased with both, and Complex IV increased with maltodextrin. In the offspring, sucrose-exposed males had greater body weight at 21 days, and females showed increased glycemia at 30 days. Overall, findings suggest that maltodextrin and sucrose intake during pregnancy and lactation can induce long-term metabolic and genetic alterations in mothers and offspring.

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母体接触蔗糖和麦芽糖糊精会改变小鼠后代的代谢和遗传毒性

宫内早期代谢事件可增加成年后对慢性疾病的易感性。富含糖的胎儿和新生儿营养可能导致肥胖、胰岛素抵抗和糖尿病等疾病。本研究评估了麦芽糊精和蔗糖摄入对妊娠和哺乳期瑞士雌性小鼠及其后代的影响。选用60日龄交配对，在交配、妊娠和哺乳期间（分别为7、21和21天）接受营养干预（麦芽糊精10%/L、蔗糖10%/L或水），共49天。遗传（彗星试验、微核试验）和生化（血糖和电子传递链）分析在母鼠和雌雄后代出生后21和30天（PND）进行。在母鼠中，监测食物摄入量和体重，而在后代中，评估人体测量参数。结果表明，这两种碳水化合物都增加了液体和卡路里的摄入量，而不影响母亲的体重。蔗糖显著提高空腹血糖。彗星分析显示，妊娠和哺乳期后DNA损伤增加，特别是在皮质中麦芽糊精（p <； 0.05），而肝脏和海马没有变化。微核试验显示麦芽糖糊精组PCE微核升高（p <； 0.05）。两种碳水化合物都增加了肝脏中复合物I的活性，而蔗糖降低了复合物II-III的活性。在皮层中，两种碳水化合物均增加复合物II并降低复合物IV；在海马体中，复合物I随两者增加，复合物IV随麦芽糊精增加。在后代中，接触蔗糖的雄性在21天时体重增加，而雌性在30天时血糖升高。总之，研究结果表明，妊娠期和哺乳期摄入麦芽糖糊精和蔗糖会导致母亲和后代的长期代谢和遗传改变。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.