Ferulic acid protects rat offspring from maternal high-fat, high-fructose diet-induced toxicity and developmental retardation through a direct effect on pancreatic islets.
{"title":"Ferulic acid protects rat offspring from maternal high-fat, high-fructose diet-induced toxicity and developmental retardation through a direct effect on pancreatic islets.","authors":"Hekmat L El-Gammal, Fatma Omar, Ayman Hyder","doi":"10.1016/j.fct.2025.115265","DOIUrl":null,"url":null,"abstract":"<p><p>Maternal obesity predisposes offspring to type 2 diabetes (T2D) through a direct chronic effect of lipids on pancreatic β-cell neogenesis. β-cells produce FABP3 to bind and metabolize fatty acids. Ferulic acid (FA) is a natural product that may inhibit fatty acids' binding to FABP3, preventing their toxicity. It is aimed to evaluate the consequences of maternal feeding on high-fat, high fructose diet (HFFD) and the role of FA on the offspring. Four-week-old female rats were fed HFFD for 9 weeks prior to and throughout gestation and lactation to develop T2D. A group of them received 50 mg/kg FA daily. Offspring were sampled on gestational day 18 (GD18), and postnatal days (PND) 3 and 30. HFFD increased offspring's blood glucose, insulin, Homa-IR, HbA1c, triglycerides, cholesterol, intrahepatic and intra-insular lipid droplets. The mechanism of islet inflammation and apoptosis, detected by Il-1b and cleaved caspase3, involved the nuclear translocation of NFκB p65. Maternal HFFD caused developmental retardations in offspring's ovaries, testes, kidney and liver. Coupling FA treatment with the maternal HFFD maintained normoglycemia, lipidemia, and healthy islets, and prevented developmental retardations. FA administration to T2D mothers revealed positive effects on the offspring that is related to its direct protective effect on pancreatic β-cells.</p>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":" ","pages":"115265"},"PeriodicalIF":3.9000,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food and Chemical Toxicology","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1016/j.fct.2025.115265","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Maternal obesity predisposes offspring to type 2 diabetes (T2D) through a direct chronic effect of lipids on pancreatic β-cell neogenesis. β-cells produce FABP3 to bind and metabolize fatty acids. Ferulic acid (FA) is a natural product that may inhibit fatty acids' binding to FABP3, preventing their toxicity. It is aimed to evaluate the consequences of maternal feeding on high-fat, high fructose diet (HFFD) and the role of FA on the offspring. Four-week-old female rats were fed HFFD for 9 weeks prior to and throughout gestation and lactation to develop T2D. A group of them received 50 mg/kg FA daily. Offspring were sampled on gestational day 18 (GD18), and postnatal days (PND) 3 and 30. HFFD increased offspring's blood glucose, insulin, Homa-IR, HbA1c, triglycerides, cholesterol, intrahepatic and intra-insular lipid droplets. The mechanism of islet inflammation and apoptosis, detected by Il-1b and cleaved caspase3, involved the nuclear translocation of NFκB p65. Maternal HFFD caused developmental retardations in offspring's ovaries, testes, kidney and liver. Coupling FA treatment with the maternal HFFD maintained normoglycemia, lipidemia, and healthy islets, and prevented developmental retardations. FA administration to T2D mothers revealed positive effects on the offspring that is related to its direct protective effect on pancreatic β-cells.
期刊介绍：
Food and Chemical Toxicology (FCT), an internationally renowned journal, that publishes original research articles and reviews on toxic effects, in animals and humans, of natural or synthetic chemicals occurring in the human environment with particular emphasis on food, drugs, and chemicals, including agricultural and industrial safety, and consumer product safety. Areas such as safety evaluation of novel foods and ingredients, biotechnologically-derived products, and nanomaterials are included in the scope of the journal. FCT also encourages submission of papers on inter-relationships between nutrition and toxicology and on in vitro techniques, particularly those fostering the 3 Rs.
The principal aim of the journal is to publish high impact, scholarly work and to serve as a multidisciplinary forum for research in toxicology. Papers submitted will be judged on the basis of scientific originality and contribution to the field, quality and subject matter. Studies should address at least one of the following:
-Adverse physiological/biochemical, or pathological changes induced by specific defined substances
-New techniques for assessing potential toxicity, including molecular biology
-Mechanisms underlying toxic phenomena
-Toxicological examinations of specific chemicals or consumer products, both those showing adverse effects and those demonstrating safety, that meet current standards of scientific acceptability.
Authors must clearly and briefly identify what novel toxic effect (s) or toxic mechanism (s) of the chemical are being reported and what their significance is in the abstract. Furthermore, sufficient doses should be included in order to provide information on NOAEL/LOAEL values.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
