Ferulic acid protects rat offspring from maternal high-fat, high-fructose diet-induced toxicity and developmental retardation through a direct effect on pancreatic islets.

IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Food and Chemical Toxicology Pub Date : 2025-01-18 DOI:10.1016/j.fct.2025.115265
Hekmat L El-Gammal, Fatma Omar, Ayman Hyder
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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.

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阿魏酸通过对胰岛的直接作用,保护大鼠后代免受母体高脂肪、高果糖饮食引起的毒性和发育迟缓。
母体肥胖通过脂质对胰腺β细胞新生的直接慢性影响,使后代易患2型糖尿病(T2D)。β-细胞产生FABP3结合和代谢脂肪酸。阿魏酸(FA)是一种天然产物,可以抑制脂肪酸与FABP3的结合,防止其毒性。本研究旨在评估高脂肪、高果糖饮食(HFFD)对后代的影响以及FA对后代的作用。4周龄的雌性大鼠在妊娠和哺乳期前和整个哺乳期喂养9周HFFD以形成T2D。每组饲喂50 mg/kg FA。子代在妊娠第18天(GD18)和产后第3和30天(PND)取样。HFFD增加子代血糖、胰岛素、Homa-IR、HbA1c、甘油三酯、胆固醇、肝内和岛内脂滴。通过Il-1b和cleaved caspase3检测,胰岛炎症和凋亡的机制与NFκB p65的核易位有关。母体HFFD导致子代卵巢、睾丸、肾脏和肝脏发育迟缓。将FA治疗与母亲HFFD结合,维持正常的血糖、血脂和健康的胰岛,并预防发育迟缓。给T2D母鼠服用FA对后代有积极作用,这与FA对胰腺β细胞的直接保护作用有关。
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来源期刊
Food and Chemical Toxicology
Food and Chemical Toxicology 工程技术-毒理学
CiteScore
10.90
自引率
4.70%
发文量
651
审稿时长
31 days
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.
期刊最新文献
The Role of GSK3β Signaling Mediated Lysosomal Biosynthesis Dysregulation in Fluoride-Induced Neurological Impairment. Corrigendum to "Maternal ochratoxin A exposure impairs meiosis progression and primordial follicle formation of F1 offspring" [Food and Chemical Toxicology 168 (2022) 113386]. Aprepitant ameliorates vancomycin-induced kidney injury: Role of GPX4/system Xc- and oxidative damage. Dexlansoprazole acts as a disruptor of the aryl hydrocarbon receptor and ITE. Ferulic acid protects rat offspring from maternal high-fat, high-fructose diet-induced toxicity and developmental retardation through a direct effect on pancreatic islets.
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