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Effect of Maternal High-Fat Diet on Offspring’s Health
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Effect of Maternal High-Fat Diet on Offspring’s Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 8835

Special Issue Editor

Prof. Dr. Hong-Ren Yu

E-Mail Website
Guest Editor
1. Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 33303, Taiwan
2. Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Tao-Yuan 33302, Taiwan
Interests: child internal medicine; pediatric thorax; child rheumatism allergy immunity department

Special Issue Information

Dear Colleagues,

The rapidly increasing of obesity has become one of the major health problems in modern society. A high-fat diet is one of the factors that contribute to the increase of obesity. Maternal obesity increases the risk of pregnant complications, including preeclampsia, gestational diabetes, caesarean section, and preterm birth. In addition, maternal high-fat diets can also influence fetal development and may lead to offspring programmed to metabolic problems in childhood, adolescence, and even adulthood stage.

The placenta is the key link between mother and the developing fetus and it performs many important functions in fetal growth. In addition to attaching the developing fetus to the uterine wall, the placenta is involved in the development of maternal immune tolerance, hormone production, nutrient assimilation, metabolic waste removal, gas exchange, and as a barrier to block harmful substances into the fetus through maternal-fetal blood supply. There is evidence that a high-fat diet in pregnant women can cause placental dysfunction and adversely affect fetal development. More research is needed to understand how a maternal high-fat diet affects the placenta to program offspring to exacerbate the development of metabolic problems in adulthood.

High-fat diet during pregnancy and lactation can impair the integrity of gut barrier and affect both maternal and offspring gut microbiomes, which may increase the risk of adverse health in offspring. The elucidation of gut microbiome adaptations and relevant molecule alteration has great implications for the prevention and treatment of healthy problem related to maternal high-fat diet.

Developmental Origins of Health and Disease (DOHaD) concept emphasis the effects of prenatal/perinatal exposure to environmental factors in determining the development of human diseases in adulthood. DOHaD concept also open a window for us early intervention to reprogram the effect of prenatal/perinatal adversities. The DOHaD concept also opens a window for early intervention, where we can re-program the effects of prenatal/perinatal adversity. More precise re-programming strategies are still urgent demanded.

The main aim of this Special Issue “Effect of maternal high-fat diet on offspring health” aims to enroll valuable studies on a broad range of targets, including maternal HF diet components, placenta pathology, microbiomes and its metabolites, future child and adult health, and re-programming strategies. Original studies, and review articles will be considered.

Prof. Dr. Hong-Ren Yu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • maternal high-fat diet
  • DOHaD
  • microbiome
  • placenta
  • fetus/offspring
  • nutritional/medication programming

Published Papers (4 papers)

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Research

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16 pages, 4029 KiB  
Communication
Perinatal Obesity Sensitizes for Premature Kidney Aging Signaling
by Jaco Selle, Katrin Bohl, Katja Höpker, Rebecca Wilke, Katharina Dinger, Philipp Kasper, Bastian Abend, Bernhard Schermer, Roman-Ulrich Müller, Christine Kurschat, Kai-Dietrich Nüsken, Eva Nüsken, David Meyer, Soni Savai Pullamsetti, Björn Schumacher, Jörg Dötsch and Miguel A. Alejandre Alcazar
Int. J. Mol. Sci. 2023, 24(3), 2508; https://doi.org/10.3390/ijms24032508 - 28 Jan 2023
Cited by 1 | Viewed by 1861
Abstract
Chronic Kidney Disease (CKD), a global health burden, is strongly associated with age-related renal function decline, hypertension, and diabetes, which are all frequent consequences of obesity. Despite extensive studies, the mechanisms determining susceptibility to CKD remain insufficiently understood. Clinical evidence together with prior [...] Read more.
Chronic Kidney Disease (CKD), a global health burden, is strongly associated with age-related renal function decline, hypertension, and diabetes, which are all frequent consequences of obesity. Despite extensive studies, the mechanisms determining susceptibility to CKD remain insufficiently understood. Clinical evidence together with prior studies from our group showed that perinatal metabolic disorders after intrauterine growth restriction or maternal obesity adversely affect kidney structure and function throughout life. Since obesity and aging processes converge in similar pathways we tested if perinatal obesity caused by high-fat diet (HFD)-fed dams sensitizes aging-associated mechanisms in kidneys of newborn mice. The results showed a marked increase of γH2AX-positive cells with elevated 8-Oxo-dG (RNA/DNA damage), both indicative of DNA damage response and oxidative stress. Using unbiased comprehensive transcriptomics we identified compartment-specific differentially-regulated signaling pathways in kidneys after perinatal obesity. Comparison of these data to transcriptomic data of naturally aged kidneys and prematurely aged kidneys of genetic modified mice with a hypomorphic allele of Ercc1, revealed similar signatures, e.g., inflammatory signaling. In a biochemical approach we validated pathways of inflammaging in the kidneys after perinatal obesity. Collectively, our initial findings demonstrate premature aging-associated processes as a consequence of perinatal obesity that could determine the susceptibility for CKD early in life. Full article
(This article belongs to the Special Issue Effect of Maternal High-Fat Diet on Offspring’s Health)
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14 pages, 3234 KiB  
Article
Maternal Metformin Treatment Reprograms Maternal High-Fat Diet-Induced Hepatic Steatosis in Offspring Associated with Placental Glucose Transporter Modifications
by Chien-Fu Huang, Mao-Meng Tiao, I-Chun Lin, Li-Tung Huang, Jiunn-Ming Sheen, You-Lin Tain, Chien-Ning Hsu, Ching-Chou Tsai, Yu-Ju Lin and Hong-Ren Yu
Int. J. Mol. Sci. 2022, 23(22), 14239; https://doi.org/10.3390/ijms232214239 - 17 Nov 2022
Cited by 3 | Viewed by 1774
Abstract
Maternal high-fat (HF) diet exposure in utero may affect fetal development and cause metabolic problems throughout life due to lipid dysmetabolism and oxidative damage. Metformin has been suggested as a potential treatment for body weight reduction and nonalcoholic fatty liver disease, but its [...] Read more.
Maternal high-fat (HF) diet exposure in utero may affect fetal development and cause metabolic problems throughout life due to lipid dysmetabolism and oxidative damage. Metformin has been suggested as a potential treatment for body weight reduction and nonalcoholic fatty liver disease, but its reprogramming effect on offspring is undetermined. This study assesses the effects of maternal metformin treatment on hepatic steatosis in offspring caused by maternal HF diet. Female rats were fed either a control or an HF diet before conception, with or without metformin treatment during gestation, and placenta and fetal liver tissues were collected. In another experiment, the offspring were fed a control diet until 120 d (adult stage). Metformin treatment during pregnancy ameliorates placental oxidative stress and enhances placental glucose transporter 1 (GLUT1), GLUT3, and GLUT4 expression levels through 5’ adenosine monophosphate-activated protein kinase (AMPK) activation. Maternal metformin treatment was shown to reprogram maternal HF diet-induced changes in offspring fatty liver with the effects observed in adulthood as well. Further validation is required to develop maternal metformin therapy for clinical applications. Full article
(This article belongs to the Special Issue Effect of Maternal High-Fat Diet on Offspring’s Health)
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13 pages, 2617 KiB  
Article
Dysregulation of Placental Lipid Hydrolysis by High-Fat/High-Cholesterol Feeding and Gestational Diabetes Mellitus in Mice
by Katharina B. Kuentzel, Ivan Bradić, Zala N. Mihalič, Melanie Korbelius, Silvia Rainer, Anita Pirchheim, Julia Kargl and Dagmar Kratky
Int. J. Mol. Sci. 2022, 23(20), 12286; https://doi.org/10.3390/ijms232012286 - 14 Oct 2022
Cited by 3 | Viewed by 1714
Abstract
Advanced maternal age and obesity are the main risk factors to develop gestational diabetes mellitus (GDM). Obesity is a consequence of the increased storage of triacylglycerol (TG). Cytosolic and lysosomal lipid hydrolases break down TG and cholesteryl esters (CE) to release fatty acids [...] Read more.
Advanced maternal age and obesity are the main risk factors to develop gestational diabetes mellitus (GDM). Obesity is a consequence of the increased storage of triacylglycerol (TG). Cytosolic and lysosomal lipid hydrolases break down TG and cholesteryl esters (CE) to release fatty acids (FA), free cholesterol, and glycerol. We have recently shown that intracellular lipases are present and active in the mouse placenta and that deficiency of lysosomal acid lipase alters placental and fetal lipid homeostasis. To date, intracellular lipid hydrolysis in GDM has been poorly studied despite the important role of FA in this condition. Therefore, we hypothesized that intracellular lipases are dysregulated in pregnancies complicated by maternal high-fat/high-cholesterol (HF/HCD) feeding with and without GDM. Placentae of HF/HCD-fed mice with and without GDM were more efficient, indicating increased nutrient transfer to the fetus. The increased activity of placental CE but not TG hydrolases in placentae of dams fed HF/HCD with or without GDM resulted in upregulated cholesterol export to the fetus and placental TG accumulation. Our results indicate that HF/HCD-induced dysregulation of placental lipid hydrolysis contributes to fetal hepatic lipid accumulation and possibly to fetal overgrowth, at least in mice. Full article
(This article belongs to the Special Issue Effect of Maternal High-Fat Diet on Offspring’s Health)
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Review

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17 pages, 1136 KiB  
Review
Maternal High-Fat Diet and Offspring Hypertension
by You-Lin Tain and Chien-Ning Hsu
Int. J. Mol. Sci. 2022, 23(15), 8179; https://doi.org/10.3390/ijms23158179 - 25 Jul 2022
Cited by 14 | Viewed by 3095
Abstract
The incidence of hypertension has increased to epidemic levels in the past decades. Increasing evidence reveals that maternal dietary habits play a crucial role in the development of hypertension in adult offspring. In humans, increased fat consumption has been considered responsible for obesity [...] Read more.
The incidence of hypertension has increased to epidemic levels in the past decades. Increasing evidence reveals that maternal dietary habits play a crucial role in the development of hypertension in adult offspring. In humans, increased fat consumption has been considered responsible for obesity and associated diseases. Maternal diets rich in saturated fats have been widely employed in animal models to study various adverse offspring outcomes. In this review, we discussed current evidence linking maternal high-fat diet to offspring hypertension. We also provided an in-depth overview of the potential mechanisms underlying hypertension of developmental origins that are programmed by maternal high-fat intake from animal studies. Furthermore, this review also presented an overview of how reprogramming interventions can prevent maternal high-fat-diet-induced hypertension in adult offspring. Overall, recent advances in understanding mechanisms behind programming and reprogramming of maternal high-fat diet on hypertension of developmental origins might provide the answers to curtail this epidemic. Still, more research is needed to translate research findings into practice. Full article
(This article belongs to the Special Issue Effect of Maternal High-Fat Diet on Offspring’s Health)
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