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Maternal and Infant Health: The Molecular Nutrition Perspective

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

Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 14058

Special Issue Editor


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Guest Editor
Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan
Interests: fetal programming; developmental origins of adult health and disease; nutritional epigenetics; obesity; metabolic syndrome; cardiovascular disease; nonalcoholic fatty liver disease (NAFLD); adipose tissue browning; metabolic health

Special Issue Information

Dear Colleagues,

Maternal nutrition plays an important role in improving the health of mothers and their children. Women with obesity, diabetes, anemia or cancer are at greater risk of developing childbirth-related complications. Furthermore, their children are more likely to experience adverse health outcomes such as cardiovascular disease, insulin resistance and many chronic metabolic diseases later in life. The “developmental origins of adult health and disease” (DOHaD) is a concept that links the state of health and risk of disease in adult life with the environmental conditions (such as maternal malnutrition and unhealthy lifestyle) of the early life (such as the embryonic stage, infancy and early childhood). Understanding the impact of maternal nutrition on offspring is particularly important. Interventions targeting early-life programming might offer new opportunities to improve the health outcomes of both mothers and offspring.

The objective of this Special Issue on “Maternal and Infant Health: The Molecular Nutrition Perspective” is to showcase the latest research capturing the breadth of DOHaD, from basic science to clinical research. As IJMS is a journal of molecular science, submissions of basic research with molecular biology experiments and/or clinical studies with biomolecular experiments are welcomed.

Prof. Dr. Fu-Jung Lin
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

  • fetal programming
  • developmental origins of adult health and disease
  • early nutrition
  • maternal obesity
  • maternal diet
  • epigenetics
  • cardiovascular disease
  • metabolism
  • metabolic disorders
  • fetus

Published Papers (5 papers)

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Research

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17 pages, 4425 KiB  
Article
The Modification of Offspring Stress-Related Behavior and the Expression of Drd1, Drd2, and Nr3c1 by a Western-Pattern Diet in Mus Musculus
by Nikki Clauss, Kelsey Brass Allen, Katie D. Billings, Mikayla D. M. Tolliver, Ray Garza, Jennifer Byrd-Craven and Polly Campbell
Int. J. Mol. Sci. 2022, 23(16), 9245; https://doi.org/10.3390/ijms23169245 - 17 Aug 2022
Viewed by 1606
Abstract
The impact of early developmental experience on neurobiological pathways that may contribute to the association between diet and behavior have not yet been elucidated. The focus of the current study was to determine whether the impact of prenatal stress (PS) could be mitigated [...] Read more.
The impact of early developmental experience on neurobiological pathways that may contribute to the association between diet and behavior have not yet been elucidated. The focus of the current study was to determine whether the impact of prenatal stress (PS) could be mitigated by a diet that stimulates the same neuroendocrine systems influenced by early stress, using a mouse model. Behavioral and genetic approaches were used to assess how a Western-pattern diet (WPD) interacts with PS and sex to impact the expression of anxiety-like behavior in an open-field arena, as well as the expression of the glucocorticoid receptor in the hippocampus, D1 dopamine receptors in the nucleus accumbens, and D2 dopamine receptors in the ventral tegmental area. Overall, the results demonstrated that a prenatal WPD mitigates the effects of maternal stress in dams and offspring. These results help to elucidate the relationship between pre- and post-natal nutrition, gene expression, and behaviors that lead to long-term health effects. Full article
(This article belongs to the Special Issue Maternal and Infant Health: The Molecular Nutrition Perspective)
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12 pages, 3463 KiB  
Article
Maternal Iron Deficiency Programs Rat Offspring Hypertension in Relation to Renin—Angiotensin System and Oxidative Stress
by Ya-Hui Chang, Wan-Hsuan Chen, Chung-Hao Su, Hong-Ren Yu, You-Lin Tain, Li-Tung Huang and Jiunn-Ming Sheen
Int. J. Mol. Sci. 2022, 23(15), 8294; https://doi.org/10.3390/ijms23158294 - 27 Jul 2022
Cited by 3 | Viewed by 1694
Abstract
Hypertension is an important public health challenge, affecting up to 30–50% of adults worldwide. Several epidemiological studies indicate that high blood pressure originates in fetal life—the so-called programming effect or developmental origin of hypertension. Iron-deficiency anemia has become one of the most prevalent [...] Read more.
Hypertension is an important public health challenge, affecting up to 30–50% of adults worldwide. Several epidemiological studies indicate that high blood pressure originates in fetal life—the so-called programming effect or developmental origin of hypertension. Iron-deficiency anemia has become one of the most prevalent nutritional problems globally. Previous animal experiments have shown that prenatal iron-deficiency anemia adversely affects offspring hypertension. However, the underlying mechanism remains unclear. We used a maternal low-iron diet Sprague Dawley rat model to study changes in blood pressure, the renal renin-angiotensin system, oxidative stress, inflammation, and sodium transporters in adult male offspring. Our study revealed that 16-week-old male offspring born to mothers with low dietary iron throughout pregnancy and the lactation period had (1) higher blood pressure, (2) increased renal cortex angiotensin II receptor type 1 and angiotensin-converting enzyme abundance, (3) decreased renal cortex angiotensin II receptor type 2 and MAS abundance, and (4) increased renal 8-hydroxy-2′-deoxyguanosine and interleukin-6 abundance. Improving the iron status of pregnant mothers could influence the development of hypertension in their offspring. Full article
(This article belongs to the Special Issue Maternal and Infant Health: The Molecular Nutrition Perspective)
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15 pages, 1414 KiB  
Article
Maternal Acetate Supplementation Reverses Blood Pressure Increase in Male Offspring Induced by Exposure to Minocycline during Pregnancy and Lactation
by Chien-Ning Hsu, Hong-Ren Yu, Julie Y. H. Chan, Wei-Chia Lee, Kay L. H. Wu, Chih-Yao Hou, Guo-Ping Chang-Chien, Sufan Lin and You-Lin Tain
Int. J. Mol. Sci. 2022, 23(14), 7924; https://doi.org/10.3390/ijms23147924 - 18 Jul 2022
Cited by 9 | Viewed by 1968
Abstract
Emerging evidence supports that hypertension can be programmed or reprogrammed by maternal nutrition. Maternal exposures during pregnancy, such as maternal nutrition or antibiotic use, could alter the offspring’s gut microbiota. Short-chain fatty acids (SCFAs) are the major gut microbiota-derived metabolites. Acetate, the most [...] Read more.
Emerging evidence supports that hypertension can be programmed or reprogrammed by maternal nutrition. Maternal exposures during pregnancy, such as maternal nutrition or antibiotic use, could alter the offspring’s gut microbiota. Short-chain fatty acids (SCFAs) are the major gut microbiota-derived metabolites. Acetate, the most dominant SCFA, has shown its antihypertensive effect. Limited information exists regarding whether maternal acetate supplementation can prevent maternal minocycline-induced hypertension in adult offspring. We exposed pregnant Sprague Dawley rats to normal diet (ND), minocycline (MI, 50 mg/kg/day), magnesium acetate (AC, 200 mmol/L in drinking water), and MI + AC from gestation to lactation period. At 12 weeks of age, four groups (n = 8/group) of male progeny were sacrificed. Maternal acetate supplementation protected adult offspring against minocycline-induced hypertension. Minocycline administration reduced plasma acetic acid level, which maternal acetate supplementation prevented. Additionally, acetate supplementation increased the protein level of SCFA receptor G protein-coupled receptor 41 in the offspring kidneys. Further, minocycline administration and acetate supplementation significantly altered gut microbiota composition. Maternal acetate supplementation protected minocycline-induced hypertension accompanying by the increases in genera Roseburia, Bifidobacterium, and Coprococcus. In sum, our results cast new light on targeting gut microbial metabolites as early interventions to prevent the development of hypertension, which could help alleviate the global burden of hypertension. Full article
(This article belongs to the Special Issue Maternal and Infant Health: The Molecular Nutrition Perspective)
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Review

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20 pages, 2335 KiB  
Review
Maternal Fructose Intake, Programmed Mitochondrial Function and Predisposition to Adult Disease
by Erin Vanessa LaRae Smith, Rebecca Maree Dyson, Freya Rebecca Weth, Mary Judith Berry and Clint Gray
Int. J. Mol. Sci. 2022, 23(20), 12215; https://doi.org/10.3390/ijms232012215 - 13 Oct 2022
Cited by 1 | Viewed by 3927
Abstract
Fructose consumption is now recognised as a major risk factor in the development of metabolic diseases, such as hyperlipidaemia, diabetes, non-alcoholic fatty liver disease and obesity. In addition to environmental, social, and genetic factors, an unfavourable intrauterine environment is now also recognised as [...] Read more.
Fructose consumption is now recognised as a major risk factor in the development of metabolic diseases, such as hyperlipidaemia, diabetes, non-alcoholic fatty liver disease and obesity. In addition to environmental, social, and genetic factors, an unfavourable intrauterine environment is now also recognised as an important factor in the progression of, or susceptibility to, metabolic disease during adulthood. Developmental trajectory in the short term, in response to nutrient restriction or excessive nutrient availability, may promote adaptation that serves to maintain organ functionality necessary for immediate survival and foetal development. Consequently, this may lead to decreased function of organ systems when presented with an unfavourable neonatal, adolescent and/or adult nutritional environment. These early events may exacerbate susceptibility to later-life disease since sub-optimal maternal nutrition increases the risk of non-communicable diseases (NCDs) in future generations. Earlier dietary interventions, implemented in pregnant mothers or those considering pregnancy, may have added benefit. Although, the mechanisms by which maternal diets high in fructose and the vertical transmission of maternal metabolic phenotype may lead to the predisposition to adult disease are poorly understood. In this review, we will discuss the potential contribution of excessive fructose intake during pregnancy and how this may lead to developmental reprogramming of mitochondrial function and predisposition to metabolic disease in offspring. Full article
(This article belongs to the Special Issue Maternal and Infant Health: The Molecular Nutrition Perspective)
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12 pages, 1106 KiB  
Review
The Role of Human Milk Lipids and Lipid Metabolites in Protecting the Infant against Non-Communicable Disease
by Alexandra D. George, Satvika Burugupalli, Sudip Paul, Toby Mansell, David Burgner and Peter J. Meikle
Int. J. Mol. Sci. 2022, 23(14), 7490; https://doi.org/10.3390/ijms23147490 - 6 Jul 2022
Cited by 10 | Viewed by 3916
Abstract
Non-communicable diseases continue to increase globally and have their origins early in life. Early life obesity tracks from childhood to adulthood, is associated with obesity, inflammation, and metabolic dysfunction, and predicts non-communicable disease risk in later life. There is mounting evidence that these [...] Read more.
Non-communicable diseases continue to increase globally and have their origins early in life. Early life obesity tracks from childhood to adulthood, is associated with obesity, inflammation, and metabolic dysfunction, and predicts non-communicable disease risk in later life. There is mounting evidence that these factors are more prevalent in infants who are formula-fed compared to those who are breastfed. Human milk provides the infant with a complex formulation of lipids, many of which are not present in infant formula, or are present in markedly different concentrations, and the plasma lipidome of breastfed infants differs significantly from that of formula-fed infants. With this knowledge, and the knowledge that lipids have critical implications in human health, the lipid composition of human milk is a promising approach to understanding how breastfeeding protects against obesity, inflammation, and subsequent cardiovascular disease risk. Here we review bioactive human milk lipids and lipid metabolites that may play a protective role against obesity and inflammation in later life. We identify key knowledge gaps and highlight priorities for future research. Full article
(This article belongs to the Special Issue Maternal and Infant Health: The Molecular Nutrition Perspective)
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