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Maternal Nutritional-Mediated Programming of Offspring Health and Disease

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition in Women".

Deadline for manuscript submissions: closed (21 December 2023) | Viewed by 23205

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Dr. Mina Desai

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Guest Editor

The Lundquist Institute, David Geffen School of Medicine, Harbor-UCLA Medical Center, University of California, Los Angeles, CA 90095, USA
Interests: metabolic disorders; reproductive health; maternal-infant nutrition

Prof. Dr. Michael Ross

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Guest Editor

Special Issue Information

Dear Colleagues,

Nutrition is unquestionably one of the cornerstones of growth, development, and health, and as such, maternal nutrition is of critical importance. The field of developmental origins of adult health and disease has incorporated this phenomenon and portends that maternal nutritional insufficiency as well as nutrient excess impact fetal/infant growth, leading to ‘programmed’ adult diseases. The essential principles which underlie the concept of programming are that nutritional manipulations cause different effects at different times in early life, rapidly growing fetuses and neonates are more vulnerable to these manipulations, and these manipulations have permanent effects. The permanent effects include altered organ structure, resetting of hormonal axes, as well as cellular, molecular, signaling, and epigenetic modifications.

The objective of this proposed Special Issue is to publish seminal papers (reviews, clinical and experimental studies) on the consequences of sub-optimal maternal nutrition prior to pregnancy and during pregnancy/lactation on offspring risk of disease. These include the development of a wide range of diseases such as metabolic abnormalities, reproductive dysfunction, cardiovascular disease, neurobehavioral and immunological disorders, allergies, and aging, to name a few. To mitigate the burden of chronic disease worldwide, a comprehensive understanding of nutrition-mediated programmed effects and mechanisms is imperative. Importantly, there are also significant implications for the generational transmission of disease.

Dr. Mina Desai
Prof. Dr. Michael Ross
Guest Editors

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Published Papers (8 papers)

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Research

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22 pages, 3037 KiB

Open AccessArticle

Maternal Vitamin C Intake during Pregnancy Influences Long-Term Offspring Growth with Timing- and Sex-Specific Effects in Guinea Pigs

by Sharna J. Coker, Mary J. Berry, Margreet C. M. Vissers and Rebecca M. Dyson

Nutrients 2024, 16(3), 369; https://doi.org/10.3390/nu16030369 - 26 Jan 2024

Viewed by 2589

Abstract

Our previous work in guinea pigs revealed that low vitamin C intake during preconception and pregnancy adversely affects fertility, pregnancy outcomes, and foetal and neonatal growth in a sex-dependent manner. To investigate the long-term impact on offspring, we monitored their growth from birth to adolescence (four months), recorded organ weights at childhood equivalence (28 days) and adolescence, and assessed physiological parameters like oral glucose tolerance and basal cortisol concentrations. We also investigated the effects of the timing of maternal vitamin C restriction (early vs. late gestation) on pregnancy outcomes and the health consequences for offspring. Dunkin Hartley guinea pigs were fed an optimal (900 mg/kg feed) or low (100 mg/kg feed) vitamin C diet ad libitum during preconception. Pregnant dams were then randomised into four feeding regimens: consistently optimal, consistently low, low during early pregnancy, or low during late pregnancy. We found that low maternal vitamin C intake during early pregnancy accelerated foetal and neonatal growth in female offspring and altered glucose homeostasis in the offspring of both sexes at an age equivalent to early childhood. Conversely, low maternal vitamin C intake during late pregnancy resulted in foetal growth restriction and reduced weight gain in male offspring throughout their lifespan. We conclude that altered vitamin C during development has long-lasting, sex-specific consequences for offspring and that the timing of vitamin C depletion is also critical, with low levels during early development being associated with the development of a metabolic syndrome-related phenotype, while later deprivation appears to be linked to a growth-faltering phenotype. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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22 pages, 6944 KiB

Open AccessArticle

Sex-Dependent Variations in Hypothalamic Fatty Acid Profile and Neuropeptides in Offspring Exposed to Maternal Obesity and High-Fat Diet

by Mayara da Nóbrega Baqueiro, Laís Angélica de Paula Simino, João Paulo Costa, Carolina Panzarin, Andressa Reginato, Marcio Alberto Torsoni, Letícia Ignácio-Souza, Marciane Milanski, Michael G. Ross, Kelly Pereira Coca, Mina Desai and Adriana Souza Torsoni

Nutrients 2024, 16(3), 340; https://doi.org/10.3390/nu16030340 - 24 Jan 2024

Cited by 1 | Viewed by 2850

Abstract

Maternal obesity and/or high-fat diet (HF) consumption can disrupt appetite regulation in their offspring, contributing to transgenerational obesity and metabolic diseases. As fatty acids (FAs) play a role in appetite regulation, we investigated the maternal and fetal levels of FAs as potential contributors to programmed hyperphagia observed in the offspring of obese dams. Female mice were fed either a control diet (CT) or HF prior to mating, and fetal and maternal blood and tissues were collected at 19 days of gestation. Elevated levels of linoleic acid were observed in the serum of HF dams as well as in the serum of their fetuses. An increased concentration of eicosadienoic acid was also detected in the hypothalamus of female HF-O fetuses. HF-O male fetuses showed increased hypothalamic neuropeptide Y (Npy) gene expression, while HF-O female fetuses showed decreased hypothalamic pro-opiomelanocortin (POMC) protein content. Both male and female fetuses exhibited reduced hypothalamic neurogenin 3 (NGN-3) gene expression. In vitro experiments confirmed that LA contributed to the decreased gene expression of Pomc and Ngn-3 in neuronal cells. During lactation, HF female offspring consumed more milk and had a higher body weight compared to CT. In summary, this study demonstrated that exposure to HF prior to and during gestation alters the FA composition in maternal serum and fetal serum and hypothalamus, particularly increasing n-6, which may play a role in the switch from POMC to NPY neurons, leading to increased weight gain in the offspring during lactation. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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15 pages, 3643 KiB

Open AccessArticle

Maternal Intake of Either Fructose or the Artificial Sweetener Acesulfame-K Results in Differential and Sex-Specific Alterations in Markers of Skin Inflammation and Wound Healing Responsiveness in Mouse Offspring: A Pilot Study

by Pania E. Bridge-Comer, Mark H. Vickers, Sandra Ferraro, Aurélie Pagnon, Clare M. Reynolds and Dominique Sigaudo-Roussel

Nutrients 2023, 15(11), 2534; https://doi.org/10.3390/nu15112534 - 29 May 2023

Cited by 2 | Viewed by 3028

Abstract

Growing evidence has demonstrated that maternal artificial sweetener (AS) consumption may not be a beneficial alternative when compared to sugar-sweetened beverages and potentially leads to metabolic dysfunction in adult offspring. Compromised skin integrity and wound healing associated with type 2 diabetes can lead to complications such as diabetic pressure injury (PI). In this context, the skin plays an important role in the maintenance of metabolic homeostasis, yet there is limited information on the influence of sugar- or AS-sweetened beverages during pregnancy on developmental programming and offspring skin homeostasis. This study examined the impact of maternal fructose or acesulfame-k consumption on offspring wound healing. Female C57Bl/6 mice received a chow diet ad libitum with either water (CD), fructose (FR; 34.7 mM fructose), or AS (AS; 12.5 mM Acesulfame-K) throughout pregnancy and lactation. PIs were induced in offspring at 9 weeks of age (n = 6/sex/diet). PIs and healthy skin biopsies were collected for later analysis. Maternal AS intake increased skin inflammatory markers in healthy biopsies while an FR diet increased Tgfb expression, and both diets induced subtle changes in inflammatory markers post-wound inducement in a sex-specific manner. Furthermore, a maternal FR diet had a significant effect on pressure wound severity and early wound healing delay, while AS maternal diet had a sex-specific effect on the course of the healing process. This study demonstrates the need for a better understanding of developmental programming as a mediator of later-life skin integrity and wound responsiveness. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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19 pages, 6381 KiB

Open AccessArticle

Programming Mechanism of Adipose Tissue Expansion in the Rat Offspring of Obese Mothers Occurs in a Sex-Specific Manner

by Carlos A. Ibáñez, Gabriela Lira-León, Luis A. Reyes-Castro, Guadalupe L. Rodríguez-González, Consuelo Lomas-Soria, Alejandra Hernández-Rojas, Eyerahí Bravo-Flores, Juan Mario Solis-Paredes, Guadalupe Estrada-Gutierrez and Elena Zambrano

Nutrients 2023, 15(10), 2245; https://doi.org/10.3390/nu15102245 - 9 May 2023

Cited by 6 | Viewed by 2524

Abstract

We investigated whether excessive retroperitoneal adipose tissue (AT) expansion programmed by maternal obesity (MO) affects adipocyte size distribution and gene expression in relation to adipocyte proliferation and differentiation in male and female offspring (F1) from control (F1C) and obese (F1MO) mothers. Female Wistar rats (F0) ate a control or high-fat diet from weaning through pregnancy and lactation. F1 were weaned onto a control diet and euthanized at 110 postnatal days. Fat depots were weighed to estimate the total AT. Serum glucose, triglyceride, leptin, insulin, and the insulin resistance index (HOMA-IR) were determined. Adipocyte size and adipogenic gene expression were examined in retroperitoneal fat. Body weight, retroperitoneal AT and adipogenesis differed between male and female F1Cs. Retroperitoneal AT, glucose, triglyceride, insulin, HOMA-IR and leptin were higher in male and female F1MO vs. F1C. Small adipocytes were reduced in F1MO females and absent in F1MO males; large adipocytes were increased in F1MO males and females vs. F1C. Wnt, PI3K-Akt, and insulin signaling pathways in F1MO males and Egr2 in F1MO females were downregulated vs. F1C. MO induced metabolic dysfunction in F1 through different sex dimorphism mechanisms, including the decreased expression of pro-adipogenic genes and reduced insulin signaling in males and lipid mobilization-related genes in females. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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13 pages, 3546 KiB

Open AccessArticle

Adverse Maternal Environments Perturb Hepatic DNA Methylome and Transcriptome Prior to the Adult-Onset Non-Alcoholic Fatty Liver Disease in Mouse Offspring

by Qi Fu, Warren A. Cheung, Amber V. Majnik, Xingrao Ke, Tomi Pastinen and Robert H. Lane

Nutrients 2023, 15(9), 2167; https://doi.org/10.3390/nu15092167 - 30 Apr 2023

Cited by 3 | Viewed by 2063

Abstract

Exposure to adverse early-life environments (AME) increases the incidence of developing adult-onset non-alcoholic fatty liver disease (NAFLD). DNA methylation has been postulated to link AME and late-onset diseases. This study aimed to investigate whether and to what extent the hepatic DNA methylome was perturbed prior to the development of NAFLD in offspring exposed to AME in mice. AME constituted maternal Western diet and late-gestational stress. Male offspring livers at birth (d0) and weaning (d21) were used for evaluating the DNA methylome and transcriptome using the reduced representation of bisulfite sequencing and RNA-seq, respectively. We found AME caused 5879 differentially methylated regions (DMRs) and zero differentially expressed genes (DEGs) at d0 and 2970 and 123, respectively, at d21. The majority of the DMRs were distal to gene transcription start sites and did not correlate with DEGs. The DEGs at d21 were significantly enriched in GO biological processes characteristic of liver metabolic functions. In conclusion, AME drove changes in the hepatic DNA methylome, which preceded perturbations in the hepatic metabolic transcriptome, which preceded the onset of NAFLD. We speculate that subtle impacts on dynamic enhancers lead to long-range regulatory changes that manifest over time as gene network alternations and increase the incidence of NAFLD later in life. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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15 pages, 3212 KiB

Open AccessArticle

Developmental Programming-Aging Interactions Have Sex-Specific and Developmental Stage of Exposure Outcomes on Life Course Circulating Corticosterone and Dehydroepiandrosterone (DHEA) Concentrations in Rats Exposed to Maternal Protein-Restricted Diets

by Elena Zambrano, Luis A. Reyes-Castro, Guadalupe L. Rodríguez-González, Roberto Chavira, Consuelo Lomas-Soria, Kenneth G. Gerow and Peter W. Nathanielsz

Nutrients 2023, 15(5), 1239; https://doi.org/10.3390/nu15051239 - 1 Mar 2023

Cited by 2 | Viewed by 2266

Abstract

The steroids corticosterone and dehydroepiandrosterone (DHEA) perform multiple life course functions. Rodent life-course circulating corticosterone and DHEA trajectories are unknown. We studied life course basal corticosterone and DHEA in offspring of rats fed protein-restricted (10% protein, R) or control (20% protein, C), pregnancy diet first letter, and/or lactation second letter, producing four offspring groups—CC, RR, CR, and RC. We hypothesize that 1. maternal diet programs are sexually dimorphic, offspring life course steroid concentrations, and 2. an aging-related steroid will fall. Both changes differ with the plastic developmental period offspring experienced R, fetal life or postnatally, pre-weaning. Corticosterone was measured by radioimmunoassay and DHEA by ELISA. Steroid trajectories were evaluated by quadratic analysis. Female corticosterone was higher than male in all groups. Male and female corticosterone were highest in RR, peaked at 450 days, and fell thereafter. DHEA declined with aging in all-male groups. DHEA: corticosterone fell in three male groups but increased in all-female groups with age. In conclusion, life course and sexually dimorphic steroid developmental programming-aging interactions may explain differences in steroid studies at different life stages and between colonies experiencing different early-life programming. These data support our hypotheses of sex and programming influences and aging-related fall in rat life course serum steroids. Life course studies should address developmental programming-aging interactions. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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14 pages, 1282 KiB

Open AccessArticle

Maternal Pea Protein Intake Provides Sex-Specific Protection against Dyslipidemia in Offspring from Obese Pregnancies

by Todd C. Rideout, Gabriella A. Andreani, Jillian Pembroke, Divya Choudhary, Richard W. Browne, Saleh Mahmood and Mulchand S. Patel

Nutrients 2023, 15(4), 867; https://doi.org/10.3390/nu15040867 - 8 Feb 2023

Cited by 7 | Viewed by 2509

Abstract

Increased consumption of dietary pulse protein has been shown to assist in body weight regulation and improve a range of metabolic health outcomes. We investigated if the exchange of casein for yellow pea protein (YPPN) in an obese-inducing maternal diet throughout pregnancy and lactation offered protection against obesity and dyslipidemia in offspring. Sixty female Sprague Dawley rats were fed a low-calorie control diet (CON), a high-caloric obesity-inducing diet (with casein protein (CP), HC-CP), or an isocaloric/macronutrient-matched HC diet supplemented with YPPN isolate (HC-PPN) in pre-pregnancy, gestation, and lactation. Body weight (BW) and metabolic outcomes were assessed in male and female offspring at weaning and in adulthood after consuming the CON diet in the postnatal period. Consumption of the HC-PPN diet did not protect against maternal obesity but did improve reproductive success compared with the HC-CP group (72.7% versus 43.7%) and reduced total energy, fat, and protein in maternal milk. Male, but not female, offspring from mothers fed the HC-CP diet demonstrated hyperphagia, obesity, dyslipidemia, and hepatic triglyceride (TG) accumulation as adults compared with CON offspring. Isocaloric exchange of CP for YPPN in a high-calorie obese-inducing diet did not protect against obesity but did improve several aspects of lipid metabolism in adult male offspring including serum total cholesterol, LDL/VLDL cholesterol, triglycerides (TGs), and hepatic TG concentration. Our results suggest that the exchange of CP for YPPN in a maternal obese-inducing diet selectively protects male offspring from the malprogramming of lipid metabolism in adulthood. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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Review

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16 pages, 2157 KiB

Open AccessReview

Maternal Malnutrition and Elevated Disease Risk in Offspring

by Kent L. Thornburg and Amy M. Valent

Nutrients 2024, 16(16), 2614; https://doi.org/10.3390/nu16162614 - 8 Aug 2024

Cited by 3 | Viewed by 4364

Abstract

US populations have seen dramatic increases in the prevalence of chronic disease over the past three generations. Rapid increases in type 2 diabetes and obesity have occurred in all the states but have been particularly striking in the Deep South. These increases have contributed to decreases in life expectancy and to painful elevations in health care costs. The causes of worsening population health are complex and incompletely understood. However, there is strong evidence that vulnerability to chronic conditions is determined in early life. Most chronic diseases are developmentally driven. There are specific stressors experienced in early life that influence epigenetic and structural changes during development. These include malnutrition, severe levels of social stress, toxic chemicals, and low oxygen levels. Most US populations have experienced a decrease in the quality of the food they consume as industrial foods have replaced garden-grown foods. Thus, the consumption of too few nutrients before and during pregnancy and during lactation influences the growth of the placenta and fetal organs and their level of resilience when faced with stresses in postnatal life and particularly as adults. Animal studies have shown that the effects of poor nutrition can be passed on to future generations. The most powerful way that the current epidemics of obesity and insulin resistance can be reversed is by providing key nutrients to prospective mothers and those already pregnant. Full article

(This article belongs to the Special Issue Maternal Nutritional-Mediated Programming of Offspring Health and Disease)

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