scholarly journals Maternal Fructose Diet-Induced Developmental Programming

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3278
Author(s):  
Michael D. Thompson ◽  
Brian J. DeBosch
Keyword(s):  
Metabolic Syndrome ◽  
Chronic Disease ◽  
Animal Models ◽  
Indirect Effects ◽  
Developmental Programming ◽  
Developmental Origins ◽  
Adult Disease ◽  
Basic Tenet ◽  
Pregnancy And Lactation ◽  
Exposure During Pregnancy

Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.

scholarly journals The Good, the Bad, and the Ugly of Pregnancy Nutrients and Developmental Programming of Adult Disease

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 894 ◽  
Author(s):  
Hsu ◽  
Tain
Keyword(s):  
Animal Models ◽  
Maternal Nutrition ◽  
Decisive Role ◽  
Developmental Programming ◽  
Adult Onset ◽  
Epidemiological Evidence ◽  
Nutritional Interventions ◽  
Adult Disease ◽  
Nutritional Programming ◽  
The Common

Maternal nutrition plays a decisive role in developmental programming of many non-communicable diseases (NCDs). A variety of nutritional insults during gestation can cause programming and contribute to the development of adult-onset diseases. Nutritional interventions during pregnancy may serve as reprogramming strategies to reverse programming processes and prevent NCDs. In this review, firstly we summarize epidemiological evidence for nutritional programming of human disease. It will also discuss evidence from animal models, for the common mechanisms underlying nutritional programming, and potential nutritional interventions used as reprogramming strategies.

scholarly journals Developmental Programming of the Metabolic Syndrome: Can We Reprogram with Resveratrol?

2018 ◽  
Vol 19 (9) ◽  
pp. 2584 ◽  
Author(s):  
You-Lin Tain ◽  
Chien-Ning Hsu
Keyword(s):  
Metabolic Syndrome ◽  
Early Life ◽  
Wide Spectrum ◽  
Molecular Targets ◽  
Developmental Programming ◽  
Developmental Origins ◽  
Polyphenolic Compound ◽  
Beneficial Effects ◽  
The Metabolic Syndrome ◽  
Health And Disease

Metabolic syndrome (MetS) is a mounting epidemic worldwide. MetS can start in early life, in a microenvironment that is now known as the developmental origins of health and disease (DOHaD). The concept of DOHaD also offers opportunities for reprogramming strategies that aim to reverse programming processes in early life. Resveratrol, a polyphenolic compound has a wide spectrum of beneficial effects on human health. In this review, we first summarize the epidemiological and experimental evidence supporting the developmental programming of MetS. This review also presents an overview of the evidence linking different molecular targets of resveratrol to developmental programming of MetS-related disorders. This will be followed by studies documenting resveratrol as a reprogramming agent to protect against MetS-related disorders. Further clinical studies are required in order to bridge the gap between animal models and clinical trials in order to establish the effective dose and therapeutic duration for resveratrol as a reprogramming therapy on MetS disorders from developmental origins.

scholarly journals Adverse Impact of Environmental Chemicals on Developmental Origins of Kidney Disease and Hypertension

2021 ◽  
Vol 12 ◽  
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Kidney Disease ◽  
Animal Studies ◽  
Kidney Development ◽  
Renin Angiotensin System ◽  
Chemical Exposure ◽  
Environmental Chemicals ◽  
Developmental Origins ◽  
Environmental Chemical ◽  
Pregnancy And Lactation ◽  
Exposure During Pregnancy

Chronic kidney disease (CKD) and hypertension are becoming a global health challenge, despite developments in pharmacotherapy. Both diseases can begin in early life by so-called “developmental origins of health and disease” (DOHaD). Environmental chemical exposure during pregnancy can affect kidney development, resulting in renal programming. Here, we focus on environmental chemicals that pregnant mothers are likely to be exposed, including dioxins, bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), polycyclic aromatic hydrocarbons (PAH), heavy metals, and air pollution. We summarize current human evidence and animal models that supports the link between prenatal exposure to environmental chemicals and developmental origins of kidney disease and hypertension, with an emphasis on common mechanisms. These include oxidative stress, renin-angiotensin system, reduced nephron numbers, and aryl hydrocarbon receptor signaling pathway. Urgent action is required to identify toxic chemicals in the environment, avoid harmful chemicals exposure during pregnancy and lactation, and continue to discover other potentially harmful chemicals. Innovation is also needed to identify kidney disease and hypertension in the earliest stage, as well as translating effective reprogramming interventions from animal studies into clinical practice. Toward DOHaD approach, prohibiting toxic chemical exposure and better understanding of underlying mechanisms, we have the potential to reduce global burden of kidney disease and hypertension.

Developmental programming of a reduced nephron endowment: more than just a baby's birth weight

2009 ◽  
Vol 296 (1) ◽  
pp. F1-F9 ◽  
Author(s):  
Karen M. Moritz ◽  
Reetu R. Singh ◽  
Megan E. Probyn ◽  
Kate M. Denton
Keyword(s):  
Birth Weight ◽  
Animal Models ◽  
Low Birth Weight ◽  
Strong Association ◽  
Underlying Mechanism ◽  
Developmental Programming ◽  
Adult Onset ◽  
Adult Disease ◽  
Nephron Endowment ◽  
Short Period

The risk of developing many adult-onset diseases, including hypertension, type 2 diabetes, and renal disease, is increased in low-birth-weight individuals. A potential underlying mechanism contributing to the onset of these diseases is the formation of a low nephron endowment during development. Evidence from the human, as well as many experimental animal models, has shown a strong association between low birth weight and a reduced nephron endowment. However, other animal models, particularly those in which the mother is exposed to elevated glucocorticoids for a short period, have shown a 20–40% reduction in nephron endowment without discernible changes in the birth weight of offspring. Such findings emphasize that a low birth weight is one, but certainly not the only, predictor of nephron endowment and suggests reduced nephron endowment and risk of developing adult-onset disease, even among normal-birth-weight individuals. Recognition of the dissociation between birth weight and nephron endowment is important for future studies aimed at elucidating the role of a reduced nephron endowment in the developmental programming of adult disease.

scholarly journals Developmental origins of health and disease: experimental and human evidence of fetal programming for metabolic syndrome

2011 ◽  
Vol 26 (7) ◽  
pp. 405-419 ◽  
Author(s):  
M L de Gusmão Correia ◽  
A M Volpato ◽  
M B Águila ◽  
C A Mandarim-de-Lacerda
Keyword(s):  
Metabolic Syndrome ◽  
Fetal Programming ◽  
Developmental Origins ◽  
Health And Disease

Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

2007 ◽  
Vol 292 (5) ◽  
pp. E1318-E1324 ◽  
Author(s):  
Lucie Šedová ◽  
Ondřej Šeda ◽  
Ludmila Kazdová ◽  
Blanka Chylíková ◽  
Pavel Hamet ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Genetic Model ◽  
Metabolic Response ◽  
Maternal Diet ◽  
Later Life ◽  
Standard Diet ◽  
Lipoprotein Subfractions ◽  
Sucrose Feeding ◽  
Pregnancy And Lactation

The importance of early environment, including maternal diet during pregnancy, is suspected to play a major role in pathogenesis of metabolic syndrome and related conditions. One of the proposed mechanisms is a mismatch between the prenatal and postnatal environments, leading to misprogramming of the metabolic and signaling pathways of the developing fetus. We assessed whether the exposure to high-sucrose diet (HSD) alleviates the detrimental effects of sucrose feeding in later life (predictive adaptive hypothesis) in a highly inbred model of metabolic syndrome, the PD/Cub rat. Rat dams were continuously fed either standard or HSD (70% calories as sucrose) starting 1 wk before breeding, throughout pregnancy, at birth, and until weaning of the offspring. After weaning, all male offspring were fed HSD until the age of 20 wk, when detailed metabolic and morphometric profiles were ascertained. The early life exposure to a sucrose-rich diet resulted in distinct responses to longtime postnatal HSD feeding. Offspring of the sucrose-fed mothers displayed higher adiposity and substantial increases in triglyceride liver content together with unfavorable distribution of cholesterol into lipoprotein subfractions. On the other hand, their adiponectin concentrations were significantly higher, and insulin sensitivity of skeletal muscle was enhanced compared with the offspring of standard diet-fed mothers. Triglycerides, free fatty acids, overall glucose tolerance, and the insulin sensitivity of adipose tissue were comparable in both groups. In the genetically identical animals, maternal HSD feeding elicited a variety of subtle effects but did not lead to predictive adaptive protection from most HSD-induced metabolic derangements.

Epigenetic Mechanisms in the Developmental Origins of Adult Disease

2011 ◽  
pp. 187-204 ◽  
Author(s):  
Keith M. Godfrey ◽  
Karen A. Lillycrop ◽  
Mark A. Hanson ◽  
Graham C. Burdge
Keyword(s):  
Epigenetic Mechanisms ◽  
Developmental Origins ◽  
Adult Disease

scholarly journals TREATMENT OF PATIENTS WITH CHRONIC DISEASE KIDNEYS OF THE PRESENCE OF LESIONS GASTRODUODENAL AREAS AND CHRONIC PYLONEPHRITIS IN COMBINATION WITH METABOLIC SYNDROME

2018 ◽  
Vol 64 ◽  
Author(s):  
O.V. Demchuk ◽  
D.A. Slobodian ◽  
А.A. Piddubna ◽  
V.V. Vivsiannyk ◽  
M.A. Vintonyak
Keyword(s):  
Metabolic Syndrome ◽  
Chronic Kidney Disease ◽  
Chronic Disease ◽  
Kidney Disease ◽  
Economic Problem ◽  
Chronic Pyelonephritis

The article deals with literature data on the theory of progression of patients with chronic kidney disease with the presence of lesions of the gastroduodenal region and chronic pyelonephritis in association with metabolic syndrome. The methods of treating these diseases are presented, because this, apart from actually clinical, also has a socio-economic problem.

scholarly journals Homage to the ‘H’ in developmental origins of health and disease

2016 ◽  
Vol 8 (1) ◽  
pp. 8-29 ◽  
Author(s):  
C. S. Rosenfeld
Keyword(s):  
Female Offspring ◽  
Postnatal Period ◽  
Environmental Chemicals ◽  
Primary Concern ◽  
Developmental Origins ◽  
Adult Health ◽  
Fetal Origins ◽  
Adult Disease ◽  
Remediation Strategies ◽  
Health And Disease

Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.

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