scholarly journals Early-Life Origins of Metabolic Syndrome: Mechanisms and Preventive Aspects

2021 ◽  
Vol 22 (21) ◽  
pp. 11872
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Wei-Hsuan Hsu ◽  
You-Lin Tain

One of the leading global public-health burdens is metabolic syndrome (MetS), despite the many advances in pharmacotherapies. MetS, now known as “developmental origins of health and disease” (DOHaD), can have its origins in early life. Offspring MetS can be programmed by various adverse early-life conditions, such as nutrition imbalance, maternal conditions or diseases, maternal chemical exposure, and medication use. Conversely, early interventions have shown potential to revoke programming processes to prevent MetS of developmental origins, namely reprogramming. In this review, we summarize what is currently known about adverse environmental insults implicated in MetS of developmental origins, including the fundamental underlying mechanisms. We also describe animal models that have been developed to study the developmental programming of MetS. This review extends previous research reviews by addressing implementation of reprogramming strategies to prevent the programming of MetS. These mechanism-targeted strategies include antioxidants, melatonin, resveratrol, probiotics/prebiotics, and amino acids. Much work remains to be accomplished to determine the insults that could induce MetS, to identify the mechanisms behind MetS programming, and to develop potential reprogramming strategies for clinical translation.

2018 ◽  
Vol 243 (10) ◽  
pp. 836-842 ◽  
Author(s):  
Jia Zheng ◽  
Qianyun Feng ◽  
Sheng Zheng ◽  
Xinhua Xiao

Osteoporosis, the most frequent metabolic disorder of bone, is a complex disease with a multifactorial origin that is influenced by genes and environments. However, the pathogenesis of osteoporosis has not been fully elucidated. The theory of “Developmental Origins of Health and Disease” indicates that early life environment exposure determines the risks of cardiometabolic diseases in adulthood. However, investigations into the effects of maternal nutrition and nutrition exposure during early life on the development of osteoporosis are limited. Recently, emerging evidence has strongly suggested that maternal nutrition has long-term influences on bone metabolism in offspring, and epigenetic modifications maybe the underlying mechanisms of this process. This review aimed to address maternal nutrition and its implications for the developmental origins of osteoporosis in offspring. It is novel in providing a theoretical basis for the early prevention of osteoporosis. Impact statement Our review aimed to address maternal nutrition and its implications for the developmental origins of osteoporosis in offspring, that can novelly provide a theoretical basis for the early prevention of osteoporosis.


2018 ◽  
Vol 19 (9) ◽  
pp. 2584 ◽  
Author(s):  
You-Lin Tain ◽  
Chien-Ning Hsu

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.


Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 623
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain

Increasing evidence suggests that fetal programming through environmental exposure during a critical window of early life leads to long-term detrimental outcomes, by so-called developmental origins of health and disease (DOHaD). Hypertension can originate in early life. Animal models are essential for providing convincing evidence of a causal relationship between diverse early-life insults and the developmental programming of hypertension in later life. These insults include nutritional imbalances, maternal illnesses, exposure to environmental chemicals, and medication use. In addition to reviewing the various insults that contribute to hypertension of developmental origins, this review focuses on the benefits of animal models in addressing the underlying mechanisms by which early-life interventions can reprogram disease processes and prevent the development of hypertension. Our understanding of hypertension of developmental origins has been enhanced by each of these animal models, narrowing the knowledge gap between animal models and future clinical translation.


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

Author(s):  
Fiona Lynch ◽  
Sharon Lewis ◽  
Ivan Macciocca ◽  
Jeffrey M. Craig

Abstract Epigenetics is likely to play a role in the mediation of the effects of genes and environment in risk for many non-communicable diseases (NCDs). The Developmental Origins of Health and Disease (DOHaD) theory presents unique opportunities regarding the possibility of early life interventions to alter the epigenetic makeup of an individual, thereby modifying their risk for a variety of NCDs. While it is important to determine how we can lower the risk of these NCDs, it is equally important to understand how the public’s knowledge and opinion of DOHaD and epigenetic concepts may influence their willingness to undertake such interventions for themselves and their children. In this review, we provide an overview of epigenetics, DOHaD, NCDs, and the links between them. We explore the issues surrounding using epigenetics to identify those at increased risk of NCDs, including the concept of predictive testing of children. We also outline what is currently understood about the public’s understanding and opinion of epigenetics, DOHaD, and their relation to NCDs. In doing so, we demonstrate that it is essential that future research explores the public’s awareness and understanding of epigenetics and epigenetic concepts. This will provide much-needed information which will prepare health professionals for the introduction of epigenetic testing into future healthcare.


2017 ◽  
Vol 9 (3) ◽  
pp. 266-269 ◽  
Author(s):  
K. Suzuki

Since its debut in a ground-breaking report by Barker and Osmond in 1986, the concept of the Developmental Origins of Health and Disease (DOHaD) has been further developed in several aspects. Its methodology and conclusions relating to proposed origins and outcomes of early life events have been developing and spreading internationally. Indeed, the DOHaD concept now seems to have influenced many fields of research. This article aims to briefly review why the DOHaD concept is important in biomedical science, how it has developed, is currently developing, and how it should develop in future.


2016 ◽  
Vol 7 (5) ◽  
pp. 433-439 ◽  
Author(s):  
S. L. Prescott ◽  
K. Allen ◽  
K. Armstrong ◽  
C. Collins ◽  
H. Dickinson ◽  
...  

The evidence underpinning the developmental origins of health and disease (DOHaD) is overwhelming. As the emphasis shifts more towards interventions and the translational strategies for disease prevention, it is important to capitalize on collaboration and knowledge sharing to maximize opportunities for discovery and replication. DOHaD meetings are facilitating this interaction. However, strategies to perpetuate focussed discussions and collaborations around and between conferences are more likely to facilitate the development of DOHaD research. For this reason, the DOHaD Society of Australia and New Zealand (DOHaD ANZ) has initiated themed Working Groups, which convened at the 2014–2015 conferences. This report introduces the DOHaD ANZ Working Groups and summarizes their plans and activities. One of the first Working Groups to form was the ActEarly birth cohort group, which is moving towards more translational goals. Reflecting growing emphasis on the impact of early life biodiversity – even before birth – we also have a Working Group titled Infection, inflammation and the microbiome. We have several Working Groups exploring other major non-cancerous disease outcomes over the lifespan, including Brain, behaviour and development and Obesity, cardiovascular and metabolic health. The Epigenetics and Animal Models Working Groups cut across all these areas and seeks to ensure interaction between researchers. Finally, we have a group focussed on ‘Translation, policy and communication’ which focusses on how we can best take the evidence we produce into the community to effect change. By coordinating and perpetuating DOHaD discussions in this way we aim to enhance DOHaD research in our region.


2018 ◽  
Vol Volume 11 ◽  
pp. 543-551
Author(s):  
Haroldo da Silva Ferreira ◽  
Antonio Fernando Silva Xavier Junior ◽  
Monica Lopes Assunção ◽  
Tainá Cardoso Caminha Uchôa ◽  
Abel Barbosa Lira-Neto ◽  
...  

2014 ◽  
Vol 38 (2) ◽  
pp. 170-175 ◽  
Author(s):  
Jamie R. Mitchell ◽  
Jiun-Jr Wang

Dr. Carl Wiggers' careful observations have provided a meaningful resource for students to learn how the heart works. Throughout the many years from his initial reports, the Wiggers diagram has been used, in various degrees of complexity, as a fundamental tool for cardiovascular instruction. Often, the various electrical and mechanical plots are the novice learner's first exposure to simulated data. As the various temporal relationships throughout a heartbeat could simply be memorized, the challenge for the cardiovascular instructor is to engage the learner so the underlying mechanisms governing the changing electrical and mechanical events are truly understood. Based on experience, we suggest some additions to the Wiggers diagram that are not commonly used to enhance cardiovascular pedagogy. For example, these additions could be, but are not limited to, introducing the concept of energy waves and their role in influencing pressure and flow in health and disease. Also, integrating concepts of exercise physiology, and the differences in cardiac function and hemodynamics between an elite athlete and normal subject, can have a profound impact on student engagement. In describing the relationship between electrical and mechanical events, the instructor may find the introduction of premature ventricular contractions as a useful tool to further understanding of this important principle. It is our hope that these examples can aid cardiovascular instructors to engage their learners and promote fundamental understanding at the expense of simple memorization.


2018 ◽  
Vol 315 (1) ◽  
pp. E15-E28 ◽  
Author(s):  
Amita Bansal ◽  
Rebecca A. Simmons

The incidence of metabolic disorders like type 2 diabetes (T2D) and obesity continue to increase. Although it is evident that the increasing incidence of diabetes confers a global societal and economic burden, the mechanisms responsible for the increased incidence of T2D are not well understood. Extensive efforts to understand the association of early-life perturbations with later onset of metabolic diseases, the founding principle of developmental origins of health and disease, have been crucial in determining the mechanisms that may be driving the pathogenesis of T2D. As the programming of the epigenome occurs during critical periods of development, it has emerged as a potential molecular mechanism that could occur early in life and impact metabolic health decades later. In this review, we critically evaluate human and animal studies that illustrated an association of epigenetic processes with development of T2D as well as intervention strategies that have been employed to reverse the perturbed epigenetic modification or reprogram the naturally occurring epigenetic marks to favor improved metabolic outcome. We highlight that although our understanding of epigenetics and its contribution toward developmental origins of T2D continues to grow, whether epigenetics is a cause, consequence, or merely a correlation remains debatable due to the many limitations/challenges of the existing epigenetic studies. Finally, we discuss the potential of establishing collaborative research efforts between different disciplines, including physiology, epigenetics, and bioinformatics, to help advance the developmental origins field with great potential for understanding the pathogenesis of T2D and developing preventive strategies for T2D.


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