scholarly journals Editorial: Developmental Programming of Metabolic Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Sarah J. Glastras ◽  
Damaskini Valvi ◽  
Amita Bansal
Keyword(s):  
Metabolic Diseases ◽  
Developmental Programming

Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences

2014 ◽  
Vol 18 (2) ◽  
Author(s):  
Analia Lorena Tomat ◽  
Francisco Javier Salazar
Keyword(s):  
Metabolic Diseases ◽  
Current Knowledge ◽  
Adult Life ◽  
Developmental Programming ◽  
Renal Diseases ◽  
Future Studies ◽  
Functional Changes ◽  
Regulatory Systems ◽  
Increased Risk ◽  
Renal Changes

AbstractA substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may “program” susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes.The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.

scholarly journals Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress

2020 ◽  
Vol 77 (23) ◽  
pp. 4861-4898
Author(s):  
Efthimia R. Christoforou ◽  
Amanda N. Sferruzzi-Perri
Keyword(s):  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Developmental Programming ◽  
In Utero ◽  
Postnatal Life ◽  
Molecular Pathways ◽  
Epigenetic Mechanisms ◽  
Metabolic Dysfunction ◽  
Rodent Models ◽  
Human Lifespan

Abstract The results of different human epidemiological datasets provided the impetus to introduce the now commonly accepted theory coined as ‘developmental programming’, whereby the presence of a stressor during gestation predisposes the growing fetus to develop diseases, such as metabolic dysfunction in later postnatal life. However, in a clinical setting, human lifespan and inaccessibility to tissue for analysis are major limitations to study the molecular mechanisms governing developmental programming. Subsequently, studies using animal models have proved indispensable to the identification of key molecular pathways and epigenetic mechanisms that are dysregulated in metabolic organs of the fetus and adult programmed due to an adverse gestational environment. Rodents such as mice and rats are the most used experimental animals in the study of developmental programming. This review summarises the molecular pathways and epigenetic mechanisms influencing alterations in metabolic tissues of rodent offspring exposed to in utero stress and subsequently programmed for metabolic dysfunction. By comparing molecular mechanisms in a variety of rodent models of in utero stress, we hope to summarise common themes and pathways governing later metabolic dysfunction in the offspring whilst identifying reasons for incongruencies between models so to inform future work. With the continued use and refinement of such models of developmental programming, the scientific community may gain the knowledge required for the targeted treatment of metabolic diseases that have intrauterine origins.

scholarly journals Maternal Exposure to the Holocaust and Health Complaints in Offspring

2011 ◽  
Vol 30 (2-3) ◽  
pp. 133-139 ◽  
Author(s):  
Janine D. Flory ◽  
Linda M. Bierer ◽  
Rachel Yehuda
Keyword(s):  
Metabolic Diseases ◽  
Holocaust Survivors ◽  
Developmental Programming ◽  
Maternal Exposure ◽  
Developmental Trajectory ◽  
Lipid Disorders ◽  
Parental Exposure ◽  
The Holocaust ◽  
The Relationship ◽  
Early Developmental

Although the link between chronic stress and the development of cardiovascular and metabolic diseases of adulthood has been known for some time, there is growing recognition that early environmental influences may result in developmental programming via epigenetic mechanisms, thereby affecting the developmental trajectory of disease progression. Previous studies support the idea that offspring of Holocaust survivors may have been subjected to early developmental programming. We evaluated the relationship between parental exposure to the Holocaust and self-reported health ratings and disorders made by their adult offspring (i.e., second generation Holocaust survivors). A total of 137 subjects were evaluated. Regression analyses demonstrated that maternal but not paternal exposure to the Holocaust was related to poorer subjective impressions of emotional and physical health. This relationship was diminished when the offspring’s own level of trait anxiety was considered. Offspring with maternal, but not paternal, Holocaust exposure also reported greater use of psychotropic and other medications, including medications for the treatment of hypertension and lipid disorders. The mechanism linking these health outcomes and maternal exposure deserves further investigation, including the possibility that fetal or early developmental programming is involved.

scholarly journals Developmental programming of metabolic diseases – a review of studies on experimental animal models

2014 ◽  
Vol 68 ◽  
pp. 899-911 ◽  
Author(s):  
Iwona Piotrowska ◽  
Paulina Zgódka ◽  
Marta Milewska ◽  
Maciej Błaszczyk ◽  
Katarzyna Grzelkowska-Kowalczyk
Keyword(s):  
Animal Models ◽  
Experimental Animal ◽  
Metabolic Diseases ◽  
Developmental Programming ◽  
Experimental Animal Models

scholarly journals Epigenetic Programming of Adipose Tissue in the Progeny of Obese Dams

2019 ◽  
Vol 20 (6) ◽  
pp. 428-437 ◽  
Author(s):  
Simon Lecoutre ◽  
Kelvin H.M. Kwok ◽  
Paul Petrus ◽  
Mélanie Lambert ◽  
Christophe Breton
Keyword(s):  
Adipose Tissue ◽  
Maternal Obesity ◽  
Metabolic Diseases ◽  
Tissue Expansion ◽  
Developmental Programming ◽  
Epigenetic Mechanisms ◽  
Epigenetic Programming ◽  
Important Player ◽  
Health And Disease ◽  
Adipose Tissue Remodeling

According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and the resulting accelerated growth in neonates predispose offspring to obesity and associated metabolic diseases that may persist across generations. In this context, the adipose tissue has emerged as an important player due to its involvement in metabolic health, and its high potential for plasticity and adaptation to environmental cues. Recent years have seen a growing interest in how maternal obesity induces long-lasting adipose tissue remodeling in offspring and how these modifications could be transmitted to subsequent generations in an inter- or transgenerational manner. In particular, epigenetic mechanisms are thought to be key players in the developmental programming of adipose tissue, which may partially mediate parts of the transgenerational inheritance of obesity. This review presents data supporting the role of maternal obesity in the developmental programming of adipose tissue through epigenetic mechanisms. Inter- and transgenerational effects on adipose tissue expansion are also discussed in this review.

scholarly journals From Mice to Men: research models of developmental programming

2012 ◽  
Vol 4 (1) ◽  
pp. 3-9 ◽  
Author(s):  
C. Rabadán-Diehl ◽  
P. Nathanielsz
Keyword(s):  
Metabolic Diseases ◽  
Time Window ◽  
Developmental Time ◽  
High Energy ◽  
Developmental Programming ◽  
Therapeutic Interventions ◽  
Diagnostic Tools ◽  
Systems Physiology ◽  
Comparative Systems ◽  
Fetus And Neonate

Developmental programming can be defined as a response to a specific challenge to the mammalian organism during a critical developmental time window that alters the trajectory of development with persistent effects on offspring phenotype and predisposition to future illness. We focus on the need for studies in relevant, well-characterized animal models in the context of recent research discoveries on the challenges, mechanisms and outcomes of developmental programming. We discuss commonalities and differences in general principles of developmental programming as they apply to several species, including humans. The consequences of these differences are discussed. Obesity, metabolic disorders and cardiovascular diseases are associated with the highest percentage of morbidity and mortality worldwide. Although many of the causes are associated with lifestyle, high-energy diets and lack of physical activity, recent evidence has linked developmental programming to the epidemic of metabolic diseases. A better understanding of comparative systems physiology of mother, fetus and neonate using information provided by rapid advances in molecular biology has the potential to improve the lifetime health of future generations by providing better women's health, diagnostic tools and preventative and therapeutic interventions in individuals exposed during their development to programming influences.

Mitochondria microcrystals deposition in some inherited diseases of lipid metabolism.

1978 ◽  
Vol 36 (2) ◽  
pp. 256-257
Author(s):  
S. Laoussadi ◽  
A. Kahan ◽  
G. Aubouy ◽  
F. Delbarre
Keyword(s):  
Synovial Tissue ◽  
Storage Disease ◽  
Metabolic Diseases ◽  
Uranyl Acetate ◽  
List Type ◽  
Type Ii ◽  
Type Number ◽  
Lipid Storage Disease ◽  
Thin Sections ◽  
Mean Size

Several patients with Fabry's, Gaucher's diseases and hyperlipoproteinemia type II and with arthropatic manifestations were observed.As no histological explanation for these symptoms was available,an ultrastructural study of synovial tissue was done to establish an anatomoclinical relation.Material and Methods :synovial membrane samples were obtained by needle biopsies of the knee from three patients with arthropatic manifestations of each disease.They were fixed in 5% glutaraldehyde, postfixed in 1% osmium tetraoxyde and embedded in Epon 812. Thin sections coloured by uranyl acetate and lead citrate were observed with an Elmiskop I Siemens electron microscope.Two important phenomena were observed in synovial tissue:Specific patterns of each lipid storage disease,which are now well known.In all the three metabolic diseases, hydroxyapatite-like crystals were found. They are characterized by their intramitochondrial localization, without any relation with cristae,an anarchic disposition and a mean size of 550 A.Crystals may be found also free in the cytoplasm of synoviocytes Some micrographs suggest an evolution in four steps :a. mitochondria with only a few microcrystalsb. mitochondria stuffed with these structuresc. disruption of mitochondria membranesd. microcrystals appear free in the cytoplasm

Investigation analysis of metabolic diseases-associated indexes in Chongqing children

2010 ◽  
Vol 34 (8) ◽  
pp. S70-S70
Author(s):  
Xiaoping WEI ◽  
Lan LIU ◽  
Jie CHEN ◽  
Youxue LIU ◽  
Yang BI ◽  
...  
Keyword(s):  
Metabolic Diseases

Flavonoids in adipose tissue inflammation and atherosclerosis: one arrow, two targets

2020 ◽  
Vol 134 (12) ◽  
pp. 1403-1432 ◽  
Author(s):  
Manal Muin Fardoun ◽  
Dina Maaliki ◽  
Nabil Halabi ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fruits And Vegetables ◽  
Metabolic Diseases ◽  
Therapeutic Agents ◽  
Adipose Tissue Inflammation ◽  
Cellular Mechanisms ◽  
Tissue Inflammation ◽  
Cholesterol Levels ◽  
Naturally Occurring ◽  
Pro Inflammatory Cytokines

Abstract Flavonoids are polyphenolic compounds naturally occurring in fruits and vegetables, in addition to beverages such as tea and coffee. Flavonoids are emerging as potent therapeutic agents for cardiovascular as well as metabolic diseases. Several studies corroborated an inverse relationship between flavonoid consumption and cardiovascular disease (CVD) or adipose tissue inflammation (ATI). Flavonoids exert their anti-atherogenic effects by increasing nitric oxide (NO), reducing reactive oxygen species (ROS), and decreasing pro-inflammatory cytokines. In addition, flavonoids alleviate ATI by decreasing triglyceride and cholesterol levels, as well as by attenuating inflammatory mediators. Furthermore, flavonoids inhibit synthesis of fatty acids and promote their oxidation. In this review, we discuss the effect of the main classes of flavonoids, namely flavones, flavonols, flavanols, flavanones, anthocyanins, and isoflavones, on atherosclerosis and ATI. In addition, we dissect the underlying molecular and cellular mechanisms of action for these flavonoids. We conclude by supporting the potential benefit for flavonoids in the management or treatment of CVD; yet, we call for more robust clinical studies for safety and pharmacokinetic values.

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.

Sign in / Sign up

Export Citation Format

Share Document