scholarly journals The role of adipokines in developmental programming: evidence from animal models

2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers
Keyword(s):  
Adipose Tissue ◽  
Animal Models ◽  
Maternal Nutrition ◽  
Adult Life ◽  
Empirical Support ◽  
Later Life ◽  
Developmental Programming ◽  
Critical Periods ◽  
Reproductive Disorders ◽  
Wide Range

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.

scholarly journals Prenatal programming of postnatal obesity: fetal nutrition and the regulation of leptin synthesis and secretion before birth

2004 ◽  
Vol 63 (3) ◽  
pp. 405-412 ◽  
Author(s):  
I. C. McMillen ◽  
B. S. Muhlhausler ◽  
J. A. Duffield ◽  
B. S. J. Yuen
Keyword(s):  
Adipose Tissue ◽  
Fat Mass ◽  
Maternal Nutrition ◽  
Adult Life ◽  
Later Life ◽  
Late Gestation ◽  
Relative Mass ◽  
Moderate Increase ◽  
Fetal Life ◽  
Fat Depots

Exposure to either an increased or decreased level of intrauterine nutrition can result in an increase in adiposity and in circulating leptin concentrations in later life. In animals such as the sheep and pig in which fat is deposited before birth, leptin is synthesised in fetal adipose tissue and is present in the fetal circulation throughout late gestation. In the sheep a moderate increase or decrease in the level of maternal nutrition does not alter fetal plasma leptin concentrations, but there is evidence that chronic fetal hyperglycaemia and hyperinsulinaemia increase fetal fat mass and leptin synthesis within fetal fat depots. Importantly, there is a positive relationship between the relative mass of the ‘unilocular’ component of fetal perirenal and interscapular adipose tissue and circulating fetal leptin concentrations in the sheep. Thus, as in the neonate and adult, circulating leptin concentrations may be a signal of fat mass in fetal life. There is also evidence that leptin can act to regulate the lipid storage, leptin synthetic capacity and potential thermogenic functions of fat before birth. Thus, leptin may act as a signal of energy supply and have a ‘lipostatic’ role before birth. Future studies are clearly required to determine whether the intrauterine and early postnatal nutrient environment programme the endocrine feedback loop between adipose tissue and the central and peripheral neuroendocrine systems that regulate energy balance, resulting in an enhanced risk of obesity in adult life.

scholarly journals Maternal Obesity, Inflammation, and Developmental Programming

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Stephanie A. Segovia ◽  
Mark H. Vickers ◽  
Clint Gray ◽  
Clare M. Reynolds
Keyword(s):  
Maternal Obesity ◽  
Later Life ◽  
Developmental Programming ◽  
Health Concern ◽  
Low Grade ◽  
Critical Periods ◽  
Omega 3 ◽  
Child Bearing ◽  
Prevalence Of Obesity ◽  
Low Grade Inflammation

The prevalence of obesity, especially in women of child-bearing age, is a global health concern. In addition to increasing the immediate risk of gestational complications, there is accumulating evidence that maternal obesity also has long-term consequences for the offspring. The concept of developmental programming describes the process in which an environmental stimulus, including altered nutrition, during critical periods of development can program alterations in organogenesis, tissue development, and metabolism, predisposing offspring to obesity and metabolic and cardiovascular disorders in later life. Although the mechanisms underpinning programming of metabolic disorders remain poorly defined, it has become increasingly clear that low-grade inflammation is associated with obesity and its comorbidities. This review will discuss maternal metainflammation as a mediator of programming in insulin sensitive tissues in offspring. Use of nutritional anti-inflammatories in pregnancy including omega 3 fatty acids, resveratrol, curcumin, and taurine may provide beneficial intervention strategies to ameliorate maternal obesity-induced programming.

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 Association of early- and adult-life socioeconomic circumstances with muscle strength in older age

2018 ◽  
Vol 47 (3) ◽  
pp. 398-407 ◽  
Author(s):  
Boris Cheval ◽  
Matthieu P Boisgontier ◽  
Dan Orsholits ◽  
Stefan Sieber ◽  
Idris Guessous ◽  
...  
Keyword(s):  
Muscle Strength ◽  
Early Life ◽  
Adult Life ◽  
Health Behaviours ◽  
Later Life ◽  
Older Age ◽  
Sensitive Period ◽  
Future Health ◽  
Mixed Effect ◽  
Wide Range

Abstract Background socioeconomic circumstances (SEC) during a person’s lifespan influence a wide range of health outcomes. However, solid evidence of the association of early- and adult-life SEC with health trajectories in ageing is still lacking. This study assessed whether early-life SEC are associated with muscle strength in later life—a biomarker of health—and whether this relationship is caused by adult-life SEC and health behaviours. Methods we used data from the Survey of Health Ageing and Retirement in Europe, a 12-year population-based cohort study with repeated measurement in six waves (2004–15) and retrospective collection of life-course data. Participants’ grip strength was assessed by using a handheld dynamometer. Confounder-adjusted logistic mixed-effect models were used to examine the associations of early- and adult-life SEC with the risk of low muscle strength (LMS) in older age. Results a total of 24,179 participants (96,375 observations) aged 50–96 living in 14 European countries were included in the analyses. Risk of LMS was increased with disadvantaged relative to advantaged early-life SEC. The association between risk of LMS and disadvantaged early-life SEC gradually decreased when adjusting for adult-life SEC for both sexes and with unhealthy behaviours for women. After adjusting for these factors, all associations between risk of LMS and early-life SEC remained significant for women. Conclusion early-life SEC are associated with muscle strength after adjusting for adult-life SEC and behavioural lifestyle factors, especially in women, which suggests that early life may represent a sensitive period for future health.

130 Early Developmental Exposure to Stress and Programming of Lifelong Gut and Immune Function

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 69-69
Author(s):  
Adam J Moeser
Keyword(s):  
Life Stress ◽  
Disease Risk ◽  
Early Life Stress ◽  
Later Life ◽  
Developmental Programming ◽  
Postnatal Life ◽  
Critical Periods ◽  
Organ Systems ◽  
High Level ◽  
The Impact

Abstract Prenatal and early postnatal life represents critical periods of development across species for many organ systems including immune, nervous, reproductive, and gastrointestinal systems. A high level of plasticity exists during these periods, and thus maternal and environmental cues including stress, immune stimulation, and nutrition, can alter the normal developmental programming of the fetus and neonate and impact the trajectory for disease risk and productivity across the lifespan. This presentation will focus on the impact of and biological mechanisms by which prenatal and early postnatal stressors, including psychological immune and nutritional stressors, alter the normal developmental programming of the immune, gastrointestinal, and neuroendocrine stress axes in the offspring and how this may link to increased disease risk and reduced productivity across the lifespan in animals and humans. Further, specifically how host factors such as biological sex interact with early life stress to shape gut and systemic neuroimmune development and later life disease risk will be discussed.

Developmental programming of cardiovascular disease by prenatal hypoxia

2013 ◽  
Vol 4 (5) ◽  
pp. 328-337 ◽  
Author(s):  
D. A. Giussani ◽  
S. T. Davidge
Keyword(s):  
Cardiovascular Health ◽  
Maternal Nutrition ◽  
Research Effort ◽  
Peripheral Resistance ◽  
Later Life ◽  
Developmental Programming ◽  
The Metabolic Syndrome ◽  
Ischaemia And Reperfusion ◽  
Health And Disease

It is now recognized that the quality of the fetal environment during early development is important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. However, in contrast to the extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only recently becoming delineated and established. This review discusses the increasing body of evidence supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the identification of plausible mechanisms and the implementation of maternal and early life interventions to protect against adverse programming.

scholarly journals In UteroProgramming of Later Adiposity: The Role of Fetal Growth Restriction

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Ousseynou Sarr ◽  
Kaiping Yang ◽  
Timothy R. H. Regnault
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Synthase ◽  
Leptin Receptor ◽  
Methylation Status ◽  
Adult Life ◽  
Later Life ◽  
Growth Restriction ◽  
Receptor Expression ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Intrauterine growth restriction (IUGR) is strongly associated with obesity in adult life. The mechanisms contributing to the onset of IUGR-associated adult obesity have been studied in animal models and humans, where changes in fetal adipose tissue development, hormone levels and epigenome have been identified as principal areas of alteration leading to later life obesity. Following an adversein uterodevelopment, IUGR fetuses display increased lipogenic and adipogenic capacity in adipocytes, hypoleptinemia, altered glucocorticoid signalling, and chromatin remodelling, which subsequently all contribute to an increased later life obesity risk. Data suggest that many of these changes result from an enhanced activity of the adipose master transcription factor regulator, peroxisome proliferator-activated receptor-γ(PPARγ) and its coregulators, increased lipogenic fatty acid synthase (FAS) expression and activity, and upregulation of glycolysis in fetal adipose tissue. Increased expression of fetal hypothalamic neuropeptide Y (NPY), altered hypothalamic leptin receptor expression and partitioning, reduced adipose noradrenergic sympathetic innervations, enhanced adipose glucocorticoid action, and modifications in methylation status in the promoter of hepatic and adipose adipogenic and lipogenic genes in the fetus also contribute to obesity following IUGR. Therefore, interventions that inhibit these fetal developmental changes will be beneficial for modulation of adult body fat accumulation.

scholarly journals The impact of early nutrition on the ageing trajectory

2014 ◽  
Vol 73 (2) ◽  
pp. 289-301 ◽  
Author(s):  
Jane L. Tarry-Adkins ◽  
Susan E. Ozanne
Keyword(s):  
Animal Models ◽  
Early Life ◽  
Structural Changes ◽  
Molecular Mechanisms ◽  
Later Life ◽  
Epidemiological Studies ◽  
Developmental Programming ◽  
Early Nutrition ◽  
Cellular Ageing ◽  
The Impact

Epidemiological studies, including those in identical twins, and in individualsin uteroduring periods of famine have provided robust evidence of strong correlations between low birth-weight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

scholarly journals Endocrine and nutritional regulation of fetal adipose tissue development

2003 ◽  
Vol 179 (3) ◽  
pp. 293-299 ◽  
Author(s):  
ME Symonds ◽  
A Mostyn ◽  
S Pearce ◽  
H Budge ◽  
T Stephenson
Keyword(s):  
Adipose Tissue ◽  
Maternal Nutrition ◽  
Uncoupling Protein ◽  
Post Partum ◽  
Critical Role ◽  
Plasma Concentrations ◽  
Later Life ◽  
Postnatal Period ◽  
Late Gestation ◽  
Nutritional Regulation

In the fetus, adipose tIssue comprises both brown and white adipocytes for which brown fat is characterised as possessing the unique uncoupling protein (UCP)1. The dual characteristics of fetal fat reflect its critical role at birth in providing lipid that is mobilised rapidly following activation of UCP1 upon cold exposure to the extra-uterine environment. A key stage in the maturation of fetal fat is the gradual rise in the abundance of UCP1. For species with a mature hypothalamic-pituitary axis at birth there is a gradual increase in the amount and activity of UCP1 during late gestation, in conjunction with an increase in the plasma concentrations of catecholamines, thyroid hormones, cortisol, leptin and prolactin. These may act individually, or in combination, to promote UCP1 expression and, following the post-partum surge in each hormone, UCP1 abundance attains maximal amounts.Adipose tIssue grows in the fetus at a much lower rate than in the postnatal period. However, its growth is under marked nutritional constraints and, in contrast to many other fetal organs that are unaffected by nutritional manipulation, fat mass can be significantly altered by changes in maternal and, therefore, fetal nutrition. Fat deposition in the fetus is enhanced during late gestation following a previous period of nutrient restriction up to mid gestation. This is accompanied by increased mRNA abundance for the receptors of IGF-I and IGF-II. In contrast, increasing maternal nutrition in late gestation results in less adipose tIssue deposition but enhanced UCP1 abundance. The pronounced nutritional sensitivity of fetal adipose tIssue to both increased and decreased maternal nutrition may explain why the consequences of an adverse nutritional environment persist into later life.

scholarly journals Prenatally undernourished rats show increased preference for wheel running v. lever pressing for food in a choice task

2008 ◽  
Vol 101 (6) ◽  
pp. 902-908 ◽  
Author(s):  
Jennifer L. Miles ◽  
Jason Landon ◽  
Michael Davison ◽  
Christian U. Krägeloh ◽  
Nichola M. Thompson ◽  
...  
Keyword(s):  
Experimental Approach ◽  
Maternal Nutrition ◽  
Wheel Running ◽  
Adult Life ◽  
Later Life ◽  
Response Lever ◽  
Control Group ◽  
Biological Origin ◽  
Lifestyle Choices ◽  
Lever Pressing

Maternal nutrition during pregnancy has a significant influence in establishing patterns of metabolism and postnatal behaviours in offspring, and therefore shapes their risk of developing disorders in later life. Although it is well established that a mismatch between food consumption and energy expenditure leads to obesity and metabolic dysregulation, little research has investigated the biological origin of such behaviour. We conducted the present experiments to investigate effects of early-life nutrition on preference between wheel running and lever pressing for food during adult life. To address this issue we employed a well-established experimental approach in the rat which has shown that offspring of mothers undernourished during pregnancy develop obesity and metabolic disorders when kept under standard laboratory conditions. Using this experimental approach, two studies were conducted where offspring of ad libitum-fed dams and dams undernourished throughout pregnancy were given the choice between wheel running and pressing a response lever for food. Across subsequent conditions, the rate at which the response lever provided food was varied from 0·22 to 6·0 (study 1) and 0·19 to 3·0 (study 2) pellets per min. Compared with the control group, offspring from dams undernourished during pregnancy showed a consistently greater preference for running over lever pressing for food throughout both experiments of the study. The results of the present study provide experimental evidence that a mother's nutrition during pregnancy can result in a long-term shift in her offspring's lifestyle choices that are relevant to obesity prevention. Such a shift, if endorsed, will have substantial and wide-ranging health consequences throughout the lifespan.

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