Looking at the Future through the Mother’s Womb: Gestational Diabetes and Offspring Fertility

Endocrinology ◽  
2021 ◽  
Author(s):  
Niharika Sinha ◽  
Gretchen Lydia Walker ◽  
Aritro Sen
Keyword(s):  
Reproductive Health ◽  
Gestational Diabetes ◽  
Maternal Obesity ◽  
Adult Life ◽  
Epidemiological Studies ◽  
Epigenetic Changes ◽  
Adverse Conditions ◽  
Long Term Effect ◽  
Increased Risk

Abstract Altered nutrition or intra-uterine exposure to various adverse conditions during fetal development or earlier in a mother’s life can lead to epigenetic changes in fetal tissues, predisposing those tissues to diseases that manifest when offspring become adults. An example is a maternal obesity associated with gestational diabetes (GDM), where fetal exposure to a hyperglycemic, hyperinsulinemic, and/or hyperlipidemic gestational environment can provoke epigenetic changes that predispose offspring to various diseased conditions later in life. While it is now well established that offspring exposed to GDM have an increased risk of developing obesity, metabolic disorders, and/or cardiovascular disease in adult life, there are limited studies assessing the reproductive health of these offspring. This mini-review discusses the long-term effect of in-utero exposure to GDM-associated adverse prenatal environment on the reproductive health of the offspring. Moreover, using evidence from various animal models and human epidemiological studies this review offers a molecular insight and understanding of how epigenetic reprogramming of genes culminates in reproductive dysfunction and the development of sub/infertility later in adult life.

scholarly journals The impact of gestational diabetes and maternal obesity on the mother and her offspring

2010 ◽  
Vol 1 (4) ◽  
pp. 208-215 ◽  
Author(s):  
P. M. Catalano
Keyword(s):  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Glucose Intolerance ◽  
Maternal Obesity ◽  
Insulin Response ◽  
Obese Women ◽  
Increased Risk ◽  
Short And Long Term ◽  
The Impact

Thein uteromaternal metabolic environment is important relative to both short and long term development of the offspring. Although poor fetal growth remains a significant factor relative to long-term outcome, fetal overgrowth is assuming greater importance because of the increase in obesity in the world’s populations. Maternal obesity and gestational diabetes are the most common metabolic complications of pregnancy related to fetal overgrowth and more specifically adiposity.Women with gestational diabetes have increased insulin resistance and inadequate insulin response compared with weight-matched controls. Gestational diabetes increases the risk of maternal hypertensive disease (preeclampsia) as well as cesarean delivery. At birth the neonate has increased adiposity and is at risk for birth injury. Multiple studies have reported that children of women with gestational diabetes have a greater prevalence childhood obesity and glucose intolerance; even at glucose concentrations less than currently used to define gestational diabetes, compared with normoglycemic women.Obese women also have increased insulin resistance, insulin response and inflammatory cytokines compared with average weight women both before and during pregnancy. They too are at increased risk for the metabolic syndrome-like disorders during pregnancy that is hypertension, hyperlipidemia, glucose intolerance and coagulation disorders. Analogous to women with gestational diabetes, neonates of obese women are heavier at delivery because of increased fat and not lean body mass. Similarly, these children have an increased risk of childhood adiposity and metabolic dysregulation. Hence, the preconceptional and perinatal period offers a unique opportunity to modify both short and long term risks for both the woman and her offspring.

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

Long-term effect of morphine administration in young rats on the analgesic opioid response in adult life

2008 ◽  
Vol 26 (6) ◽  
pp. 561-565 ◽  
Author(s):  
Joanna Ripoll Rozisky ◽  
Giovana Dantas ◽  
Lauren Spezia Adachi ◽  
Viviane Soares Alves ◽  
Maria Beatriz Cardoso Ferreira ◽  
...  
Keyword(s):  
Adult Life ◽  
Term Effect ◽  
Young Rats ◽  
Long Term Effect ◽  
Morphine Administration

Air Pollution as Risk Factor for Mental Disorders: In Search for a Possible Link with Alzheimer’s Disease and Schizophrenia

2021 ◽  
Author(s):  
Luigi Attademo ◽  
Francesco Bernardini
Keyword(s):  
Mental Health ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Risk Factor ◽  
Air Pollutants ◽  
Epidemiological Studies ◽  
Increased Risk ◽  
The Central Nervous System

As a global problem that has increasingly been causing worldwide concern, air pollution poses a significant and serious environmental risk to health. Risks of cardiovascular and respiratory diseases, as well as various types of cancer, have been consistently associated with the exposure to air pollutants. More recently, various studies have also shown that the central nervous system is also attacked by air pollution. Air pollution appears to be strongly associated with a higher risk of cognitive defects, neurodevelopmental (e.g., schizophrenia) and neurodegenerative (e.g., Alzheimer’s disease) disorders. Subjects with schizophrenia, as well as subjects with Alzheimer’s disease, experience a variety of neuropsychological deficits and cognitive impairments. This determines an adverse effect on social and professional functioning, and it contributes to the long-term disease burden. However, no final conclusions have been drawn on the matter of the direct relationship between schizophrenia and Alzheimer’s disease. In recent years, the topic of urbanicity and mental health has become increasingly important. Urban exposure to environmental toxins and pollution is currently described as a reliable risk factor for schizophrenia and other psychoses, and it has been demonstrated more and more how exposure to air pollutants is associated with increased risk of dementia. Pathways by which air pollution can target and damage the brain, leading to an increased risk for developing schizophrenia and Alzheimer’s disease, are multiple and complex. Results from epidemiological studies suggest potential associations, but are still insufficient to confirm causality. Further studies are needed in order to verify this hypothesis. And if confirmed, the clinical implications could be of substantial relevance for both public and mental health.

Previous gestational diabetes impairs long-term endothelial function in a mouse model of complicated pregnancy

2010 ◽  
Vol 299 (3) ◽  
pp. R862-R870 ◽  
Author(s):  
Joanna L. Stanley ◽  
Sowndramalingam Sankaralingam ◽  
Philip N. Baker ◽  
Sandra T. Davidge
Keyword(s):  
Endothelial Dysfunction ◽  
Gestational Diabetes ◽  
Mouse Model ◽  
Endothelial Function ◽  
Fluorescence Intensity ◽  
Mean Fluorescence Intensity ◽  
Mesenteric Arteries ◽  
Superoxide Production ◽  
Increased Risk

Women who develop gestational diabetes mellitis (GDM) display endothelial dysfunction up to 1 yr after pregnancy, despite a return to normoglycemia. It is unknown whether this dysfunction was preexisting or whether GDM pregnancy leads to long-term endothelial dysfunction. A mouse model that spontaneously develops GDM ( Lepr db/+) was used to determine whether the endothelial dysfunction that develops during GDM is evident in later life. Heterozygous and wild-type (WT) controls were allowed to litter once, then age to 9–10 mo, and were compared with virgin controls. Vascular function of small mesenteric arteries was assessed using wire myography. Concentration response curves to the thromboxane A2mimetic U46619 and the endothelium-dependent vasodilator methacholine were constructed. Superoxide production and peroxynitrite formation was also measured. Mice with previous GDM displayed blood glucose concentrations similar to previously pregnant WT mice (8.0 ± 0.1 vs. 7.1 ± 0.3 mmol/l, P > 0.05). Arteries from mice with previous GDM displayed increased sensitivity to U46619 (EC50 5.2 ± 0.7 vs. 45.2 ± 1.0 nmol/l, P < 0.01) and impaired endothelium-dependent relaxation compared with WT controls (29 ± 8 vs. 58 ± 16 percent relaxation, P < 0.05). This was associated with increased superoxide production (93.3 ± 2.3 vs. 64.6 ± 1.6 mean fluorescence intensity, P < 0.001) and increased peroxynitrite formation (173.5 ± 11.0 vs. 57.4 ± 16.2 mean fluorescence intensity, P < 0.01) compared with virgin controls. In summary, endothelial dysfunction was evident in mice with previous GDM compared with previously healthy pregnant mice or virgin controls. These data suggest that GDM affects endothelial function and may contribute to an increased risk of cardiovascular disease.

Growing healthy muscles to optimise metabolic health into adult life

2014 ◽  
Vol 5 (6) ◽  
pp. 420-434 ◽  
Author(s):  
S. A. Bayol ◽  
C. R. Bruce ◽  
G. D. Wadley
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Maternal Obesity ◽  
Adult Life ◽  
Metabolic Health ◽  
Skeletal Muscle Development ◽  
Pregnancy And Lactation ◽  
Functional Consequences ◽  
And Function

The importance of skeletal muscle for metabolic health and obesity prevention is gradually gaining recognition. As a result, interventions are being developed to increase or maintain muscle mass and metabolic function in adult and elderly populations. These interventions include exercise, hormonal and nutritional therapies. Nonetheless, growing evidence suggests that maternal malnutrition and obesity during pregnancy and lactation impede skeletal muscle development and growth in the offspring, with long-term functional consequences lasting into adult life. Here we review the role of skeletal muscle in health and obesity, providing an insight into how this tissue develops and discuss evidence that maternal obesity affects its development, growth and function into adult life. Such evidence warrants the need to develop early life interventions to optimise skeletal muscle development and growth in the offspring and thereby maximise metabolic health into adult life.

Is benzodiazepine use a risk factor for cognitive decline and dementia? A literature review of epidemiological studies

2004 ◽  
Vol 35 (3) ◽  
pp. 307-315 ◽  
Author(s):  
HELENE VERDOUX ◽  
RAJAA LAGNAOUI ◽  
BERNARD BEGAUD
Keyword(s):  
General Population ◽  
Cognitive Decline ◽  
Epidemiological Studies ◽  
Cognitive Outcome ◽  
Public Health Issue ◽  
Hand Search ◽  
Increased Risk ◽  
Benzodiazepine Use

Background. A major public health issue is to determine whether long-term benzodiazepine use may induce cognitive deficits persisting after withdrawal. The aim of the present review was to examine findings from prospective studies carried out in general population samples exploring whether exposure to benzodiazepines is associated with an increased risk of incident cognitive decline.Method. Using a MEDLINE search and a hand-search of related references in selected papers, we retrieved original studies published in peer-reviewed journals that explored in general population samples the association between benzodiazepine exposure and change in cognitive performance between baseline and follow-up assessment.Results. Six papers met the inclusion criteria. Two studies reported a lower risk of cognitive decline in former or ever users, two found no association whatever the category of user, and three found an increased risk of cognitive decline in benzodiazepine users.Conclusions. The discrepant findings obtained by studies examining the link between benzodiazepine exposure and risk of cognitive decline may be due to methodological differences, especially regarding the definitions of exposure and cognitive outcome. As a large proportion of subjects are exposed to benzodiazepines, a small increase in the risk of cognitive decline may have marked deleterious consequences for the health of the general population. This issue needs to be explored further by pharmaco-epidemiological studies.

scholarly journals Impact of Maternal Obesity on Fetal Programming of Cardiovascular Disease

Physiology ◽  
2015 ◽  
Vol 30 (3) ◽  
pp. 224-231 ◽  
Author(s):  
Victoria H. J. Roberts ◽  
Antonio E. Frias ◽  
Kevin L. Grove
Keyword(s):  
Cardiovascular Disease ◽  
Health Risks ◽  
Fetal Programming ◽  
Maternal Obesity ◽  
Later Life ◽  
Epidemiological Studies ◽  
Cardiovascular Development ◽  
Mechanistic Studies ◽  
In Utero Environment

The in utero environment is a key determinant of long-term health outcomes; poor maternal metabolic state and placental insufficiency are strongly associated with these long-term health risks. Human epidemiological studies link maternal obesity and offspring cardiovascular disease in later life, but mechanistic studies in animal models are limited. Here, we review the literature pertaining to maternal consequences of obesity during pregnancy and the subsequent impact on fetal cardiovascular development.

scholarly journals AN ECONOMIC ANALYSIS OF AWARENESS ON RURAL HEALTH PROGARMMES IN MUDIKANDANALLUR VILLAGE, SRIMUSHNAM TALUK,CUDDALORE DISTRICT,TAMILNADU

YMER Digital ◽  
2021 ◽  
Vol 20 (12) ◽  
pp. 769-779
Author(s):  
Dr. C Ramesh ◽  
Keyword(s):  
Reproductive Health ◽  
Rural Health ◽  
Adult Life ◽  
Physical Growth ◽  
World Health ◽  
Bottom Of The Pyramid ◽  
Sustainable Business ◽  
Increased Risk ◽  
Growth And Change ◽  
Health Organization

World Health Organization (WHO) defines adolescence as the period of life between 10and 19 year of age. The adolescent experiences not only physical growth and change but also emotional, psychological, social, and mental change and growth. Physiological changes change lead to sexual maturity and usually occur during the first several year of this period. Adolescence represents a window of opportunity to prepare for a healthy adult life. The world’s adolescent population-1200 million persons, 10-19 year of age or about 19% of the total population-faces series of serious challenges not affecting their growth and development but also their livelihood as adults. Yet adolescents remain a largely neglected, difficult-to-measure, and hard-to-reach population, in which the needs of adolescent girls in particular are often ignored. Adolescence is period of increased risk taking and therefore susceptibility to behavioural problems at the time of puberty and new concerns about reproductive health. Majority of adolescents still do not have access to information and education on sexuality, reproduction, and sexual and reproductive health and rights, nor do they have access to preventive and preventive curative service. Commercial innovation to address health needs at the bottom of the pyramid for more than 800 million men, women and children across India living on USD 1-3 ADAY, the idea if accessible and affordable medicine is often as remote as their rural homes. Arogya Parivar (“health family’’ in Hindi) is a for-profit social initiative developed by Novartis to reach the undeserved million living at the bottom of the pyramid in rural India. After just years, Arogya Parivar is proving to be both a force for improving rural health programme in rural community and a sustainable business.

scholarly journals Gestational Diabetes Mellitus Affects Offspring’s Epigenome. Is There a Way to Reduce the Negative Consequences?

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2792
Author(s):  
Monika Słupecka-Ziemilska ◽  
Piotr Wychowański ◽  
Monika Puzianowska-Kuznicka
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnancy Complication ◽  
Epigenetic Changes ◽  
Negative Consequences ◽  
Short Term ◽  
Related Factors ◽  
Epigenetic Programming

Gestational diabetes mellitus (GDM) is the most common pregnancy complication worldwide and may result in short-term and long-term consequences for offspring. The present review highlights evidence of epigenetic programming, mostly from human studies, which occurs in offspring exposed to maternal GDM during different stages of development, paying special attention to the differences in sensitivity of offspring to maternal hyperglycemia as a result of sex-related factors. We also aim to answer the following question: If these epigenetic changes are constant throughout the lifetime of the offspring, how do they present phenotypically?

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