Maternal nutrition during pregnancy and health of the offspring

2006 ◽  
Vol 34 (5) ◽  
pp. 779-782 ◽  
Author(s):  
M.S. Martin-Gronert ◽  
S.E. Ozanne
Keyword(s):  
Animal Studies ◽  
Molecular Mechanisms ◽  
Maternal Nutrition ◽  
Critical Factor ◽  
The Body ◽  
Long Term Effects ◽  
Insulin Dependent ◽  
Fetal Malnutrition ◽  
And Function ◽  
Maternal Overnutrition

The ability of mother to provide nutrients and oxygen for her baby is a critical factor for fetal health and its survival. Failure in supplying the adequate amount of nutrients to meet fetal demand can lead to fetal malnutrition. The fetus responds and adapts to undernutrition but by doing so it permanently alters the structure and function of the body. Maternal overnutrition also has long-lasting and detrimental effects on the health of the offspring. There is growing evidence that maternal nutrition can induce epigenetic modifications of the fetal genome. Only relatively recently has evidence from epidemiological and animal studies emerged suggesting that fetal responses to the intrauterine environment may underlie the prevalence of many chronic diseases of adulthood including Type 2 (non-insulin-dependent) diabetes. It is now of crucial importance to gain the understanding of the molecular mechanisms underlying the relationship between fetal alterations to the intra-uterine environment and their long-term effects on the health of an individual.

scholarly journals Gut Microbiota as Important Mediator Between Diet and DNA Methylation and Histone Modifications in the Host

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 597 ◽  
Author(s):  
Patrizia D’Aquila ◽  
Laurie Lynn Carelli ◽  
Francesco De Rango ◽  
Giuseppe Passarino ◽  
Dina Bellizzi
Keyword(s):  
Dna Methylation ◽  
Gut Microbiota ◽  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Current Evidence ◽  
Long Term Effects ◽  
Metabolic Functions ◽  
Complex Ecosystem ◽  
Short And Long Term ◽  
And Function

The human gut microbiota is a complex ecosystem consisting of trillions of microorganisms that inhabit symbiotically on and in the human intestine. They carry out, through the production of a series of metabolites, many important metabolic functions that complement the activity of mammalian enzymes and play an essential role in host digestion. Interindividual variability of microbiota structure, and consequently of the expression of its genes (microbiome), was largely ascribed to the nutritional regime. Diet influences microbiota composition and function with short- and long-term effects. In spite of the vast literature, molecular mechanisms underlying these effects still remain elusive. In this review, we summarized the current evidence on the role exerted by gut microbiota and, more specifically, by its metabolites in the establishment of the host epigenome. The interest in this topic stems from the fact that, by modulating DNA methylation and histone modifications, the gut microbiota does affect the cell activities of the hosting organism.

scholarly journals Ozone: A Review of Recent Experimental, Clinical and Epidemiological Evidence, with Notes on Causation—Part 1

1995 ◽  
Vol 2 (1) ◽  
pp. 25-31 ◽  
Author(s):  
David V Bates
Keyword(s):  
Clinical Studies ◽  
Animal Studies ◽  
Human Subjects ◽  
Ozone Exposure ◽  
Long Term Effects ◽  
Mechanisms Of Adaptation ◽  
Living Tissues ◽  
And Function ◽  
Theoretical Issues

Part 1 of this review is concerned with theoretical issues of ozone dosimetry, animal and cellular studies that illustrate the mechanism of action of ozone on living tissues, and with clinical studies. Animal studies have indicated that there are long term effects from low level long term ozone exposure. Clinical studies involve controlled ozone exposures on human subjects, both normals and asthmatics. Exercise concomitant with the ozone exposure increases the effect of the gas. It is concluded that the induction of an inflammatory response in the airway, both in the nose and in the lung, is the striking and earliest feature of ozone exposure. Current unexplained observations include: the dissociation between the inflammatory and function test response; the mechanisms of ‘adaptation’ and of airway hyperresponsiveness; and the phenomena that underlie the effect of ozone on maximal athletic performance.

scholarly journals Analytical and preparative biosynthesis of S100B recombinant protein using the pBT7-N-His vector system and preliminary studies of structure and function of this protein

2018 ◽  
pp. 161-164
Author(s):  
О.Л. Терёхина ◽  
М.К. Нурбеков ◽  
О.П. Дмитренко ◽  
Д.М. Давыдов
Keyword(s):  
Recombinant Protein ◽  
Molecular Mechanisms ◽  
The Body ◽  
S100b Protein ◽  
Vector System ◽  
Diagnostic Systems ◽  
E Coli ◽  
Sds Page ◽  
Bacterial Clone ◽  
And Function

С целью исследований структуры и функций белка S100B в клетке и в тканях был проведен цикл работ по оптимизации экспрессии рекомбинантного белка (рекS100B) в E. coli. Проведены процедуры аналитической экспрессии рекS100B в составе рекомбинантной плазмиды pBT7-N-His-S100B03. При SDS-ПААГЭ лизатов клонов бактерий выявлена четко экспрессирующаяся полоса в 10 кДа, которая была идентифицирована как мономерная форма белка. Перспективы исследований рекS100B связаны с потенциальным его использованием для изучения тонких молекулярных механизмов PPI взаимодействий в системе S100B/RAGE рецептор как ключевого звена передачи сигналов в клетке и организме и в качестве перспективного объекта создания диагностических систем мониторинга состояний организма в норме и при патологии связанной с нарушениями регуляции гена и/или функций S100B белка. To study structure and functions of the S100B protein in cells and tissues, a series of studies was conducted to optimize the recombinant protein (recS100B) expression in E. coli. Procedures for analytical expression of recS100B in the pBT7-N-His-S100B03 recombinant plasmid were performed. In SDS-PAGE of bacterial clone lysate, a clear 10 kDa band expression was detected, which was identified as a monomeric form of the protein. Prospects for the S100B study are related with its potential use for investigating molecular mechanisms of PPI interactions in the S100B/RAGE system as a key signal transducer in the cell and body and as a promising object for developing diagnostic systems for monitoring the body state in normal and pathological conditions associated with impaired regulation of the gene and/or functions of the S100B protein.

An Exploration of ADHD and Comorbidity With Substance Abuse and Brain Development

2021 ◽  
pp. 245-258
Author(s):  
York Williams
Keyword(s):  
Brain Development ◽  
Animal Studies ◽  
Primary Treatment ◽  
Treatment Team ◽  
Long Term Effects ◽  
Hyperactivity Disorder ◽  
Brain Structure And Function ◽  
And Function ◽  
Psychodynamic Therapies

Methylphenidate (MPH) is the most commonly used drug to treat attention deficit/hyperactivity disorder (ADHD) in children effectively and safely. However, in spite of its widespread application throughout what is considered one of the most plastic and sensitive phases of brain development in children, very little is known to date about its long-term effects on brain structure and function leading well into later adolescence and adulthood. Additionally, there is scant information available to parents, clinicians, and clients with ADD/ADHD about the influence of MPH on brain development. More importantly, recent human and animal studies suggest that MPH alters the dopaminergic system with long-term effects beyond the termination of treatment. As such, a multimodal treatment with psychodynamic therapies can assist the treatment team to support the development of the client's pro-social skills in addition to medication treatment, thus reducing full reliance on MPH as the primary treatment for ADD/ADHD.

scholarly journals Glycosphingolipids and neuroinflammation in Parkinson’s disease

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Karim Belarbi ◽  
Elodie Cuvelier ◽  
Marie-Amandine Bonte ◽  
Mazarine Desplanque ◽  
Bernard Gressier ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Lewy Bodies ◽  
Inflammasome Activation ◽  
Nigrostriatal Pathway ◽  
Neurodegenerative Process ◽  
And Function ◽  
The Brain

Abstract Parkinson's disease is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons of the nigrostriatal pathway and the formation of neuronal inclusions known as Lewy bodies. Chronic neuroinflammation, another hallmark of the disease, is thought to play an important role in the neurodegenerative process. Glycosphingolipids are a well-defined subclass of lipids that regulate crucial aspects of the brain function and recently emerged as potent regulators of the inflammatory process. Deregulation in glycosphingolipid metabolism has been reported in Parkinson’s disease. However, the interrelationship between glycosphingolipids and neuroinflammation in Parkinson’s disease is not well known. This review provides a thorough overview of the links between glycosphingolipid metabolism and immune-mediated mechanisms involved in neuroinflammation in Parkinson’s disease. After a brief presentation of the metabolism and function of glycosphingolipids in the brain, it summarizes the evidences supporting that glycosphingolipids (i.e. glucosylceramides or specific gangliosides) are deregulated in Parkinson’s disease. Then, the implications of these deregulations for neuroinflammation, based on data from human inherited lysosomal glycosphingolipid storage disorders and gene-engineered animal studies are outlined. Finally, the key molecular mechanisms by which glycosphingolipids could control neuroinflammation in Parkinson’s disease are highlighted. These include inflammasome activation and secretion of pro-inflammatory cytokines, altered calcium homeostasis, changes in the blood-brain barrier permeability, recruitment of peripheral immune cells or production of autoantibodies.

scholarly journals Air Pollution and COVID-19: A Possible Dangerous Synergy for Male Fertility

2021 ◽  
Vol 18 (13) ◽  
pp. 6846
Author(s):  
Luigi Montano ◽  
Francesco Donato ◽  
Pietro Massimiliano Bianco ◽  
Gennaro Lettieri ◽  
Antonino Guglielmino ◽  
...  
Keyword(s):  
Air Pollution ◽  
Male Fertility ◽  
Molecular Mechanisms ◽  
Semen Quality ◽  
Synergistic Effects ◽  
Epidemiological Data ◽  
The Body ◽  
Reproductive Capacity ◽  
Long Term Effects ◽  
Male Reproductive Function

Several studies indicate that semen quality has strongly declined in the last decades worldwide. Air pollution represents a significant co-factor with the COVID-19 impact and has negative effects on the male reproductive system, through pro-oxidant, inflammatory and immune-dysregulating mechanisms. It has recently been reported that chronic exposure to PM2.5 causes overexpression of the alveolar ACE2 receptor, the entry route of SARS-CoV-2 into the organism shared by the lungs and testis where expression is highest in the body. In the testis, the ACE2/Ang-(1–7)/MasR pathway plays an important role in the regulation of spermatogenesis and an indirect mechanism of testicular damage could be due to the blockade of the ACE2 receptor by SARS-CoV-2. This prevents the conversion of specific angiotensins, and their excess causes inflammation with the overproduction of cytokines. PM2.5-induced overexpression of the alveolar ACE2 receptor, in turn, could increase local viral load in patients exposed to pollutants, producing ACE2 receptor depletion and compromising host defenses. By presenting an overall view of epidemiological data and molecular mechanisms, this manuscript aims to interpret the possible synergistic effects of both air pollution and COVID-19 on male reproductive function, warning that the spread of SARS-CoV-2 in the fertile years may represent a significant threat to global reproductive health. All of this should be of great concern, especially for men of the age of maximum reproductive capacity, and an important topic of debate for policy makers. Altered environmental conditions, together with the direct and indirect short- and long-term effects of viral infection could cause a worsening of semen quality with important consequences for male fertility, especially in those areas with higher environmental impact.

Influence of maternal overnutrition and gestational diabetes on the programming of metabolic health outcomes in the offspring: experimental evidence

2015 ◽  
Vol 93 (5) ◽  
pp. 438-451 ◽  
Author(s):  
Troy J. Pereira ◽  
Brittany L. Moyce ◽  
Stephanie M. Kereliuk ◽  
Vernon W. Dolinsky
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Maternal Obesity ◽  
Obesity And Diabetes ◽  
Intergenerational Effect ◽  
Major Factors ◽  
Maternal Overnutrition

The incidence of obesity and type 2 diabetes mellitus have risen across the world during the past few decades and has also reached an alarming level among children. In addition, women are currently more likely than ever to enter pregnancy obese. As a result, the incidence of gestational diabetes mellitus is also on the rise. While diet and lifestyle contribute to these trends, population health data show that maternal obesity and diabetes during pregnancy during critical stages of development are major factors that contribute to the development of chronic disease in adolescent and adult offspring. Fetal programming of metabolic function, through physiological and (or) epigenetic mechanisms, may also have an intergenerational effect, and as a result may perpetuate metabolic disorders in the next generation. In this review, we summarize the existing literature that characterizes how maternal obesity and gestational diabetes mellitus contribute to metabolic and cardiovascular disorders in the offspring. In particular, we focus on animal studies that investigate the molecular mechanisms that are programmed by the gestational environment and lead to disease phenotypes in the offspring. We also review interventional studies that prevent disease with a developmental origin in the offspring.

Development and neurotransmitter-environmental interactions

1996 ◽  
Vol 8 (1) ◽  
pp. 183-199 ◽  
Author(s):  
Graham A. Rogeness ◽  
Erin B. McClure
Keyword(s):  
Emotionally Disturbed ◽  
Animal Studies ◽  
Long Term Effects ◽  
Behavioral Systems ◽  
Environmental Interactions ◽  
History Of ◽  
The Individual ◽  
And Function ◽  
The Brain

AbstractNorepinephrine (NE), dopamine (DA), and serotonin (5HT) are three of the more than thirty neurotransmitters (NTs) in the brain. Axons from a relatively small number of cell bodies located in the midbrain and brainstem branch out to connect with virtually all areas of the brain. Via these connections, these three NTs participate in the regulation of several behavioral systems that help modulate the interaction of the individual with his/her environment. Because the NT systems continue to develop after birth, interactions between the individual and his/her environment after birth may affect the development of these systems and have long-term effects on the individual's behavior. Animal studies indicate that early experience affects behavior and biogenic amine systems in the adult. For instance, one study showed that maternal deprivation, which is analogous to human neglect, affects the NE system in monkeys and may have a long-lasting effect on its development and function. In a previous study, similar relationships between early neglect and the NE system in humans were examined. Our results show that emotionally disturbed children with a history of neglect have lower dopamine-β-hydroxylase (DβH) activity, an enzyme involved in the synthesis of NE, than do children with no history of neglect. Additionally, the children with a history of neglect have lower systolic and diastolic blood pressure, both of which are functions mediated by the NE system, than the other children studied. These results support findings in animal studies that neglect affects the development of the NE system in a long-lasting, if not permanent way.

scholarly journals Maternal Obesity: A Focus on Maternal Interventions to Improve Health of Offspring

2021 ◽  
Vol 8 ◽  
Author(s):  
Akriti Shrestha ◽  
Madison Prowak ◽  
Victoria-Marie Berlandi-Short ◽  
Jessica Garay ◽  
Latha Ramalingam
Keyword(s):  
Animal Studies ◽  
Maternal Obesity ◽  
Maternal Nutrition ◽  
The United States ◽  
Oxidative Capacity ◽  
Cardiovascular Complications ◽  
Adverse Outcomes ◽  
Long Term Effects ◽  
Nutritional Interventions ◽  
Offspring Health

Maternal obesity has many implications for offspring health that persist throughout their lifespan that include obesity and cardiovascular complications. Several different factors contribute to obesity and they encompass interplay between genetics and environment. In the prenatal period, untreated obesity establishes a foundation for a myriad of symptoms and negative delivery experiences, including gestational hypertensive disorders, gestational diabetes, macrosomia, and labor complications. However, data across human and animal studies show promise that nutritional interventions and physical activity may rescue much of the adverse effects of obesity on offspring metabolic health. Further, these maternal interventions improve the health of the offspring by reducing weight gain, cardiovascular disorders, and improving glucose tolerance. Mechanisms from animal studies have also been proposed to elucidate the signaling pathways that regulate inflammation, lipid metabolism, and oxidative capacity of the tissue, ultimately providing potential specific courses of treatment. This review aims to pinpoint the risks of maternal obesity and provide plausible intervention strategies. We delve into recent research involving both animal and human studies with maternal interventions. With the increasing concerning of obesity rates witnessed in the United States, it is imperative to acknowledge the long-term effects posed on future generations and specifically modify maternal nutrition and care to mitigate these adverse outcomes.

scholarly journals Chronic Stress Effects on Tumor: Pathway and Mechanism

2021 ◽  
Vol 11 ◽  
Author(s):  
Hanqing Hong ◽  
Min Ji ◽  
Dongmei Lai
Keyword(s):  
Chronic Stress ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Emotional Experience ◽  
Stress Hormones ◽  
Chemotherapy Resistance ◽  
Immune Monitoring ◽  
The Body ◽  
Endocrine Disease ◽  
Stress Effects

Chronic stress is an emotional experience that occurs when people encounter something they cannot adapt to. Repeated chronic stress increases the risk of a variety of diseases, such as cardiovascular disease, depression, endocrine disease, inflammation and cancer. A growing body of research has shown that there is a link between chronic stress and tumor occurrence in both animal studies and clinical studies. Chronic stress activates the neuroendocrine system (hypothalamic-pituitary-adrenal axis) and sympathetic nervous system. Stress hormones promote the occurrence and development of tumors through various mechanisms. In addition, chronic stress also affects the immune function of the body, leading to the decline of immune monitoring ability and promote the occurrence of tumors. The mechanisms of chronic stress leading to tumor include inflammation, autophagy and epigenetics. These factors increase the proliferation and invasion capacity of tumor cells and alter the tumor microenvironment. Antagonists targeting adrenergic receptors have played a beneficial role in improving antitumor activity, as well as chemotherapy resistance and radiation resistance. Here, we review how these mechanisms contribute to tumor initiation and progression, and discuss whether these molecular mechanisms might be an ideal target to treat tumor.

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