scholarly journals Fetal Programming of the Neuroendocrine-Immune System and Metabolic Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
R. E. Fisher ◽  
M. Steele ◽  
N. A. Karrow
Keyword(s):  
Metabolic Disease ◽  
Immune System ◽  
Metabolic Diseases ◽  
The Body ◽  
Intrauterine Environment ◽  
Maternal Malnutrition ◽  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
Increased Risk ◽  
The Individual

Adverse uterine environments experienced during fetal development can alter the projected growth pattern of various organs and systems of the body, leaving the offspring at an increased risk of metabolic disease. The thrifty phenotype hypothesis has been demonstrated as an alteration to the growth trajectory to improve the survival and reproductive fitness of the individual. However, when the intrauterine environment does not match the extrauterine environment problems can arise. With the increase in metabolic diseases in both Westernized and developing countries, it is becoming apparent that there is an environmental disconnect with the extrauterine environment. Therefore, the focus of this paper will be to explore the effects of maternal malnutrition on the offspring’s susceptibility to metabolic disorders such as obesity, cardiovascular disease, and diabetes with emphasis on programming of the neuroendocrine-immune system.

Immunometabolism of obesity and diabetes: microbiota link compartmentalized immunity in the gut to metabolic tissue inflammation

2015 ◽  
Vol 129 (12) ◽  
pp. 1083-1096 ◽  
Author(s):  
Joseph B. McPhee ◽  
Jonathan D. Schertzer
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Immune Responses ◽  
Metabolic Diseases ◽  
The Body ◽  
Tissue Inflammation ◽  
Gut Barrier Function ◽  
Inflammatory Status ◽  
Obesity And Diabetes

The bacteria that inhabit us have emerged as factors linking immunity and metabolism. Changes in our microbiota can modify obesity and the immune underpinnings of metabolic diseases such as Type 2 diabetes. Obesity coincides with a low-level systemic inflammation, which also manifests within metabolic tissues such as adipose tissue and liver. This metabolic inflammation can promote insulin resistance and dysglycaemia. However, the obesity and metabolic disease-related immune responses that are compartmentalized in the intestinal environment do not necessarily parallel the inflammatory status of metabolic tissues that control blood glucose. In fact, a permissive immune environment in the gut can exacerbate metabolic tissue inflammation. Unravelling these discordant immune responses in different parts of the body and establishing a connection between nutrients, immunity and the microbiota in the gut is a complex challenge. Recent evidence positions the relationship between host gut barrier function, intestinal T cell responses and specific microbes at the crossroads of obesity and inflammation in metabolic disease. A key problem to be addressed is understanding how metabolite, immune or bacterial signals from the gut are relayed and transferred into systemic or metabolic tissue inflammation that can impair insulin action preceding Type 2 diabetes.

scholarly journals The Long and Short of It: The Role of Telomeres in Fetal Origins of Adult Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Stephanie E. Hallows ◽  
Timothy R. H. Regnault ◽  
Dean H. Betts
Keyword(s):  
Intrauterine Growth Restriction ◽  
The Body ◽  
Premature Aging ◽  
Fetal Origins ◽  
Maternal Malnutrition ◽  
Adult Disease ◽  
Increased Risk

Placental insufficiency, maternal malnutrition, and other causes of intrauterine growth restriction (IUGR) can significantly affect short-term growth and long-term health. Following IUGR, there is an increased risk for cardiovascular disease and Type 2 Diabetes. The etiology of these diseases is beginning to be elucidated, and premature aging or cellular senescence through increased oxidative stress and DNA damage to telomeric ends may be initiators of these disease processes. This paper will explore the areas where telomere and telomerase biology can have significant effects on various tissues in the body in IUGR outcomes.

scholarly journals Maternal obesity increases the risk of metabolic disease and impacts renal health in offspring

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Sarah J. Glastras ◽  
Hui Chen ◽  
Carol A. Pollock ◽  
Sonia Saad
Keyword(s):  
Metabolic Disease ◽  
Kidney Disease ◽  
Maternal Obesity ◽  
Disease Risk ◽  
Reproductive Age ◽  
Intrauterine Environment ◽  
Alcoholic Fatty Liver ◽  
Increased Risk ◽  
Epigenetic Modulation

Obesity, together with insulin resistance, promotes multiple metabolic abnormalities and is strongly associated with an increased risk of chronic disease including type 2 diabetes (T2D), hypertension, cardiovascular disease, non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The incidence of obesity continues to rise in astronomical proportions throughout the world and affects all the different stages of the lifespan. Importantly, the proportion of women of reproductive age who are overweight or obese is increasing at an alarming rate and has potential ramifications for offspring health and disease risk. Evidence suggests a strong link between the intrauterine environment and disease programming. The current review will describe the importance of the intrauterine environment in the development of metabolic disease, including kidney disease. It will detail the known mechanisms of fetal programming, including the role of epigenetic modulation. The evidence for the role of maternal obesity in the developmental programming of CKD is derived mostly from our rodent models which will be described. The clinical implication of such findings will also be discussed.

scholarly journals Hormonal Contraception and the Development of Autoimmunity: A Review of the Literature

2017 ◽  
Vol 84 (3) ◽  
pp. 275-295 ◽  
Author(s):  
William V. Williams
Keyword(s):  
Crohn’S Disease ◽  
Immune System ◽  
Crohn's Disease ◽  
Autoimmune Diseases ◽  
Interstitial Cystitis ◽  
White Blood Cells ◽  
The Body ◽  
Hormonal Contraceptives ◽  
Chemical Components ◽  
Increased Risk

Estrogens and progestins are known to have profound effects on the immune system and may modulate the susceptibility to autoimmune diseases. A comprehensive literature search was carried out using PubMed for any of 153 autoimmune disease terms and the terms contraception, contraceptive, or their chemical components with limits of Humans + Title or Abstract. Over 1,800 titles were returned and scanned, 352 papers retrieved and reviewed in depth and an additional 70 papers retrieved from the bibliographies. Based on this review, substantial evidence exists linking the use of combined oral contraceptives to a lower incidence of hyperthyroidism, an increase in multiple sclerosis, ulcerative colitis, Crohn's disease, Systemic Lupus Erythematosus, and interstitial cystitis. Progesterone only contraceptives are linked to progesterone dermatitis and in one large developing world concurrent cohort study are associated with increases in arthropathies and related disorders, eczema and contact dermatitis, pruritis and related conditions, alopecia, acne, and urticaria. Hormonal contraceptives modulate the immune system and may influence the susceptibility to autoimmune diseases with significant increases in risk for several autoimmune diseases. Summary Hormonal contraceptives (HCs), such as the “pill,” Norplant, and vaginal rings, are very potent hormones that have effects on the immune system, which is made up of white blood cells and lymph nodes and normally defends the body against invading bacteria, viruses and parasites. This review looked at the association of HC use to the development of autoimmune diseases, where the immune system turns against the body and causes damage to organs. There is good evidence that HC use is associated with an increased risk of several serious autoimmune diseases such as Crohn's disease (which causes inflammation of the bowels), Lupus (which causes inflammation in many organs), and interstitial cystitis (which causes inflammation in the bladder). Several other rarer autoimmune diseases are also linked to HC use. People contemplating the use of HCs should be informed of these risks.

scholarly journals Diabetic and Metabolic Programming: Mechanisms Altering the Intrauterine Milieu

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Claudia Eberle ◽  
Christoph Ament
Keyword(s):  
Metabolic Syndrome ◽  
Cardiovascular Diseases ◽  
Maternal Health ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Experimental Studies ◽  
Cardiovascular Changes ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome ◽  
Thrifty Phenotype Hypothesis

A wealth of epidemiological, clinical, and experimental studies have been linked to poor intrauterine conditions as well as metabolic and associated cardiovascular changes postnatal. These are novel perspectives connecting the altered intrauterine milieu to a rising number of metabolic diseases, such as diabetes, obesity, and hypercholesterolemia as well as the Metabolic Syndrome (Met S). Moreover, metabolic associated atherosclerotic diseases are connected to perigestational maternal health. The “Thrifty Phenotype Hypothesis” introduced cross-generational links between poor conditions during gestation and metabolic as well as cardiovascular alterations postnatal. Still, mechanisms altering the intrauterine milieu causing metabolic and associated atherosclerotic diseases are currently poorly understood. This paper will give novel insights in fundamental concepts connected to specific molecular mechanisms “programming” diabetes and associated metabolic as well as cardiovascular diseases.

scholarly journals The Interplay between Immune System and Microbiota in Osteoporosis

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Pietro Locantore ◽  
Valeria Del Gatto ◽  
Silvia Gelli ◽  
Rosa Maria Paragliola ◽  
Alfredo Pontecorvi
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Bone Cells ◽  
Bone Microarchitecture ◽  
Interleukin 17 ◽  
Mineral Density ◽  
Increased Risk ◽  
Long Term Treatment ◽  
Wide Range

Osteoporosis is a disease characterized by low bone mass and alterations of bone microarchitecture, with an increased risk of fractures. It is a multifactorial disorder that is more frequent in postmenopausal women but can be associated to other diseases (inflammatory and metabolic diseases). At present, several options are available to treat osteoporosis trying to block bone reabsorption and reduce the risk of fracture. Anyway, these drugs have safety and tolerance problems in long-term treatment. Recently, gut microbiota has been highlighted to have strong influence on bone metabolism, becoming a potential new target to modify bone mineral density. Such evidences are mainly based on mouse models, showing an involvement in modulating the interaction between the immune system and bone cells. Germ-free mice represent a basic model to understand the interaction between microbiota, immune system, and bone cells, even though data are controversial. Anyway, such models have unequivocally demonstrated a connection between such systems, even if the mechanism is unclear. Gut microbiota is a complex system that influences calcium and vitamin D absorption and modulates gut permeability, hormonal secretion, and immune response. A key role is played by the T helper 17 lymphocytes, TNF, interleukin 17, and RANK ligand system. Other important pathways include NOD1, NOD2, and Toll-like receptor 5. Prebiotics and probiotics are a wide range of substances and germs that can influence and modify microbiota. Several studies demonstrated actions by different prebiotics and probiotics in different animals, differing according to sex, age, and hormonal status. Data on the effects on humans are poor and controversial. Gut microbiota manipulation appears a possible strategy to prevent and treat osteopenia and/or osteoporosis as well as other possible bone alterations, even though further clinical studies are necessary to identify correct procedures in humans.

scholarly journals Hormone-Related Cancer and Autoimmune Diseases: A Complex Interplay to be Discovered

2022 ◽  
Vol 12 ◽  
Author(s):  
A Losada-García ◽  
SA Cortés-Ramírez ◽  
M Cruz-Burgos ◽  
M Morales-Pacheco ◽  
Carlos D Cruz-Hernández ◽  
...  
Keyword(s):  
Immune System ◽  
Autoimmune Diseases ◽  
Molecular Mechanisms ◽  
Continuous Process ◽  
Clinical Signs ◽  
The Body ◽  
Future Research ◽  
Adaptive Immune ◽  
Increased Risk ◽  
Risk Of Cancer

Neoplasic transformation is a continuous process that occurs in the body. Even before clinical signs, the immune system is capable of recognizing these aberrant cells and reacting to suppress them. However, transformed cells acquire the ability to evade innate and adaptive immune defenses through the secretion of molecules that inhibit immune effector functions, resulting in tumor progression. Hormones have the ability to modulate the immune system and are involved in the pathogenesis of autoimmune diseases, and cancer. Hormones can control both the innate and adaptive immune systems in men and women. For example androgens reduce immunity through modulating the production of pro-inflammatory and anti-inflammatory mediators. Women are more prone than men to suffer from autoimmune diseases such as systemic lupus erythematosus, psoriasis and others. This is linked to female hormones modulating the immune system. Patients with autoimmune diseases consistently have an increased risk of cancer, either as a result of underlying immune system dysregulation or as a side effect of pharmaceutical treatments. Epidemiological data on cancer incidence emphasize the link between the immune system and cancer. We outline and illustrate the occurrence of hormone-related cancer and its relationship to the immune system or autoimmune diseases in this review. It is obvious that some observations are contentious and require explanation of molecular mechanisms and validation. As a result, future research should clarify the molecular pathways involved, including any causal relationships, in order to eventually allocate information that will aid in the treatment of hormone-sensitive cancer and autoimmune illness.

scholarly journals DNA Methylation as a Marker of Body Shape in Premenopausal Women

2021 ◽  
Vol 12 ◽  
Author(s):  
Adeline Divoux ◽  
Alexey Eroshkin ◽  
Edina Erdos ◽  
Katalin Sandor ◽  
Timothy F. Osborne ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
Body Fat ◽  
Body Shape ◽  
Metabolic Diseases ◽  
Premenopausal Women ◽  
Fat Distribution ◽  
The Body ◽  
Fat Depots ◽  
Increased Risk

Preferential accumulation of fat in the gluteo-femoral (GF) depot (pear shape) rather than in the abdominal (A) depot (apple shape), protects against the development of metabolic diseases but the underlying molecular mechanism is still unknown. Recent data, including our work, suggest that differential epigenetic marking is associated with regulation of genes attributed to distinct fat distribution. Here, we aimed to compare the genomic DNA methylation signatures between apple and pear-shaped premenopausal women. To investigate the contribution of upper and lower body fat, we used paired samples of A-FAT and GF-FAT, analyzed on the BeadChip Methylation Array and quantified the differentially methylated sites between the 2 groups of women. We found unique DNA methylation patterns within both fat depots that are significantly different depending on the body fat distribution. Around 60% of the body shape specific DNA methylation sites identified in adipose tissue are maintained ex vivo in cultured preadipocytes. As it has been reported before in other cell types, we found only a hand full of genes showing coordinated differential methylation and expression levels. Finally, we determined that more than 50% of the body shape specific DNA methylation sites could also be detected in whole blood derived DNA. These data reveal a strong DNA methylation program associated with adipose tissue distribution with the possibility that a simple blood test could be used as a predictive diagnostic indicator of young women who are at increased risk for progressing to the apple body shape with a higher risk of developing obesity related complications.Clinical Trial Registration:https://clinicaltrials.gov/ct2/show/NCT02728635 and https://clinicaltrials.gov/ct2/show/NCT02226640, identifiers NCT02728635 and NCT02226640.

scholarly journals The Molecular Effects of Dietary Acid Load on Metabolic Disease (The Cellular PasaDoble: The Fast-Paced Dance of pH Regulation)

2021 ◽  
Vol 1 ◽  
Author(s):  
Morgan Williamson ◽  
Naima Moustaid-Moussa ◽  
Lauren Gollahon
Keyword(s):  
Metabolic Disease ◽  
Mammalian Cells ◽  
Metabolic Diseases ◽  
Prolonged Exposure ◽  
The Body ◽  
Calcium Excretion ◽  
Ph Homeostasis ◽  
Acid Base ◽  
Dietary Analysis ◽  
Wide Range

Metabolic diseases are becoming more common and more severe in populations adhering to western lifestyle. Since metabolic conditions are highly diet and lifestyle dependent, it is suggested that certain diets are the cause for a wide range of metabolic dysfunctions. Oxidative stress, excess calcium excretion, inflammation, and metabolic acidosis are common features in the origins of most metabolic disease. These primary manifestations of “metabolic syndrome” can lead to insulin resistance, diabetes, obesity, and hypertension. Further complications of the conditions involve kidney disease, cardiovascular disease, osteoporosis, and cancers. Dietary analysis shows that a modern “Western-style” diet may facilitate a disruption in pH homeostasis and drive disease progression through high consumption of exogenous acids. Because so many physiological and cellular functions rely on acid-base reactions and pH equilibrium, prolonged exposure of the body to more acids than can effectively be buffered, by chronic adherence to poor diet, may result in metabolic stress followed by disease. This review addresses relevant molecular pathways in mammalian cells discovered to be sensitive to acid - base equilibria, their cellular effects, and how they can cascade into an organism-level manifestation of Metabolic Syndromes. We will also discuss potential ways to help mitigate this digestive disruption of pH and metabolic homeostasis through dietary change.

scholarly journals Are anti-CTL4 and anti-PD-1 an effective biomarker in immunotherapy?

2022 ◽  
Vol 3 (1) ◽  
pp. 01-04
Author(s):  
Hasibe Vural
Keyword(s):  
Immune System ◽  
Cancer Therapy ◽  
The Body ◽  
Self Knowledge ◽  
The Individual ◽  
The Brain

The task of the immune system is to prevent foreign organisms from entering the body, if microbes have entered the body, to destroy them, to prevent or delay their spread. One of the most important features of the immune system is that it has the ability to recognize and distinguish millions of different microbes that are foreign to it. The immune system, like the brain, evaluates and synthesizes the situation, which is this breeding organ, and produces different training and special responses to microbes, cancer. This is a feature that does not exist in any system or organ except the brain and immune system. In summary, the task of the immune system is to protect the essence of the individual. For this reason, he knows himself first and does not harm the essence. In this context, it can be said that the immune system spends as much effort on self-knowledge as it does on fighting the enemy. This rewiev article is intended to provide an overview of the CTLA-4 and PD-1 pathways and the description of their efficacy in cancer therapy or immunotherapy.

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