Commentary on the Role of Prenatal Stress in Developmental Programming of Obesity and Metabolic Dysfunction

2013 ◽  
pp. 121-126 ◽  
Keyword(s):  
Prenatal Stress ◽  
Developmental Programming ◽  
Metabolic Dysfunction

Gut Microbiota and Antipsychotics Induced Metabolic Alteration

2019 ◽  
pp. 131-143
Author(s):  
Dong-Yu Kan ◽  
Su-Juan Li ◽  
Chen-Chen Liu ◽  
Ren-Rong Wu
Keyword(s):  
Gut Microbiota ◽  
Body Weight Gain ◽  
Neuropsychiatric Disorders ◽  
Elevated Risk ◽  
Metabolic Disturbance ◽  
Metabolic Dysfunction ◽  
Sequencing Technology ◽  
Severe Mental Disorder ◽  
Metabolic Alteration

Schizophrenia is a chronic and severe mental disorder with antipsychotics as primary medications, but the antipsychotic-induced metabolic side effects may contribute to the elevated risk of overall morbidity and mortality in patients with psych-iatric diseases. With the development in sequencing technology and bioinformatics, dysbiosis has been shown to contribute to body weight gain and metabolic dysfunction. However, the role of gut microbiota in the antipsychotic-induced metabolic alteration remains unknown. In this paper, we reviewed the recent studies of the gut microbiota with psychiatric disorders and antipsychotic-induced metabolic dysfunction. Patients with neuropsychiatric disorders may have a different composi-tion of gut microbiota compared with healthy controls. In addition, it seems that the use of antipsychotics is concurrently associated with both altered composition of gut microbiota and metabolic disturbance. Further study is needed to address the role of gut microbiota in the development of neuropsychiatric disorders and antipsychotic-induced metabolic disturbance, to develop novel therapeutics for both neuropsychiatric disorders and metabolic dysfunction.

scholarly journals Adipose Tissue Immunomodulation and Treg/Th17 Imbalance in the Impaired Glucose Metabolism of Children with Obesity

Children ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 554
Author(s):  
Stefania Croce ◽  
Maria Antonietta Avanzini ◽  
Corrado Regalbuto ◽  
Erika Cordaro ◽  
Federica Vinci ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Th17 Cells ◽  
Metabolic Disorders ◽  
Potential Role ◽  
Immune Monitoring ◽  
Metabolic Dysfunction ◽  
Impaired Glucose Metabolism ◽  
T Cell Infiltration

In the last few decades, obesity has increased dramatically in pediatric patients. Obesity is a chronic disease correlated with systemic inflammation, characterized by the presence of CD4 and CD8 T cell infiltration and modified immune response, which contributes to the development of obesity related diseases and metabolic disorders, including impaired glucose metabolism. In particular, Treg and Th17 cells are dynamically balanced under healthy conditions, but imbalance occurs in inflammatory and pathological states, such as obesity. Some studies demonstrated that peripheral Treg and Th17 cells exhibit increased imbalance with worsening of glucose metabolic dysfunction, already in children with obesity. In this review, we considered the role of adipose tissue immunomodulation and the potential role played by Treg/T17 imbalance on the impaired glucose metabolism in pediatric obesity. In the patient care, immune monitoring could play an important role to define preventive strategies of pediatric metabolic disease treatments.

scholarly journals Role of Insulin Resistance in MAFLD

2021 ◽  
Vol 22 (8) ◽  
pp. 4156
Author(s):  
Yoshitaka Sakurai ◽  
Naoto Kubota ◽  
Toshimasa Yamauchi ◽  
Takashi Kadowaki
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo Lipogenesis ◽  
Hepatic Insulin Resistance ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD.

Prenatal Stress Leads to Intrauterine Dysfunction: The Role of Microbes and Microglia

2021 ◽  
Vol 89 (9) ◽  
pp. S191
Author(s):  
Helen Chen ◽  
Allison Bischoff ◽  
Adrienne Antonson ◽  
Therese Rajasekera ◽  
Tamar Gur
Keyword(s):  
Prenatal Stress

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

scholarly journals Maternal antioxidant treatment prevents behavioural and neural changes in offspring exposed to prenatal social stress

2019 ◽  
Author(s):  
H Scott ◽  
TJ Phillips ◽  
Y Sze ◽  
A Alfieri ◽  
MF Rogers ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Prenatal Stress ◽  
Social Stress ◽  
Maternal Stress ◽  
Later Life ◽  
Neuronal Cultures ◽  
Antioxidant Treatment ◽  
Foetal Brain ◽  
Increased Risk

AbstractMaternal exposure to social stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. However, the mechanism through which the effects of maternal stress are transmitted to the foetus is unclear. Using a rat model, we explored the mechanisms by which maternal social stress is conveyed to the foetus and the potential for targeted treatment to prevent disease in the offspring. Maternal stress increased circulating corticosterone in the mother, but not the foetuses. Maternal stress also induced oxidative stress in the placenta, but not in the foetal brain, and this was prevented by administration of a nanoparticle-bound antioxidant. Moreover, antioxidant treatment prevented prenatal stress-induced anxiety-like behaviour in the adult male offspring, along with several stress-induced neuroanatomical, neurochemical and gene expression changes in the offspring brain. Importantly, many of these neural effects were mimicked in neuronal cultures by application of placental-conditioned medium or foetal plasma from stressed pregnancies. Both placental-conditioned medium and foetal plasma contained differentially abundant extracellular microRNAs following prenatal stress. The present study highlights the crucial role of the placenta, and the molecules it secretes, in foetal brain development and provides evidence of the potential for treatment that can prevent maternal stress-induced foetal programming of neurological disease.

scholarly journals Role of NO and the NADPH Oxidase in Hyperhomocysteinemia induced Cardiac Metabolic Dysfunction in Pregnancy.

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Su Song ◽  
Harer Huang ◽  
Caroline Ojaimi ◽  
Pavel Kaminski ◽  
Suhua Zhang ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Metabolic Dysfunction ◽  
In Pregnancy

scholarly journals Genetic ablation of adipocyte PD-L1 reduces tumor growth but accentuates obesity-associated inflammation

2020 ◽  
Vol 8 (2) ◽  
pp. e000964 ◽  
Author(s):  
Bogang Wu ◽  
Huai-Chin Chiang ◽  
Xiujie Sun ◽  
Bin Yuan ◽  
Payal Mitra ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumor Growth ◽  
Body Weight Gain ◽  
High Body Mass Index ◽  
Human Adipose Tissue ◽  
Mrna Levels ◽  
Metabolic Dysfunction ◽  
Genetic Ablation ◽  
Tumor Immunosuppression

The programmed death-ligand 1 (PD-L1)-dependent immune checkpoint attenuates host immunity and maintains self-tolerance. Imbalance between protective immunity and immunopathology due to altered PD-L1 signaling can lead to autoimmunity or tumor immunosuppression. The role of the PD-L1-dependent checkpoint in non-immune system is less reported. We previously found that white adipocytes highly express PD-L1. Here we show that adipocyte-specific PD-L1 knockout mice exhibit enhanced host anti-tumor immunity against mammary tumors and melanoma with low or no tumor PD-L1. However, adipocyte PD-L1 ablation in tumor-free mice also exacerbates diet-induced body weight gain, pro-inflammatory macrophage infiltration into adipose tissue, and insulin resistance. Low PD-L1 mRNA levels in human adipose tissue correlate with high body mass index and presence of type 2 diabetes. Therefore, our mouse genetic approach unequivocally demonstrates a cell-autonomous function of adipocyte PD-L1 in promoting tumor growth and inhibiting antitumor immunity. In addition, our work uncovers a previously unrecognized role of adipocyte PD-L1 in mitigating obesity-related inflammation and metabolic dysfunction.

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