scholarly journals The Alterations in and the Role of the Th17/Treg Balance in Metabolic Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Siwen Zhang ◽  
Xiaokun Gang ◽  
Shuo Yang ◽  
Mengzhao Cui ◽  
Lin Sun ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Metabolic Diseases ◽  
Treg Cells ◽  
Metabolic Dysfunction ◽  
T Helper ◽  
T Helper 17 ◽  
Glucose And Lipid Metabolism ◽  
Underlying Mechanisms

Chronic inflammation plays an important role in the development of metabolic diseases. These include obesity, type 2 diabetes mellitus, and metabolic dysfunction-associated fatty liver disease. The proinflammatory environment maintained by the innate immunity, including macrophages and related cytokines, can be influenced by adaptive immunity. The function of T helper 17 (Th17) and regulatory T (Treg) cells in this process has attracted attention. The Th17/Treg balance is regulated by inflammatory cytokines and various metabolic factors, including those associated with cellular energy metabolism. The possible underlying mechanisms include metabolism-related signaling pathways and epigenetic regulation. Several studies conducted on human and animal models have shown marked differences in and the important roles of Th17/Treg in chronic inflammation associated with obesity and metabolic diseases. Moreover, Th17/Treg seems to be a bridge linking the gut microbiota to host metabolic disorders. In this review, we have provided an overview of the alterations in and the functions of the Th17/Treg balance in metabolic diseases and its role in regulating immune response-related glucose and lipid metabolism.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: Gut microbiota in patients with type 2 diabetes mellitus

2015 ◽  
Vol 172 (4) ◽  
pp. R167-R177 ◽  
Author(s):  
Kristine H Allin ◽  
Trine Nielsen ◽  
Oluf Pedersen
Keyword(s):  
Type 2 Diabetes ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Short Chain Fatty Acids ◽  
Intestinal Content ◽  
Low Grade ◽  
Bacterial Fermentation ◽  
Underlying Mechanisms

Perturbations of the composition and function of the gut microbiota have been associated with metabolic disorders including obesity, insulin resistance and type 2 diabetes. Studies on mice have demonstrated several underlying mechanisms including host signalling through bacterial lipopolysaccharides derived from the outer membranes of Gram-negative bacteria, bacterial fermentation of dietary fibres to short-chain fatty acids and bacterial modulation of bile acids. On top of this, an increased permeability of the intestinal epithelium may lead to increased absorption of macromolecules from the intestinal content resulting in systemic immune responses, low-grade inflammation and altered signalling pathways influencing lipid and glucose metabolism. While mechanistic studies on mice collectively support a causal role of the gut microbiota in metabolic diseases, the majority of studies in humans are correlative of nature and thus hinder causal inferences. Importantly, several factors known to influence the risk of type 2 diabetes, e.g. diet and age, have also been linked to alterations in the gut microbiota complicating the interpretation of correlative studies. However, based upon the available evidence, it is hypothesised that the gut microbiota may mediate or modulate the influence of lifestyle factors triggering development of type 2 diabetes. Thus, the aim of this review is to critically discuss the potential role of the gut microbiota in the pathophysiology and pathogenesis of type 2 diabetes.

Retinol binding protein 4 and its membrane receptors: a metabolic perspective

2015 ◽  
Vol 22 (1) ◽  
Author(s):  
Ronja Fedders ◽  
Matthias Muenzner ◽  
Michael Schupp
Keyword(s):  
Metabolic Diseases ◽  
Binding Protein ◽  
Current Data ◽  
Membrane Receptors ◽  
Retinol Binding Protein ◽  
Metabolic Effects ◽  
Retinol Binding Protein 4 ◽  
Underlying Mechanisms

AbstractNearly a decade of intense research has passed since the first report linking circulating retinol binding protein 4 (RBP4) to the development of insulin resistance. By now, a variety of underlying mechanisms have been identified; some of them are adherent to the canonical role of this circulating protein, which is to transport and deliver retinol to target tissues, and others that seem rather independent of retinol transport. Despite all these efforts, a consensus in the basic principles of RBP4’s metabolic effects has not been reached and some controversy remains. Using this as an opportunity, we here review and discuss current data on RBP4’s action on insulin sensitivity and its dependency on retinol homeostasis. We pay special attention to the involvement of RBP4 membrane receptors that were identified during these years, such as ‘stimulated by retinoic acid 6’ (STRA6), and whose identification added another layer of complexity to RBP4’s diverse actions. A better understanding of RBP4’s functions might allow its therapeutic exploitations, urgently needed in our period that is defined by an epidemic increase in metabolic diseases such as obesity and type 2 diabetes.

Glucocorticoid hormones and energy homeostasis

2014 ◽  
Vol 19 (2) ◽  
Author(s):  
Roldan M. de Guia ◽  
Adam J. Rose ◽  
Stephan Herzig
Keyword(s):  
Energy Homeostasis ◽  
Target Genes ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Metabolic Dysfunction ◽  
Endocrine Control ◽  
Regulatory Pathways ◽  
Glucose And Lipid Metabolism ◽  
Steroid Binding

AbstractGlucocorticoids (GC) and their cognate intracellular receptor, the glucocorticoid receptor (GR), have been characterised as critical checkpoints in the endocrine control of energy homeostasis in mammals. Indeed, aberrant GC action has been linked to a variety of severe metabolic diseases, including obesity, insulin resistance and type 2 diabetes. As a steroid-binding member of the nuclear receptor superfamily of transcription factors, the GR translocates into the cell nucleus upon GC binding where it serves as a transcriptional regulator of distinct GC-responsive target genes that are – in many cases – associated with glucose and lipid regulatory pathways and thereby intricately control both physiological and pathophysiological systemic energy homeostasis. Here, we summarize the current knowledge of GC/GR function in energy metabolism and systemic metabolic dysfunction, particularly focusing on glucose and lipid metabolism.

scholarly journals Electroacupuncture Improves Blood Pressure in SHRs by Regulating the Immune Balance between Th17 and Treg

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yang Wang ◽  
Lili Zhang ◽  
Li Li ◽  
Hantong Hu ◽  
Pan Pan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Th17 Cells ◽  
Spontaneously Hypertensive Rats ◽  
Treg Cells ◽  
T Helper ◽  
Hypertensive Rats ◽  
T Helper 17 ◽  
Spontaneously Hypertensive ◽  
Immune Balance

The present study investigated the effects of electroacupuncture on blood pressure in spontaneously hypertensive rats (SHRs) by regulating the immune balance of T helper 17 cells (Th17 cells) and regulatory T cells (Treg cells). This study investigated the role of electroacupuncture in the immune balance of SHRs using Western blot, flow cytometry, and ELISA techniques. Electroacupuncture significantly improved blood pressure, downregulated the expression of RORγt, and upregulated the expression of Foxp3, reduced the production of Th17 cells, promoted the production of Treg cells, reduced the secretion of IL-6 and IL-17, and increased the secretion of TGF-β1 and IL-10. These findings suggest that electroacupuncture therapy effectively improved the systolic blood pressure of SHRs, and its mechanism may be related to promotion of the immune balance between Th17 and Treg.

scholarly journals ANGPTL8 in metabolic homeostasis: more friend than foe?

Open Biology ◽  
2021 ◽  
Vol 11 (9) ◽  
Author(s):  
Chang Guo ◽  
Chenxi Wang ◽  
Xia Deng ◽  
Jianqiang He ◽  
Ling Yang ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Hepatic Glucose Production ◽  
Physiological Role ◽  
Glucose Production ◽  
Peripheral Tissues ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose

ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.

scholarly journals Th17 and Treg Cells in Bone Related Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Min Wang ◽  
Tian Tian ◽  
Shuang Yu ◽  
Na He ◽  
Daoxin Ma
Keyword(s):  
Bone Marrow ◽  
Molecular Mechanisms ◽  
Treg Cells ◽  
Bone Diseases ◽  
Reciprocal Relationship ◽  
T Helper ◽  
Therapeutic Approaches ◽  
T Helper 17 ◽  
And Function

Bone-related diseases share the process of immune response that targets bone tissue and bone marrow and then induce adverse effects on structure and function. In recent years, reciprocal relationship between immune cells and bone systems has been uncovered gradually. Regulatory T (Treg) and T helper 17 (Th17) cells are newly identified subsets of CD4+ T cells, and the balance between them is particularly essential for maintaining immune homeostasis. Accumulated data have demonstrated quantitative or functional imbalance between Th17 and Treg in bone related diseases, suggesting that Th17 and Treg cells are involved in these bone diseases. Understanding the molecular mechanisms regulating Th17 and Treg cells will create opportunities for the development of therapeutic approaches. This review will present the role of Th17 and Treg cells in the inflammatory bone diseases and bone marrow malignancies and find the potential therapeutic target for immunotherapy.

scholarly journals The role of Th17/Treg-mediated immunoregulation in abortion mice

2018 ◽  
Vol 16 ◽  
pp. 205873921876035 ◽  
Author(s):  
Ning Li ◽  
Qinglan Qu ◽  
Qian Yan
Keyword(s):  
Spontaneous Abortion ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Normal Pregnancy ◽  
Treg Cells ◽  
Vital Role ◽  
Orphan Receptor ◽  
T Helper ◽  
T Helper 17

In the study, we investigated the immune factors related to T helper 17 (Th17) cells and T regulatory (Treg) cells in spontaneous abortion mice. The expression of Th17 was analyzed by interleukin (IL)-6, IL-17A secretion, RAR-related orphan receptor γt (RORγt) expression, and proportion of CD4+IL-17+ cells. The levels of IL-10, transforming growth factor β (TGF-β), Foxp3, and CD4+Foxp3+ cells were presented the Treg expression. Higher embryo absorption rate was found in spontaneous abortion group than that in normal pregnancy group ( P < 0.01). Compared with the normal pregnancy mice, spontaneous abortion mice showed higher levels of IL-6 and IL-17A and lower levels of IL-10 and TGF-β in serum and in decidua ( P < 0.05). Furthermore, the expressions of Foxp3 and CD4+Foxp3+ cells were significantly decreased in spontaneous abortion mice than those in normal pregnancy mice ( P < 0.05). However, the levels of RORγt and CD4+IL-17+ cells remarkably increased in spontaneous abortion mice ( P < 0.05). The results reveal that Th17/Treg cells may play a vital role in immunoregulation during pregnancy.

scholarly journals The Immunoregulation of Th17 in Host against Intracellular Bacterial Infection

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Yonghong Li ◽  
Chaojun Wei ◽  
Hui Xu ◽  
Jing Jia ◽  
Zhenhong Wei ◽  
...  
Keyword(s):  
Protective Immunity ◽  
Bacterial Infections ◽  
Cytokine Production ◽  
T Helper ◽  
T Regulatory Cell ◽  
T Helper 17 ◽  
Socioeconomic Burden ◽  
Production Pattern ◽  
Underlying Mechanisms

T helper 17 cells (Th17) constitute a distinct subset of helper T cells with a unique transcriptional profile (STAT3, RORγ, and RORα), cytokine production pattern (IL17 family), and requirement of specific cytokines for their differentiation (TGF-β, IL6, IL21, and IL23). Recent studies involving experimental animals and humans have shown that Th17/IL17 plays a crucial role in host defense against a variety of pathogens, including bacteria and viruses. The underlying mechanisms by which Th17 performs include dendritic cell (DC) regulation, neutrophil recruitment, Th1 modulation, and T regulatory cell (Treg) balance. In recent years, researchers have generated an accumulating wealth of evidence on the role of Th17/IL17 in protective immunity to intracellular bacterial pathogens, such asMycobacterium tuberculosisandChlamydia trachomatis, which are one of the most important pathogens that inflict significant socioeconomic burden across the globe. In this article, we reviewed the current literature on the functions and mechanisms by which Th17/IL17 responds to intracellular bacterial infections. A better understanding of Th17/IL17 immunity to pathogens would be crucial for developing effective prophylactics and therapeutics.

N6-methyladenine RNA Modification (m6A): An Emerging Regulator of Metabolic Diseases

2020 ◽  
Vol 21 (11) ◽  
pp. 1056-1067 ◽  
Author(s):  
Hui Zhong ◽  
Hui-Fang Tang ◽  
Yin Kai
Keyword(s):  
Inflammatory Response ◽  
Messenger Rna ◽  
Metabolic Diseases ◽  
Rna Modification ◽  
Metabolic Dysfunction ◽  
Dynamic Regulation ◽  
Rna Methylation ◽  
New Ideas

N6-methyladenine RNA modification (m6A) is an RNA methylation modification catalyzed by methyltransferase at the 6th position nitrogen atom of adenine (A), which is the most common chemical modification of eukaryotic messenger RNA (mRNA). Recently, m6A has been found to play an important role in the dynamic regulation of RNA, which is crucial for some physiological and pathophysiological processes such as adipogenesis, cell differentiation, and the immune/inflammatory response. Metabolic diseases are a series of chronic inflammatory disorders caused by metabolic dysfunction of proteins, glucose, and lipids. Emerging studies have shown that m6A plays an important role in the process of metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) via regulation of glucose/lipid metabolism and the immune/inflammatory response. In this review, we will summarize the role of m6A in metabolic diseases, which may provide new ideas for the prevention and treatment of metabolic diseases.

scholarly journals Extracellular vesicles in metabolic disease

Diabetologia ◽  
2019 ◽  
Vol 62 (12) ◽  
pp. 2179-2187 ◽  
Author(s):  
Naveed Akbar ◽  
Valerio Azzimato ◽  
Robin P. Choudhury ◽  
Myriam Aouadi
Keyword(s):  
Metabolic Disease ◽  
Extracellular Vesicles ◽  
Metabolic Regulation ◽  
Metabolic Diseases ◽  
Recipient Cell ◽  
Plasma Concentrations ◽  
Parent Cell ◽  
Metabolic Dysfunction

Abstract Extracellular vesicles (EVs) are submicron-sized lipid envelopes that are produced and released from a parent cell and can be taken up by a recipient cell. EVs are capable of mediating cellular signalling by carrying nucleic acids, proteins, lipids and cellular metabolites between cells and organs. Metabolic dysfunction is associated with changes in plasma concentrations of EVs as well as alterations in their EV cargo. Since EVs can act as messengers between parent and recipient cells, they could be involved in cell-to-cell and organ-to-organ communication in metabolic diseases. Recent literature has shown that EVs are produced by cells within metabolic tissues, such as adipose tissue, pancreas, muscle and liver. These vesicles have therefore been proposed as a novel intercellular communication mode in systemic metabolic regulation. In this review, we will describe and discuss the current literature that investigates the role of adipose-derived EVs in the regulation of obesity-associated metabolic disease. We will particularly focus on the EV-dependent communication between adipocytes, the vasculature and immune cells in type 2 diabetes.

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