44-OR: PAR2-Regulated MIF Secretion from Non-Immune Cells in Adipose Tissue Is a Key Mechanism Involved in the Development of Metabolic Dysfunction

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 44-OR
Author(s):  
YIHENG HUANG ◽  
LIUJUN CHEN ◽  
YADAN QI ◽  
DAKE QI
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Metabolic Dysfunction

scholarly journals B Lymphocytes and Adipose Tissue Inflammation

2020 ◽  
Vol 40 (5) ◽  
pp. 1110-1122 ◽  
Author(s):  
Prasad Srikakulapu ◽  
Coleen A. McNamara
Keyword(s):  
Adipose Tissue ◽  
B Cell ◽  
Immune Cells ◽  
Immune Cell ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Cell Type ◽  
Tissue Inflammation ◽  
B Cell Subsets

The immune system plays an important role in obesity-induced adipose tissue inflammation and the resultant metabolic dysfunction, which can lead to hypertension, dyslipidemia, and insulin resistance and their downstream sequelae of type 2 diabetes mellitus and cardiovascular disease. While macrophages are the most abundant immune cell type in adipose tissue, other immune cells are also present, such as B cells, which play important roles in regulating adipose tissue inflammation. This brief review will overview B-cell subsets, describe their localization in various adipose depots and summarize our knowledge about the function of these B-cell subsets in regulating adipose tissue inflammation, obesity-induced metabolic dysfunction and atherosclerosis.

scholarly journals Adipocyte Oncostatin Receptor Regulates Adipose Tissue Homeostasis and Inflammation

2021 ◽  
Vol 11 ◽  
Author(s):  
David Sanchez-Infantes ◽  
Jacqueline M. Stephens
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Oncostatin M ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Fat Depots ◽  
Disease States ◽  
Inflammatory State ◽  
And Function ◽  
Oncostatin M Receptor

Adipocytes are the largest cell type in terms of volume, but not number, in adipose tissue. Adipocytes are prominent contributors to systemic metabolic health. Obesity, defined by excess adipose tissue (AT), is recognized as a low-grade chronic inflammatory state. Cytokines are inflammatory mediators that are produced in adipose tissue (AT) and function in both AT homeostatic as well as pathological conditions. AT inflammation is associated with systemic metabolic dysfunction and obesity-associated infiltration and proliferation of immune cells occurs in a variety of fat depots in mice and humans. AT immune cells secrete a variety of chemokines and cytokines that act in a paracrine manner on adjacent adipocytes. TNFα, IL-6, and MCP-1, are well studied mediators of AT inflammation. Oncostatin M (OSM) is another proinflammatory cytokine that is elevated in AT in human obesity, and its specific receptor (OSMRβ) is also induced in conditions of obesity and insulin resistance. OSM production and paracrine signaling in AT regulates adipogenesis and the functions of AT. This review summarizes the roles of the oncostatin M receptor (OSMRβ) as a modulator of adipocyte development and function its contributions to immunological adaptations in AT in metabolic disease states.

scholarly journals Metabolic dysfunction induced by high-fat diet modulates hematopoietic stem and myeloid progenitor cells in brown adipose tissue of mice

2021 ◽  
Author(s):  
Kyle T Mincham ◽  
Kunjal Panchal ◽  
Prue H Hart ◽  
Robyn M Lucas ◽  
Martin Feelisch ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Adipose Tissue ◽  
Progenitor Cells ◽  
Immune Cells ◽  
High Fat Diet ◽  
Low Dose ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Hematopoietic Stem ◽  
Brown Adipose

AbstractBrown adipose tissue (BAT) may be an important metabolic regulator of whole-body glucose. While important roles have been ascribed to macrophages in regulating metabolic functions in BAT, little known is known of the roles of other immune cells subsets, particularly dendritic cells (DCs). Eating a high fat diet may compromise the development of hematopoietic stem and progenitor cells (HSPC) – which give rise to DCs – in bone marrow, with less known of its effects in BAT. We have previously demonstrated that ongoing exposure to low-dose ultraviolet radiation (UVR) significantly reduced the ‘whitening’ effect of eating a high-fat diet upon interscapular (i)BAT of mice. Here, we examined whether this observation may be linked to changes in the phenotype of HSPC and myeloid-derived immune cells in iBAT and bone marrow of mice using 12-colour flow cytometry. Many HSPC subsets declined in both iBAT and bone marrow with increasing metabolic dysfunction. Conversely, with rising adiposity and metabolic dysfunction, conventional (c)DCs increased in both of these tissues. When compared to low-fat diet, consumption of high-fat diet significantly reduced proportions of myeloid, common myeloid and megakaryocyte-erythrocyte progenitors in iBAT, and short-term hematopoietic stem cells in bone marrow. In mice fed a high-fat diet, exposure to low-dose UVR significantly reduced proportions of cDCs in iBAT, independently of nitric oxide release from irradiated skin (blocked using the scavenger, cPTIO), but did not significantly modify HSPC subsets in either tissue. Further studies are needed to determine whether changes in these cell populations contribute towards metabolic dysfunction.

scholarly journals The role of immune cells in the development of adipose tissue dysfunction in cardiovascular diseases

2019 ◽  
pp. 92-98 ◽  
Author(s):  
E. G. Uchasova ◽  
O. V. Gruzdeva ◽  
Yu. A. Dyleva ◽  
E. V. Belik ◽  
O. L. Barbarash
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Vascular Diseases ◽  
Inflammatory Cells ◽  
Metabolic Dysfunction ◽  
Perivascular Adipose Tissue ◽  
Cytokines And Chemokines ◽  
Adipose Tissue Dysfunction ◽  
Physiological Properties ◽  
Cellular Signal

Adipose tissue dysfunction characterized by a loss of homeostatic functions It is observed in patients with obesity, insulin resistance and diabetes. In case of violation of the physiological properties in adipose tissue, an increased production of cytokines and chemokines occurs with the infiltration of tissue by immune cells. In turn, immune cells also produce cytokines, metalloproteinases, reactive oxygen species and chemokines, which are involved in tissue remodeling, cellular signal transduction and immunity regulation. The presence of inflammatory cells in adipose tissue affects organs and tissues. So in the blood vessels, inflammation of perivascular adipose tissue leads to vascular remodeling, superoxide production, endothelial dysfunction with loss of the bioavailability of nitric oxide, contributing to the development of various vascular diseases. In adipose tissue dysfunction, adipokines are also produced, such as leptin, resistin, and visfatin. These substances contribute to metabolic dysfunction, alter systemic homeostasis, sympathetic outflow, glucose regulation, and insulin sensitivity. Thus, the study of the mechanisms of interaction between immune cells and adipose tissue is promising and may be an important therapeutic target.

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 Orphan GPR116 mediates the insulin sensitizing effects of the hepatokine FNDC4 in adipose tissue

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Anastasia Georgiadi ◽  
Valeria Lopez-Salazar ◽  
Rabih El- Merahbi ◽  
Rhoda Anane Karikari ◽  
Xiaochuan Ma ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Dependent Manner ◽  
Metabolic Dysfunction ◽  
Functional Interaction ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Obesity And Diabetes ◽  
Adhesion Gpcr ◽  
Circulating Levels

AbstractThe proper functional interaction between different tissues represents a key component in systemic metabolic control. Indeed, disruption of endocrine inter-tissue communication is a hallmark of severe metabolic dysfunction in obesity and diabetes. Here, we show that the FNDC4-GPR116, liver-white adipose tissue endocrine axis controls glucose homeostasis. We found that the liver primarily controlled the circulating levels of soluble FNDC4 (sFNDC4) and lowering of the hepatokine FNDC4 led to prediabetes in mice. Further, we identified the orphan adhesion GPCR GPR116 as a receptor of sFNDC4 in the white adipose tissue. Upon direct and high affinity binding of sFNDC4 to GPR116, sFNDC4 promoted insulin signaling and insulin-mediated glucose uptake in white adipocytes. Indeed, supplementation with FcsFNDC4 in prediabetic mice improved glucose tolerance and inflammatory markers in a white-adipocyte selective and GPR116-dependent manner. Of note, the sFNDC4-GPR116, liver-adipose tissue axis was dampened in (pre) diabetic human patients. Thus our findings will now allow for harnessing this endocrine circuit for alternative therapeutic strategies in obesity-related pre-diabetes.

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 Female adipose tissue-specific Bscl2 knockout mice develop only moderate metabolic dysfunction when housed at thermoneutrality and fed a high-fat diet

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
George D. Mcilroy ◽  
Sharon E. Mitchell ◽  
Weiping Han ◽  
Mirela Delibegović ◽  
Justin J. Rochford
Keyword(s):  
Adipose Tissue ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Tissue Specific

scholarly journals Repeated clodronate-liposome treatment results in neutrophilia and is not effective in limiting obesity-linked metabolic impairments

2019 ◽  
Vol 316 (3) ◽  
pp. E358-E372 ◽  
Author(s):  
Jackie E. Bader ◽  
Reilly T. Enos ◽  
Kandy T. Velázquez ◽  
Meredith S. Carson ◽  
Alex T. Sougiannis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Intake ◽  
Complete Blood Count ◽  
Therapeutic Option ◽  
Intraperitoneal Administration ◽  
Direct Result ◽  
Metabolic Dysfunction ◽  
Macrophage Depletion ◽  
Clodronate Liposome ◽  
Metabolic Impairments

Depletion of macrophages is thought to be a therapeutic option for obesity-induced inflammation and metabolic dysfunction. However, whether the therapeutic effect is a direct result of reduced macrophage-derived inflammation or secondary to decreases in fat mass is controversial, as macrophage depletion has been shown to disrupt energy homeostasis. This study was designed to determine if macrophage depletion via clodronate-liposome (CLD) treatment could serve as an effective intervention to reduce obesity-driven inflammatory and metabolic impairments independent of changes in energy intake. After 16 wk on a high-fat diet (HFD) or the AIN-76A control (low-fat) diet (LFD) ( n = 30/diet treatment), male C57BL/6J mice were assigned to a CLD- or PBS-liposome treatment ( n = 15/group) for 4 wk. Liposomes were administered biweekly via intraperitoneal injections (8 administrations in total). PBS-liposome-treated groups were pair-fed to their CLD-treated dietary counterparts. Metabolic function was assessed before and after liposome treatment. Adipose tissue, as well as the liver, was investigated for macrophage infiltration and the presence of inflammatory mediators. Additionally, a complete blood count was performed. CLD treatment reduced energy intake. When controlling for energy intake, CLD treatment was unable to regress metabolic dysfunction or nonalcoholic fatty liver disease and impaired adipose tissue insulin action. Moreover, repeated CLD treatment induced neutrophilia and anemia, increased adipose tissue mRNA expression of the proinflammatory cytokines IL-6 and IL-1β, and augmented circulating IL-6 and monocyte chemoattractant protein-1 concentrations ( P < 0.05). This study suggests that repeated intraperitoneal administration of CLD to deplete macrophages attenuates obesity by limiting energy intake. Moreover, after controlling for the benefits of weight loss, the accompanying detrimental side effects limit regular CLD treatment as an effective therapeutic strategy.

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