scholarly journals Adipose tissue inflammation by intermittent hypoxia: mechanistic link between obstructive sleep apnoea and metabolic dysfunction

2017 ◽  
Vol 595 (8) ◽  
pp. 2423-2430 ◽  
Author(s):  
Silke Ryan
Keyword(s):  
Adipose Tissue ◽  
Obstructive Sleep Apnoea ◽  
Intermittent Hypoxia ◽  
Sleep Apnoea ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Obstructive Sleep

scholarly journals Adipose tissue as a key player in obstructive sleep apnoea

2019 ◽  
Vol 28 (152) ◽  
pp. 190006 ◽  
Author(s):  
Silke Ryan ◽  
Claire Arnaud ◽  
Susan F. Fitzpatrick ◽  
Jonathan Gaucher ◽  
Renaud Tamisier ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Obstructive Sleep Apnoea ◽  
Sleep Apnoea ◽  
Experimental Models ◽  
Complex Interaction ◽  
Health Concern ◽  
Metabolic Dysfunction ◽  
Major Health ◽  
Multiple Organs ◽  
Obstructive Sleep

Obstructive sleep apnoea (OSA) is a major health concern worldwide and adversely affects multiple organs and systems. OSA is associated with obesity in >60% of cases and is independently linked with the development of numerous comorbidities including hypertension, arrhythmia, stroke, coronary heart disease and metabolic dysfunction. The complex interaction between these conditions has a significant impact on patient care and mortality. The pathophysiology of cardiometabolic complications in OSA is still incompletely understood; however, the particular form of intermittent hypoxia (IH) observed in OSA, with repetitive short cycles of desaturation and re-oxygenation, probably plays a pivotal role. There is fast growing evidence that IH mediates some of its detrimental effects through adipose tissue inflammation and dysfunction. This article aims to summarise the effects of IH on adipose tissue in experimental models in a comprehensive way. Data from well-designed controlled trials are also reported with the final goal of proposing new avenues for improving phenotyping and personalised care in OSA.

scholarly journals Intermittent hypoxia in obstructive sleep apnoea mediates insulin resistance through adipose tissue inflammation

2017 ◽  
Vol 49 (4) ◽  
pp. 1601731 ◽  
Author(s):  
Aoife M. Murphy ◽  
Amandine Thomas ◽  
Sophie J. Crinion ◽  
Brian D. Kent ◽  
Murtaza M. Tambuwala ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Obstructive Sleep Apnoea ◽  
Intermittent Hypoxia ◽  
Insulin Signalling ◽  
Sleep Apnoea ◽  
M1 Macrophage ◽  
Insulin Signalling Pathway ◽  
Obstructive Sleep ◽  
Inflammatory Phenotype

Obstructive sleep apnoea (OSA) is increasingly associated with insulin resistance. The underlying pathophysiology remains unclear but intermittent hypoxia (IH)-mediated inflammation and subsequent dysfunction of the adipose tissue has been hypothesised to play a key role.We tested this hypothesis employing a comprehensive translational approach using a murine IH model of lean and diet-induced obese mice, an innovative IH system for cell cultures and a tightly controlled patient cohort.IH led to the development of insulin resistance in mice, corrected for the degree of obesity, and reduced insulin-mediated glucose uptake in 3T3-L1 adipocytes, associated with inhibition of the insulin-signalling pathway and downregulation of insulin-receptor substrate-1 mRNA. Providing mechanistic insight, IH induced a pro-inflammatory phenotype of visceral adipose tissue in mice with pro-inflammatory M1 macrophage polarisation correlating with the severity of insulin resistance. Complimentaryin vitroanalysis demonstrated that IH led to M1 polarisation of THP1-derived macrophages. In subjects without comorbidities (n=186), OSA was independently associated with insulin resistance. Furthermore, we found an independent correlation of OSA severity with the M1 macrophage inflammatory marker sCD163.This study provides evidence that IH induces a pro-inflammatory phenotype of the adipose tissue, which may be a crucial link between OSA and the development of insulin resistance.

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 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.

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