scholarly journals α-Mangostin remodels visceral adipose tissue inflammation to ameliorate age-related metabolic disorders in mice

Aging ◽  
2019 ◽  
Vol 11 (23) ◽  
pp. 11084-11110 ◽  
Author(s):  
Dan Li ◽  
Qianyu Liu ◽  
Xiuqiang Lu ◽  
Zhengqiu Li ◽  
Chunming Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Metabolic Disorders ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Age Related ◽  
Visceral Adipose

scholarly journals Progression from High Insulin Resistance to Type 2 Diabetes Does Not Entail Additional Visceral Adipose Tissue Inflammation

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e48155 ◽  
Author(s):  
Nuria Barbarroja ◽  
Chary Lopez-Pedrera ◽  
Lourdes Garrido-Sanchez ◽  
Maria Dolores Mayas ◽  
Wilfredo Oliva-Olivera ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
High Insulin ◽  
Visceral Adipose

Genetic Deficiency of TRAF5 Promotes Adipose Tissue Inflammation and Aggravates Diet-Induced Obesity in Mice

2021 ◽  
Author(s):  
Mark Colin Gissler ◽  
Nathaly Anto-Michel ◽  
Jan Pennig ◽  
Philipp Scherrer ◽  
Xiaowei Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Obese Patients ◽  
Adipose Tissue Inflammation ◽  
Metabolic Complications ◽  
Tissue Inflammation ◽  
Diet Induced Obesity ◽  
Genetic Deficiency ◽  
Obesity In Mice ◽  
Visceral Adipose

Objective: The accumulation of inflammatory leukocytes is a prerequisite of adipose tissue inflammation during cardiometabolic disease. We previously reported that a genetic deficiency of the intracellular signaling adaptor TRAF5 (TNF [tumor necrosis factor] receptor–associated factor 5) accelerates atherosclerosis in mice by increasing inflammatory cell recruitment. Here, we tested the hypothesis that an impairment of TRAF5 signaling modulates adipose tissue inflammation and its metabolic complications in a model of diet-induced obesity in mice. Approach and Results: To induce diet-induced obesity and adipose tissue inflammation, wild-type or Traf5 −/− mice consumed a high-fat diet for 18 weeks. Traf5 −/− mice showed an increased weight gain, impaired insulin tolerance, and increased fasting blood glucose. Weight of livers and peripheral fat pads was increased in Traf5 −/− mice, whereas lean tissue weight and growth were not affected. Flow cytometry of the stromal vascular fraction of visceral adipose tissue from Traf5 −/− mice revealed an increase in cytotoxic T cells, CD11c + macrophages, and increased gene expression of proinflammatory cytokines and chemokines. At the level of cell types, expression of TNFα, MIP (macrophage inflammatory protein)-1α, MCP (monocyte chemoattractant protein)-1, and RANTES (regulated on activation, normal T-cell expressed and secreted) was significantly upregulated in Traf5 -deficient adipocytes but not in Traf5 -deficient leukocytes from visceral adipose tissue. Finally, Traf5 expression was lower in adipocytes from obese patients and mice and recovered in adipose tissue of obese patients one year after bariatric surgery. Conclusions: We show that a genetic deficiency of TRAF5 in mice diet-induced obesity and its metabolic derangements by a proinflammatory response in adipocytes. Our data indicate that TRAF5 may promote anti-inflammatory and obesity-preventing signaling events in adipose tissue.

scholarly journals Neurotensin Is a Lipid-Induced Gastrointestinal Peptide Associated with Visceral Adipose Tissue Inflammation in Obesity

Nutrients ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 526 ◽  
Author(s):  
Ilaria Barchetta ◽  
Flavia Cimini ◽  
Danila Capoccia ◽  
Laura Bertoccini ◽  
Valentina Ceccarelli ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Visceral Adipose

scholarly journals Involvement of adipose tissue inflammation and dysfunction in virus-induced type 1 diabetes

2018 ◽  
Vol 238 (1) ◽  
pp. 61-75 ◽  
Author(s):  
James C Needell ◽  
Madalyn N Brown ◽  
Danny Zipris
Keyword(s):  
Type 1 Diabetes ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Poly I:C ◽  
Adipose Tissue Inflammation ◽  
Β Cell ◽  
Tissue Inflammation ◽  
Macrophage Recruitment ◽  
Visceral Adipose

The etiopathogenesis of type 1 diabetes (T1D) remains poorly understood. We used the LEW1.WR1 rat model of Kilham rat virus (KRV)-induced T1D to better understand the role of the innate immune system in the mechanism of virus-induced disease. We observed that infection with KRV results in cell influx into visceral adipose tissue soon following infection prior to insulitis and hyperglycemia. In sharp contrast, subcutaneous adipose tissue is free of cellular infiltration, whereas β cell inflammation and diabetes are observed beginning on day 14 post infection. Immunofluorescence studies further demonstrate that KRV triggers CD68+ macrophage recruitment and the expression of KRV transcripts and proinflammatory cytokines and chemokines in visceral adipose tissue. Adipocytes from naive rats cultured in the presence of KRV express virus transcripts and upregulate cytokine and chemokine gene expression. KRV induces apoptosis in visceral adipose tissue in vivo, which is reflected by positive TUNEL staining and the expression of cleaved caspase-3. Moreover, KRV leads to an oxidative stress response and downregulates the expression of adipokines and genes associated with mediating insulin signaling. Activation of innate immunity with Poly I:C in the absence of KRV leads to CD68+ macrophage recruitment to visceral adipose tissue and a decrease in adipokine expression detected 5 days following Poly (I:C) treatment. Finally, proof-of-principle studies show that brief anti-inflammatory steroid therapy suppresses visceral adipose tissue inflammation and protects from virus-induced disease. Our studies provide evidence raising the hypothesis that visceral adipose tissue inflammation and dysfunction may be involved in early mechanisms triggering β cell autoimmunity.

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