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 ◽  
...  



Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Katharina Hess ◽  
Nikolaus Marx ◽  
Martin Wabitsch ◽  
Thomas Skurk ◽  
Hans Hauner ◽  
...  

Background: Adipose tissue inflammation may play a critical role in the pathogenesis of insulin resistance (IR) and arteriosclerosis. Previous work has mainly focused on the role of macrophages in human adipose tissue, but little is known about pro-inflammatory T-lymphocytes. Therefore the present study examined the role of CD4-positive lymphocytes in adipose tissue inflammation and IR. Results: Both, CD4-positive lymphocytes and macrophages are present in human visceral adipose tissue as determined by immunohistochemical staining. Most macrophages were HLA-DR positive, reflecting activation through IFNγ, a cytokine released from CD4-positive lymphocytes. Furthermore, SDF-1α, a T-cell chemotactic protein, was also detectable in human adipose tissue. RT-PCR analyses confirmed the expression of IFNγ and SDF1α in visceral adipose tissue. Freshly isolated human adipocytes as well SGBS adipocyte cells express SDF-1α with a down regulation of its expression during adipocyte differentiation in both cell types. In a mouse model of IR, high fat diet induced IR already after 5 weeks which was associated with a marked lymphocyte infiltration in visceral adipose tissue as determined by immunohistochemical staining and RT-PCR. In contrast, macrophages were absent after 5 weeks of diet but could be detected at week 10, suggesting early infiltration of lymphocytes during the development of IR. Conclusion: Pro-inflammatory T-lymphocytes are present in visceral adipose tissue and may contribute to local inflammatory cell activation before the appearance of macrophages. These data suggest that lymphocytes may play an important role in the initiation and perpetuation of adipose tissue inflammation as well as the development of insulin resistance.



Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1790-P ◽  
Author(s):  
GRETHA J. BOERSMA ◽  
KERSTIN HEURLING ◽  
MARIA J. PEREIRA ◽  
EMIL JOHANSSON ◽  
MARK LUBBERINK ◽  
...  


2020 ◽  
Vol 37 (7) ◽  
pp. 1192-1201 ◽  
Author(s):  
N. E. Antonio‐Villa ◽  
O. Y Bello‐Chavolla ◽  
A. Vargas‐Vázquez ◽  
R. Mehta ◽  
C. A. Aguilar‐Salinas ◽  
...  




2016 ◽  
Vol 17 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Ilija Jeftic ◽  
Marina Miletic-Kovacevic ◽  
Nemanja Jovicic ◽  
Jelena Pantic ◽  
Nebojsa Arsenijevic ◽  
...  

Abstract Obesity and type 2 diabetes mellitus (T2DM) constitute major health problems worldwide. Increased visceral adiposity enhances the risk of insulin resistance and type 2 diabetes. The mechanisms involved in obesity-associated chronic inflammation in metabolic tissues (metaflammation) that lead to insulin resistance and dysregulated glucose metabolism are incompletely defined. Galectin-3 (Gal-3), a β-galactoside-binding lectin, modulates immune/inflammatory responses and specifically binds to metabolic danger molecules. To dissect the role of Gal-3 in obesity and diabetes, Gal-3-deficient (LGALS3-/-) and wild-type (WT) C57Bl/6 male mice were placed on a high-fat diet (HFD, 60% kcal fat) or a standard chow diet (10% kcal fat) for 6 months and metabolic, histological and immunophenotypical analyses of the visceral adipose tissue were performed. HFD-fed LGALS3-/- mice had higher body weights and more body weight gain, visceral adipose tissue (VAT), hyperglycaemia, hyperinsulinemia, insulin resistance and hyperlipidemia than diet-matched WT mice. Compared to WT mice, the enlarged VAT in obese LGALS3-/- mice contained larger adipocytes. Additionally, we demonstrate enhanced inflammation in the VAT of LGALS3-/- mice compared with diet-matched WT mice. The VAT of LGALS3-/- mice fed a HFD contained more numerous dendritic cells and proinflammatory F4/80+CD11c+CD11b+ and F4/80high macrophages. In contrast to WT mice, the numbers of CXCR3+ and CD8+ T cells were increased in the VAT of Gal-3-deficient mice after 6 months of high-fat feeding. We provide evidence that Gal-3 ablation results in enhanced HFD-induced adiposity, inflammation in the adipose tissue, insulin resistance and hyperglycaemia. Thus, Gal-3 represents an important regulator of obesity-associated immunometabolic alterations.



2015 ◽  
Vol 46 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Andoni Lancha ◽  
Santiago López-Garrido ◽  
Amaia Rodríguez ◽  
Victoria Catalán ◽  
Beatriz Ramírez ◽  
...  


Cell ◽  
2015 ◽  
Vol 160 (4) ◽  
pp. 745-758 ◽  
Author(s):  
Rachel J. Perry ◽  
João-Paulo G. Camporez ◽  
Romy Kursawe ◽  
Paul M. Titchenell ◽  
Dongyan Zhang ◽  
...  


Sign in / Sign up

Export Citation Format

Share Document