scholarly journals T Cell–Derived IL-22 Amplifies IL-1β–Driven Inflammation in Human Adipose Tissue: Relevance to Obesity and Type 2 Diabetes

Diabetes ◽  
2014 ◽  
Vol 63 (6) ◽  
pp. 1966-1977 ◽  
Author(s):  
Elise Dalmas ◽  
Nicolas Venteclef ◽  
Charles Caer ◽  
Christine Poitou ◽  
Isabelle Cremer ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
T Cell ◽  
Human Adipose Tissue

1973-P: Single-Nuclei Transcriptomics of Human Adipose Tissue Identify Distinct Adipocyte Progenitor Subpopulations in Type 2 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1973-P
Author(s):  
CLARISSA STRIEDER-BARBOZA ◽  
CARMEN G. FLESHER ◽  
LYNN M. GELETKA ◽  
ROBERT W. OROURKE ◽  
CAREY N. LUMENG
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Human Adipose Tissue

Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes

2007 ◽  
Vol 292 (3) ◽  
pp. E740-E747 ◽  
Author(s):  
S. J. Creely ◽  
P. G. McTernan ◽  
C. M. Kusminski ◽  
ff. M. Fisher ◽  
N. F. Da Silva ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Protein Expression ◽  
Serum Insulin ◽  
Human Adipose Tissue ◽  
Innate Immune ◽  
System Response ◽  
Low Grade ◽  
Tnf Α

Type 2 diabetes (T2DM) is associated with chronic low-grade inflammation. Adipose tissue (AT) may represent an important site of inflammation. 3T3-L1 studies have demonstrated that lipopolysaccharide (LPS) activates toll-like receptors (TLRs) to cause inflammation. For this study, we 1) examined activation of TLRs and adipocytokines by LPS in human abdominal subcutaneous (AbdSc) adipocytes, 2) examined blockade of NF-κB in human AbdSc adipocytes, 3) examined the innate immune pathway in AbdSc AT from lean, obese, and T2DM subjects, and 4) examined the association of circulating LPS in T2DM subjects. The findings showed that LPS increased TLR-2 protein expression twofold ( P < 0.05). Treatment of AbdSc adipocytes with LPS caused a significant increase in TNF-α and IL-6 secretion (IL-6, Control: 2.7 ± 0.5 vs. LPS: 4.8 ± 0.3 ng/ml; P < 0.001; TNF-α, Control: 1.0 ± 0.83 vs. LPS: 32.8 ± 6.23 pg/ml; P < 0.001). NF-κB inhibitor reduced IL-6 in AbdSc adipocytes (Control: 2.7 ± 0.5 vs. NF-κB inhibitor: 2.1 ± 0.4 ng/ml; P < 0.001). AbdSc AT protein expression for TLR-2, MyD88, TRAF6, and NF-κB was increased in T2DM patients ( P < 0.05), and TLR-2, TRAF-6, and NF-κB were increased in LPS-treated adipocytes ( P < 0.05). Circulating LPS was 76% higher in T2DM subjects compared with matched controls. LPS correlated with insulin in controls ( r = 0.678, P < 0.0001). Rosiglitazone (RSG) significantly reduced both fasting serum insulin levels (reduced by 51%, P = 0.0395) and serum LPS (reduced by 35%, P = 0.0139) in a subgroup of previously untreated T2DM patients. In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.

Validation of Endogenous Control Genes in Human Adipose Tissue: Relevance to Obesity and Obesity-associated Type 2 Diabetes Mellitus

2007 ◽  
Vol 39 (7) ◽  
pp. 495-500 ◽  
Author(s):  
V. Catalán ◽  
J. Gómez-Ambrosi ◽  
F. Rotellar ◽  
C. Silva ◽  
A. Rodríguez ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Endogenous Control

The Impact of Exercise on DNA Methylation of Genes Associated with Type 2 Diabetes and Obesity in Human Adipose Tissue

2014 ◽  
Vol 10 (01) ◽  
pp. 64 ◽  
Author(s):  
Tina Rönn ◽  
Charlotte Ling ◽  
◽  
Keyword(s):  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Short Review ◽  
Methylation Pattern ◽  
Cellular Level ◽  
Genetic And Environmental Factors ◽  
The Impact

It is well established that exercise promotes health, and reduces people’s risks for developing type 2 diabetes and becoming obese. But just how exercise performs this, at a cellular level, and what molecular and physiologic steps are involved and in what order, are still not fully understood. Metabolic disorders are often influenced by interactions between genetic and environmental factors. One possible explanation for how the environment may influence the genome is through epigenetic mechanisms–that is–chemical modifications to the DNA itself. Epigenetic factors include, for example, DNA methylation, histone modifications, and different RNA-mediated processes, which all have the ability to bind to DNA or affect the chromatin structure and thereby change how specific genes are interpreted and expressed. In this short review, we focus on describing how exercise influences the genome-wide DNA methylation pattern, including candidate genes for obesity and type 2 diabetes, in human adipose tissue.

scholarly journals Expression of caveolin-1 in human adipose tissue is upregulated in obesity and obesity-associated type 2 diabetes mellitus and related to inflammation

2007 ◽  
Vol 0 (0) ◽  
pp. 070907132242015-??? ◽  
Author(s):  
Victoria Catalán ◽  
Javier Gómez-Ambrosi ◽  
Amaia Rodríguez ◽  
Camilo Silva ◽  
Fernando Rotellar ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Caveolin 1

miR‐20b, miR‐296, and Let‐7f Expression in Human Adipose Tissue is Related to Obesity and Type 2 Diabetes

Obesity ◽  
2018 ◽  
Vol 27 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Adriana‐Mariel Gentile ◽  
Said Lhamyani ◽  
Leticia Coín‐Aragüez ◽  
Mercedes Clemente‐Postigo ◽  
Wilfredo Oliva Olivera ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Human Adipose Tissue

Vaspin gene expression in human adipose tissue: Association with obesity and type 2 diabetes

2006 ◽  
Vol 339 (1) ◽  
pp. 430-436 ◽  
Author(s):  
Nora Klöting ◽  
Janin Berndt ◽  
Susan Kralisch ◽  
Peter Kovacs ◽  
Mathias Fasshauer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Human Adipose Tissue

Altered Expression of Adrenomedullin 2 and its Receptor in the Adipose Tissue of Obese Patients

2019 ◽  
Vol 105 (3) ◽  
pp. e583-e596 ◽  
Author(s):  
Jimin Kim ◽  
Seul Ki Lee ◽  
Donguk Kim ◽  
Han Choe ◽  
Yeon Jin Jang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bariatric Surgery ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Receptor Expression ◽  
Receptor Complex ◽  
Obese Patients ◽  
Fat Depots ◽  
Receptor Component

Abstract Context Adrenomedullin 2 (AM2) plays protective roles in the renal and cardiovascular systems. Recent studies in experimental animals demonstrated that AM2 is an adipokine with beneficial effects on energy metabolism. However, there is little information regarding AM2 expression in human adipose tissue. Objective To investigate the pattern and regulation of the expression of AM2 and its receptor component in human adipose tissue, in the context of obesity and type 2 diabetes. Methods We measured metabolic parameters, serum AM2, and expression of ADM2 and its receptor component genes in abdominal subcutaneous and visceral adipose tissue in obese (with or without type 2 diabetes) and normal-weight women. Serum AM2 was assessed before and 6 to 9 months after bariatric surgery. Expression/secretion of AM2 and its receptor were assessed in human adipocytes. Results ADM2 mRNA in both fat depots was higher in obese patients, whether diabetic or not. Although serum AM2 was significantly lower in obese patients, it was not changed after bariatric surgery. AM2 and its receptor complex were predominantly expressed by adipocytes, and the expression of CALCRL, encoding a component of the AM2 receptor complex, was lower in both fat depots of obese patients. Incubating adipocytes with substances mimicking the microenvironment of obese adipose tissue increased ADM2 mRNA but reduced both AM2 secretion into culture media and CALCRL mRNA expression. Conclusions Our data indicate that AM2 signaling is suppressed in adipose tissue in obesity, involving lower receptor expression and ligand availability, likely contributing to insulin resistance and other aspects of the pathophysiology associated with obesity.

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