scholarly journals The C3a Anaphylatoxin Receptor Is a Key Mediator of Insulin Resistance and Functions by Modulating Adipose Tissue Macrophage Infiltration and Activation

Diabetes ◽  
2009 ◽  
Vol 58 (9) ◽  
pp. 2006-2017 ◽  
Author(s):  
Y. Mamane ◽  
C. Chung Chan ◽  
G. Lavallee ◽  
N. Morin ◽  
L.-J. Xu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

scholarly journals Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

2007 ◽  
Vol 117 (10) ◽  
pp. 2877-2888 ◽  
Author(s):  
Takashi Nomiyama ◽  
Diego Perez-Tilve ◽  
Daisuke Ogawa ◽  
Florence Gizard ◽  
Yue Zhao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

scholarly journals Blocking IL-6 trans-Signaling Prevents High-Fat Diet-Induced Adipose Tissue Macrophage Recruitment but Does Not Improve Insulin Resistance

2015 ◽  
Vol 21 (3) ◽  
pp. 403-416 ◽  
Author(s):  
Michael J. Kraakman ◽  
Helene L. Kammoun ◽  
Tamara L. Allen ◽  
Virginie Deswaerte ◽  
Darren C. Henstridge ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Tissue Macrophage ◽  
Macrophage Recruitment ◽  
Adipose Tissue Macrophage ◽  
Improve Insulin Resistance

scholarly journals Adipose tissue macrophage burden, systemic inflammation, and insulin resistance

2020 ◽  
Vol 319 (2) ◽  
pp. E254-E264 ◽  
Author(s):  
Qingyi Jia ◽  
Maria E. Morgan-Bathke ◽  
Michael D. Jensen
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Multivariate Regression ◽  
Metabolic Parameters ◽  
Model Assessment ◽  
Adipocyte Size ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

Adipose tissue inflammation, as defined by macrophage accumulation, is proposed to cause insulin resistance and systemic inflammation. Because the strength of this relationship for humans is unclear, we tested whether adipose tissue macrophage (ATM) burden is correlated with these health indicators. Using immunohistochemistry, we measured abdominal subcutaneous CD68+ (total ATM), CD14+ (proinflammatory/M1), and CD206+ (anti-inflammatory/M2) ATM in 97 volunteers (BMI 20–38 kg/m2, in addition to body composition, adipocyte size, homeostasis model assessment of insulin resistance, ADIPO-IR, adipose tissue insulin resistance measured by palmitate, plasma lipids, TNF, and IL-6 concentrations. There were several significant univariate correlations between metabolic parameters to IL-6 and ATM per 100 adipocytes, but not ATM per gram tissue; adipocyte size was a confounding variable. We used matching strategies and multivariate regression analyses to investigate the relationships between ATM and inflammatory/metabolic parameters independent of adipocyte size. Matching approaches revealed that the groups discordant for CD206 but concordant for adipocyte size had significantly different fasting insulin and IL-6 concentrations. However, groups discordant for adipocyte size but concordent for ATM differeded in that visceral fat, plasma triglyceride, glucose, and TNF concentrations were greater in those with large adipocytes. Multivariate regression analysis indicated that indexes of insulin resistance and fasting triglycerides were predicted by body composition; the predictive value of ATM per 100 adipocytes or per gram tissue was variable between males and females. We conclude that the relationship between ATM burden and metabolic/inflammatory variables is confounded by adipocyte size/body composition and that ATM do not predict insulin resistance, systemic inflammation, or dyslipidemia. ATM may primarily play a role in tissue remodeling rather than in metabolic pathology.

Abstract 81: Pharmacological Inhibition of Calpain Attenuates Adipose Tissue Apoptosis, Macrophage Accumulation and Inflammation in Diet-induced Obese Mice

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Venkateswaran Subramanian ◽  
Anju Balakrishnan ◽  
Deborah A Howatt ◽  
Jessica J Moorleghen ◽  
Wendy S Katz
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Obese Mice ◽  
Tissue Macrophage ◽  
Pharmacological Inhibition ◽  
Adipose Tissue Macrophage ◽  
Insulin Tolerance ◽  
Calpain Inhibition ◽  
Macrophage Accumulation

Background and Objective Obesity is associated with low-grade chronic inflammation and apoptosis that contributes to development of insulin resistance and other metabolic complications. Adipose tissue macrophages have been proposed as a link between obesity and insulin resistance. However, the mechanisms underlying these processes are not defined. Calpains are calcium-dependent neutral cysteine proteases that are essential for multiple cellular functions, such as cytoskeletal remodeling and apoptotic cell death. Recent studies have demonstrated that activated calpain promotes adipocyte differentiation in vitro, and enhances macrophage recruitment during nephropathy. However, the functional role of calpain activation in adipose tissue macrophage accumulation and obesity remains to be elucidated. The purpose of this study was to define whether pharmacological inhibition of calpain influences diet-induced obesity and adipose tissue macrophage accumulation in mice. Methods and Results Male C57BL/6 mice (8 weeks old; n=10 per group) were fed either low (10% kcal) or high (60% kcal) fat diet for 12 weeks. Calpeptin, a calpain inhibitor (2.5 mg/kg/day) or vehicle (DMSO) was administered daily by osmotic mini-pumps for 12 weeks. Calpeptin administration did not influence high fat diet induced body weight and fat mass gain throughout the study. Calpain inhibition had no effect on glucose and insulin tolerance in obese mice. However, calpain inhibition highly reduced adipocyte apoptosis, adipose tissue collagen and macrophage accumulation as evident by TUNEL, Picro Sirius and CD68 immunostaining. Real-time PCR analysis showed that calpain inhibition significantly suppressed inflammatory cytokines (TNFα, IL-6, MCP-1, F4/80) expression in adipose tissue (P<0.05 vs vehicle). In addition, Oil Red O staining revealed that calpain inhibition also suppressed accumulation of hepatic fat. Conclusion Pharmacological inhibition of calpain attenuated macrophage accumulation, adipocyte apoptosis, fibrosis and inflammation in diet-induced obese mice without influencing body weight gain and insulin tolerance.

scholarly journals Telmisartan Improves Insulin Resistance and Modulates Adipose Tissue Macrophage Polarization in High-Fat-Fed Mice

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1789-1799 ◽  
Author(s):  
Shiho Fujisaka ◽  
Isao Usui ◽  
Yukiko Kanatani ◽  
Masashi Ikutani ◽  
Ichiro Takasaki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Macrophage Polarization ◽  
High Fat ◽  
Adipose Tissues ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage ◽  
Visceral Adipose

Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor blocker and a peroxisome proliferator-activated receptor-γ agonist, reportedly has more beneficial effects on insulin sensitivity than other angiotensin II type 1 receptor blockers. In this study, we studied the effects of telmisartan on the adipose tissue macrophage phenotype in high-fat-fed mice. Telmisartan was administered for 5 wk to high-fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in visceral adipose tissues were then examined. An insulin- or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight, and adipocyte size without affecting the amount of energy intake. Telmisartan reduced the mRNA expression of CD11c and TNF-α, M1 macrophage markers, and significantly increased the expressions of M2 markers, such as CD163, CD209, and macrophage galactose N-acetyl-galactosamine specific lectin (Mgl2), in a quantitative RT-PCR analysis. A flow cytometry analysis showed that telmisartan decreased the number of M1 macrophages in visceral adipose tissues. In conclusion, telmisartan improves insulin sensitivity and modulates adipose tissue macrophage polarization to an antiinflammatory M2 state in high-fat-fed mice.

scholarly journals Angiopoietin Like Protein 2 (ANGPTL2) Promotes Adipose Tissue Macrophage and T lymphocyte Accumulation and Leads to Insulin Resistance

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0131176 ◽  
Author(s):  
Yusuke Sasaki ◽  
Masayuki Ohta ◽  
Dhruv Desai ◽  
Jose-Luiz Figueiredo ◽  
Mary C. Whelan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
T Lymphocyte ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage
Sign in / Sign up

Export Citation Format

Share Document