Advanced search
1 file | 1.48 MB

Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance

(2012) DIABETES. 61(3). p.615-625
Author
Organization
Abstract
The stress protein heat shock protein 60 (Hsp60) induces secretion of proinflammatory mediators from murine adipocytes. This study aimed to study Hsp60 as a mediator of adipose tissue inflammation and skeletal muscle cell (SkMC) insulin sensitivity and to quantify plasma Hsp60 concentrations in lean and obese individuals. Regulation of Hsp60 release and Hsp60-induced cytokine secretion and signaling was measured in human adipocytes and SkMCs. Adipocytes exhibited higher Hsp60 release than preadipocytes and SkMCs, which was further stimulated by cytokines and Toll-like receptor (TLR)-4 activation. Hsp60 activated extracellular signal-related lcinase (ERK)-1/2, Jun NH2-terminal kinase (JNK), p38, nuclear factor (NF)-kappa B, and impaired insulin-stimulated Akt phosphorylation in adipocytes. Furthermore, Hsp60 stimulated adipocytes to secrete tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8. In SkMCs, Hsp60 activated ERK1/2, JNK, and NF-kappa B and inhibits insulin signaling and insulin-stimulated glucose uptake. SkMCs released IL-6, IL-8, and monocyte chemoattractant protein-1 on Hsp60 stimulation. Plasma Hsp60 was higher in obese males than in lean males and correlated positively with BMI, blood pressure, leptin, and homeostasis model assessment-insulin resistance. In summary, Hsp60 is released by human adipocytes, increased in plasma of obese humans, and induces insulin resistance. This is accompanied by activation of proinflammatory signaling in human adipocytes and SkMCs. Thus, Hsp60 might be a factor underlying adipose tissue inflammation and obesity-associated metabolic disorders.
Keywords
INNATE IMMUNE CELLS, HEAT-SHOCK PROTEINS, SKELETAL-MUSCLE, FAT-CELLS, RECEPTOR, OBESITY, HSP60, ADIPOCYTES, TRAFFICKING, MACROPHAGES

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 1.48 MB

Citation

Please use this url to cite or link to this publication:

Chicago
Märker, Tina, Henrike Sell, Pia Zillessen, Anja Glöde, Jennifer Kriebel, D Margriet Ouwens, Piet Pattyn, et al. 2012. “Heat Shock Protein 60 as a Mediator of Adipose Tissue Inflammation and Insulin Resistance.” Diabetes 61 (3): 615–625.
APA
Märker, T., Sell, H., Zillessen, P., Glöde, A., Kriebel, J., Ouwens, D. M., Pattyn, P., et al. (2012). Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance. DIABETES, 61(3), 615–625.
Vancouver
1.
Märker T, Sell H, Zillessen P, Glöde A, Kriebel J, Ouwens DM, et al. Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance. DIABETES. 2012;61(3):615–25.
MLA
Märker, Tina, Henrike Sell, Pia Zillessen, et al. “Heat Shock Protein 60 as a Mediator of Adipose Tissue Inflammation and Insulin Resistance.” DIABETES 61.3 (2012): 615–625. Print.
@article{3092677,
  abstract     = {The stress protein heat shock protein 60 (Hsp60) induces secretion of proinflammatory mediators from murine adipocytes. This study aimed to study Hsp60 as a mediator of adipose tissue inflammation and skeletal muscle cell (SkMC) insulin sensitivity and to quantify plasma Hsp60 concentrations in lean and obese individuals. Regulation of Hsp60 release and Hsp60-induced cytokine secretion and signaling was measured in human adipocytes and SkMCs. Adipocytes exhibited higher Hsp60 release than preadipocytes and SkMCs, which was further stimulated by cytokines and Toll-like receptor (TLR)-4 activation. Hsp60 activated extracellular signal-related lcinase (ERK)-1/2, Jun NH2-terminal kinase (JNK), p38, nuclear factor (NF)-kappa B, and impaired insulin-stimulated Akt phosphorylation in adipocytes. Furthermore, Hsp60 stimulated adipocytes to secrete tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8. In SkMCs, Hsp60 activated ERK1/2, JNK, and NF-kappa B and inhibits insulin signaling and insulin-stimulated glucose uptake. SkMCs released IL-6, IL-8, and monocyte chemoattractant protein-1 on Hsp60 stimulation. Plasma Hsp60 was higher in obese males than in lean males and correlated positively with BMI, blood pressure, leptin, and homeostasis model assessment-insulin resistance. In summary, Hsp60 is released by human adipocytes, increased in plasma of obese humans, and induces insulin resistance. This is accompanied by activation of proinflammatory signaling in human adipocytes and SkMCs. Thus, Hsp60 might be a factor underlying adipose tissue inflammation and obesity-associated metabolic disorders.},
  author       = {M{\"a}rker, Tina and Sell, Henrike and Zillessen, Pia and Gl{\"o}de, Anja and Kriebel, Jennifer and Ouwens, D Margriet and Pattyn, Piet and Ruige, Johannes and Famulla, Susanne and Roden, Michael and Eckel, J{\"u}rgen and Habich, Christiane},
  issn         = {0012-1797},
  journal      = {DIABETES},
  language     = {eng},
  number       = {3},
  pages        = {615--625},
  title        = {Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance},
  url          = {http://dx.doi.org/10.2337/db10-1574},
  volume       = {61},
  year         = {2012},
}

Altmetric
View in Altmetric
Web of Science
Times cited: