Funding agencies: Financial assistance from Capes, FAPEMIG and CNPq is gratefully acknowledged.
Acute and sustained inflammation and metabolic dysfunction induced by high refined carbohydrate-containing diet in mice
Article first published online: 21 MAY 2013
Copyright © 2012 The Obesity Society
Volume 21, Issue 9, pages E396–E406, September 2013
How to Cite
Oliveira, M. C., Menezes-Garcia, Z., Henriques, M. C. C., Soriani, F. M., Pinho, V., Faria, A. M. C., Santiago, A. F., Cara, D. C., Souza, D. G., Teixeira, M. M. and Ferreira, A. V. M. (2013), Acute and sustained inflammation and metabolic dysfunction induced by high refined carbohydrate-containing diet in mice. Obesity, 21: E396–E406. doi: 10.1002/oby.20230
Relevant conflicts of interest/financial disclosures: The authors declare no conflict of interest.
- Issue published online: 23 SEP 2013
- Article first published online: 21 MAY 2013
- Accepted manuscript online: 12 DEC 2012 11:15AM EST
- Manuscript Accepted: 18 NOV 2012
- Manuscript Received: 21 DEC 2011
- Financial assistance from Capes
- CNPq is gratefully acknowledged
The effects of high-refined carbohydrate-containing diet (HC) on inflammatory parameters and metabolic disarrangement of adipose tissue are poorly understood. The aim of this study was to evaluate the timing and progression of metabolic and inflammatory dysfunction induced by HC diet in mice.
Design and Methods
BALB/c mice were fed chow or HC diet for 1 and 3 days, 1, 2, 4, 6, 8, 10, and 12 weeks.
Animals given HC diet exhibited acute and sustained increase in visceral adiposity, glucose intolerance, low insulin sensitivity, hyperlipemia, acute increase in mRNA expression of ACC, LPL, PPARγ, SREBP-1, and ChREBP and altered circulating levels of adiponectin, resistin, and leptin. There was leucocyte rolling and adhesion on adipose tissue microvessels already at 3 days and until 8 weeks of HC diet. Adipose tissue of mice had increased number of macrophages (M1 and M2), lymphocytes (CD8+ and CD4+Foxp3+), and neutrophils (GR1+) already at 3 days after initiation of HC diet. Overall, concentration of cytokines and chemokines, TNF-α, IL-6, IL-10, TGF-β1, CCL2, and CXCL1, in adipose tissue was elevated throughout the experimental period. Levels of IL-10 and TGF-β1 tended to reach baseline levels at 12 weeks of HC diet.
We describe a novel murine model of fat pad expansion induced by HC diet that is characterized by early onset and sustained adipose tissue inflammation and metabolic disarrangement. The acute inflammatory response in adipose tissue occurs very early and is sustained, suggesting that adipose tissue inflammation is a homeostatic mechanism to regulate nutrient overload and adipose expansion.