Kefir inhibits 3T3-L1 adipocyte differentiation through down-regulation of adipogenic transcription factor expression
Version of Record online: 20 JUL 2012
Copyright © 2012 Society of Chemical Industry
Journal of the Science of Food and Agriculture
Volume 93, Issue 3, pages 485–490, February 2013
How to Cite
Ho, J.-N., Choi, J.-W., Lim, W.-C., Kim, M.-K., Lee, I.-Y. and Cho, H.-Y. (2013), Kefir inhibits 3T3-L1 adipocyte differentiation through down-regulation of adipogenic transcription factor expression. J. Sci. Food Agric., 93: 485–490. doi: 10.1002/jsfa.5792
- Issue online: 28 JAN 2013
- Version of Record online: 20 JUL 2012
- Manuscript Accepted: 6 JUN 2012
- Manuscript Revised: 30 MAY 2012
- Manuscript Received: 31 MAY 2011
- glycerol-3-phosphate dehydrogenase (GPDH);
BACKGROUND: Kefir, a traditional fermented milk composed of microbial symbionts, is reported to have various health benefits such as anti-tumour, anti-inflammatory, anti-neoplastic and pro-digestive effects. In this study, to elucidate the effects of kefir on adipocyte differentiation and lipid accumulation, three fractions were prepared from kefir culture broth. The inhibitory effects of kefir liquid culture broth fraction (Fr-1), soluble fraction (Fr-2) and insoluble fraction (Fr-3), prepared by sonication of kefir solid culture broth, on adipocyte differentiation in 3T3-L1 preadipocytes were examined.
RESULTS: Fr-3 (0.1 mg mL−1) significantly decreased lipid accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity by 60 and 68% respectively without affecting cell viability. In addition, Fr-3 treatment down-regulated the mRNA expression of adipogenic transcription factors including C/EBPα (32%), PPARγ (46%) and SREBP-1c (34%) during adipocyte differentiation compared with untreated control cells. The mRNA expression of adipocyte-specific genes (aP2, FAS and ACC) was also clearly decreased.
CONCLUSION: The results suggest that the insoluble fraction of kefir (Fr-3) mediates anti-adipogenic effects through the inhibition of adipocyte differentiation, partly via suppression of the C/EBPα-, SREBP-1c- and PPARγ-dependent pathways. © 2012 Society of Chemical Industry