Silk peptides inhibit adipocyte diferentiation through modulation of the Notch pathway in C3H10T1/2 cells

Title
Silk peptides inhibit adipocyte diferentiation through modulation of the Notch pathway in C3H10T1/2 cells
Authors
정소라송노준황현숙안재진조용준권해영Seok-Woo Kang이광길윤기정김병준노주원최수영박계원
Keywords
silk peptide; adipocyte differentiation; notch pathway; obesity; PPARγ; C3H10T1/2 cells
Issue Date
2011-09
Publisher
Nutrition research
Citation
VOL 31, NO 9, 723-730
Abstract
Silk protein is a biocompatible material that has been used in many biotechnological applications and exhibits body fat–lowering effects. Recent studies have shown that silk peptides increase expression of osteogenic markers in osteoblast-like cells. Because osteogenic and adipogenic differentiation from common mesenchymal progenitor cells are inverse processes and often regulated reciprocally, we hypothesized that silk peptides might suppress adipocyte differentiation. We therefore endeavored to evaluate the effects of silk peptides on adipocyte differentiation in C3H10T1/2 cells. We find that silk peptides inhibit lipid accumulation and morphological differentiation in these cells. Molecular studies show that silk peptides block expression of adipocyte-specific genes such as peroxisome proliferator-activated receptor γ and its targets, including aP2, Cd36, CCAAT enhancer binding protein α. Silk peptides appear to inhibit adipogenesis by suppression of the Notch pathway, repressing the Notch target genes Hes-1 and Hey-1. In addition, these peptides inhibit endogenous Notch activation, as shown by a reduction in generation of Notch intracellular domain. N-[N-(3.5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butylester, compound E, and WPE-III-31C, which are all known Notch signaling inhibitors, block adipocyte differentiation to an extent similar to silk peptides. Together, our data demonstrate that silk peptides can modulate adipocyte differentiation through inhibition of the Notch signaling and further suggest potential future strategies for treating obesity and its related metabolic diseases.
URI
http://pubs.kist.re.kr/handle/201004/41084
ISSN
0271-5317
Appears in Collections:
KIST Publication > Article
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