Chito-Oligosaccharide Inhibits the De-Methylation of a CpG Island within the Leptin (LEP) Promoter during Adipogenesis of 3T3-L1 Cells

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Title: Chito-Oligosaccharide Inhibits the De-Methylation of a CpG Island within the Leptin (LEP) Promoter during Adipogenesis of 3T3-L1 Cells
Authors: Bahar, Bojlul
O'Doherty, John
O'Doherty, Alan
Sweeney, Torres
Permanent link: http://hdl.handle.net/10197/6500
Date: 27-Mar-2013
Abstract: Chito-oligosaccharide (COS) is a natural bioactive compound, which has been shown to suppress lipid metabolic genes and lipid accumulation in differentiating adipocytes. Leptin has been identified as a key regulator of energy homeostasis and is known to be under epigenetic regulation during adipogenesis. Hence, the first objective of this experiment was to compare leptin gene (LEP) expression and leptin secretion during the different stages of adipogenesis and to investigate the effect of COS on these processes. As COS inhibited LEP expression during adipogenesis, the second aim was to investigate the methylation dynamics of a ¿CpG¿ island in the proximal region of the LEP promoter during adipogenesis and to determine the effect of COS on this process. Mouse 3T3-L1 cells were stimulated to differentiate in the absence or presence of COS and the levels of leptin mRNA and protein were evaluated on days 0, 2, 4 and 6 post-induction of differentiation (PID). The extent of de-methylation of six CpG sites was evaluated. LEP mRNA transcript and protein could not be detected on either day 0PID or 2PID. In contrast, both were detected on day 4PID (P<0.05) and 6PID (P<0.001) and both were inhibited by COS (P<0.001). Of the six CpG sites analyzed, CpG_52, CpG_62 and CpG_95 became 11.5, 5.0 and 5.0% de-methylated between day 2PID and 6PID, respectively. COS blocked this de-methylation event at CpG_52 (P<0.001), CpG_62 (P<0.01) and CpG_95 (P<0.01) on day 6PID. These data suggest that COS can have an epigenetic effect on differentiating adipocytes, a novel biological function of COS which has potential applications for the manipulation of leptin gene expression, adipogenesis, and conditions within the metabolic syndrome spectrum.
Funding Details: Department of Agriculture, Food and the Marine
Type of material: Journal Article
Publisher: Public Library of Science
Copyright (published version): 2013 the Authors
Keywords: Obesity;Adipogenesis;LEP gene expression;Leptin secretion;Conserved methylation sites (CpG);Chito-oligosaccharide (COS)
DOI: 10.1371/journal.pone.0060011
Language: en
Status of Item: Peer reviewed
Appears in Collections:Medicine Research Collection
Agriculture and Food Science Research Collection
Veterinary Medicine Research Collection

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