3-Chloro-4,5-dihydroxybenzaldehyde inhibits adipogenesis in 3T3-L1 adipocytes by regulating expression of adipogenic transcription factors and AMPK activation
- Authors
- Kang, Min-Cheol; Ding, Yuling; Kim, Junseong; Kim, Eun-A; Fernando, I. P. Shanura; Heo, Soo-Jin; Lee, Seung-Hong
- Issue Date
- 1-May-2018
- Publisher
- Elsevier BV
- Keywords
- Adipogenesis; 3T3-L1; 3-Chloro-4,5-dihydroxybenzaldehyde; Anti-obesity; Adipocytes
- Citation
- Chemico-Biological Interactions, v.287, pp 27 - 31
- Pages
- 5
- Journal Title
- Chemico-Biological Interactions
- Volume
- 287
- Start Page
- 27
- End Page
- 31
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5976
- DOI
- 10.1016/j.cbi.2018.04.001
- ISSN
- 0009-2797
1872-7786
- Abstract
- Obesity is a serious health issue in many industrialized countries. It is a medical condition with excessive levels of fat accumulated in adipocytes. The objective of the present study was to determine the inhibitory effect of 3-chloro-4,5-dihydroxybenzaldehyde (CDB) on adipogenesis in 3T3-L1 adipocyte cells. CDB suppressed the differentiation and decreased lipid accumulation and triglycerides contents in 3T3-L1 adipocytes. Its suppression effect on fat accumulation was mediated via expression of adipogenesis factors (C/EBP alpha, SREBP-1c, PPAR gamma, and adiponectin) during adipocyte differentiation in white adipocyte cells. CDB's ability to suppress fat accumulation was increased in a concentration-dependent manner. It inhibited fatty acid synthesis related proteins including FAS, FABP4, leptin, and perilipin. It also increased expression of phosphorylated AMPK in adipocytes cells. These observations suggest that CDB has potential anti-obesity effect with ability to improve metabolic diseases.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Medical Sciences > Department of Pharmaceutical Engineering > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.