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Tschimganidine reduces lipid accumulation through AMPK activation and alleviates high-fat diet-induced metabolic diseases

Authors
 Min-Seon Hwang  ;  Jung-Hwan Baek  ;  Jun-Kyu Song  ;  In Hye Lee  ;  Kyung-Hee Chun 
Citation
 BMB REPORTS, Vol.56(4) : 246-251, 2023-04 
Journal Title
BMB REPORTS
ISSN
 1976-6696 
Issue Date
2023-04
MeSH
3T3-L1 Cells ; AMP-Activated Protein Kinases / metabolism ; Adipocytes / metabolism ; Adipogenesis ; Animals ; Anti-Obesity Agents* / metabolism ; Anti-Obesity Agents* / pharmacology ; Anti-Obesity Agents* / therapeutic use ; Diabetes Mellitus, Type 2* / metabolism ; Diet, High-Fat / adverse effects ; Lipids ; Mice ; Mice, Inbred C57BL ; Obesity / drug therapy ; Obesity / metabolism
Abstract
Obesity increases the risk of mortality and morbidity because it results in hypertension, heart disease, and type 2 diabetes. Therefore, there is an urgent need for pharmacotherapeutic drugs to treat obesity. We performed a screening assay using natural products with anti-adipogenic properties in 3T3-L1 cells and determined that tschimganidine, a terpenoid from the Umbelliferae family, inhibited adipogenesis. To evaluate the anti-obesity effects of tschimganidine in vivo. Mice were fed either a normal chow diet (NFD) or a high-fat chow diet (HFD) with or without tschimganidine for 12 weeks. Treatment with tschimganidine decreased lipid accumulation and adipogenesis, accompanied by reduced expression of adipogenesis and lipid accumulation-related factors. Tschimganidine significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and decreased that of AKT. Depletion of AMPK relieved the reduction in lipid accumulation resulting from tschimganidine treatment. Moreover, tschimganidine administration drastically reduced the weight and size of both gonadal white adipose tissue (WAT) and blood glucose levels in high-fat diet-induced obese mice. We suggest that tschimganidine is a potent antiobesity agent, which impedes adipogenesis and improves glucose homeostasis. Tschimganidine can then be evaluated for clinical application as a therapeutic agent. [BMB Reports 2023; 56(4): 246-251].
Files in This Item:
T202303531.pdf Download
DOI
10.5483/bmbrep.2022-0211
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Baek, Jung Hwan(백정환) ORCID logo https://orcid.org/0000-0002-2250-1557
Chun, Kyung Hee(전경희) ORCID logo https://orcid.org/0000-0002-9867-7321
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/195540
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