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Tschimganidine reduces lipid accumulation through AMPK activation and alleviates high-fat diet-induced metabolic diseases
Min-Seon Hwang1,2,# (Graduate student), Jung-Hwan Baek1,2,# (Research worker), Jun-Kyu Song1 (Research worker), In Hye Lee3 (Professor), Kyung-hee Chun1,2,* (Professor)
1Department of Biochemistry & Molecular Biology, Yonsei University College of Medicine,
2Brain Korea 21 PLUS Project for Medical Science, Yonsei University,
3Department of Life Science, College of Natural Science, Ewha Womans University
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 anti-obesity agent, which impedes adipogenesis and improves glucose homeostasis. Tschimganidine can then be evaluated for clinical application as a therapeutic agent.
Abstract, Accepted Manuscript(in press) [Submitted on December 29, 2022, Accepted on January 10, 2023]
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