2. Academic Validation
  3. 1,2-Dilinoleoyl-sn-glycero-3-phosphocholine increases insulin sensitivity in palmitate-treated myotubes and induces lipolysis in adipocytes

1,2-Dilinoleoyl-sn-glycero-3-phosphocholine increases insulin sensitivity in palmitate-treated myotubes and induces lipolysis in adipocytes

  • Biochem Biophys Res Commun. 2020 Nov 26;533(1):162-167. doi: 10.1016/j.bbrc.2020.09.019.
Jinwoo Park 1,  Tae Woo Jung 1,  Yoon Hee Chung 2,  Eon Sub Park 3,  Ji Hoon Jeong 4
Affiliations

Affiliations

  • 1 Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
  • 2 Department of Anatomy, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
  • 3 Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea; Department of Global Innovative Drug, the Graduate School of Chung-Ang University, Seoul, Republic of Korea; Department of Pathology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea. Electronic address: esp@cau.ac.kr.
  • 4 Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea; Department of Global Innovative Drug, the Graduate School of Chung-Ang University, Seoul, Republic of Korea. Electronic address: jhjeong3@cau.ac.kr.
PMID: 32943187 DOI: 10.1016/j.bbrc.2020.09.019
Abstract

Obesity causes the development of Insulin resistance and type 2 diabetes. Phosphatidylcholine (PPC) has been reported to increase hepatic Insulin sensitivity and lipolysis in adipose tissue to resolve local obesity. In this study, we proposed 1,2-dilinoleoyl-sn-glycero-3-phosphocholine (DLPC), the main active species of PPC, as an effective substance for the treatment of obesity-mediated disorders such as impaired fat metabolism and Insulin resistance. Therefore, we investigated the potential lipolytic effects of DLPC on adipocytes and Insulin signaling in muscle cells. In this study, DLPC-treated 3T3-L1 adipocytes showed enhanced tumor necrosis factor α (TNF-α) release. Suppression of TNF-α by short interfering RNA (siRNA) mitigated DLPC-induced lipolysis and Apoptosis. DLPC treatment increased Peroxisome Proliferator-activated Receptor α (PPARα) expression levels in C2C12 myocytes. siRNA-mediated suppression of PPARα abrogated the suppressive effects of DLPC on palmitate-induced inflammation and Insulin resistance. In conclusion, DLPC enhanced lipolysis and Apoptosis via a TNFα-dependent pathway in adipocytes and attenuated palmitate-induced Insulin resistance through PPARα-mediated suppression of inflammation in myocytes.

Keywords

3T3-L1 adipocyte; C2C12 myocyte; DLPC; PPARα; PPC; TNFα.

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