이승훈 (한국기초과학지원연구원)

황금숙 (한국기초과학지원연구원)

이승훈 (한국기초과학지원연구원)

정영애 (한국기초과학지원연구원)

황금숙 (한국기초과학지원연구원)

Obesity is a metabolic disorder characterized by reduced energy expenditure, resulting from decreased UCP1-mediated thermogenesis in brown adipocytes and excessive lipid accumulation (whitening) in white adipocytes. A promising therapeutic approach involves the conversion (browning) of white adipocytes into thermogenic beige adipocytes. This study investigated lipidomic alterations induced by HET0016, a selective CYP4A inhibitor, in 3T3-L1 adipocytes under palmitate-induced obese conditions.

The experimental model was divided into three groups: obese control (OC), palmitate-treated obese (OPA), and palmitate + HET0016-treated obese (OPT). Lipid profiling was performed using Liquid Chromatography/Quadrupole-Time-of-Flight Mass Spectrometry (LC/Q-TOF MS).

Multivariate analysis revealed clear separation among the OC, OPA, and OPT groups in positive and negative ionization modes. A total of 320 lipid species in 19 lipid classes were identified. Three lipid classes including lysophosphatidylethanolamine (LysoPE), ether-linked phosphatidylcholine (PC-O) and sphingomyelin (SM) showed significant alterations following HET0016 treatment. Compositions of LysoPE were elevated under obese conditions and subsequently decreased following HET0016 treatment. In contrast, compositions of PC-O and SM decreased with obesity but were restored after treatment.

These results suggest that HET0016 may ameliorate obesity-associated lipid dysregulation by restoring levels of specific lipid classes such as LysoPE, PC-O and SM.

Such lipidomic alterations may therefore serve as potential biomarkers and therapeutic targets for the treatment of obesity.