Korea University · Medicine
Professor Sung-Joon Lee's research lab focuses on molecular mechanisms underlying metabolic diseases, aging, and lipid homeostasis, with a particular emphasis on nuclear receptors such as PPAR-α and PPAR-γ as therapeutic targets. The lab investigates natural compounds—including resveratrol, ursolic acid, lemon balm essential oil, and azelaic acid—that modulate energy metabolism, insulin sensitivity, and lipolysis to combat obesity, type 2 diabetes, and cardiovascular diseases. Using integrative approaches combining molecular biology, transcriptomics, and in vivo models, the lab explores how phytochemicals and olfactory receptors in peripheral tissues regulate systemic metabolism. A key research direction involves identifying novel ligands and signaling pathways that rewire lipid metabolism to improve metabolic health.
Figures are computed from collected data and may differ slightly.
Aging gradually decreases cellular biological functions and increases the risk of age-related diseases. Cancer, type 2 diabetes mellitus, cardiovascular disease, and neurological disorders are commonly classified as age-related diseases that can affect the lifespan and health of individuals. Aging is a complicated and sophisticated biological process involving damage to biochemical macromolecules including DNA, proteins, and cellular organelles such as mitochondria. Aging causes multiple alterat
LDL with apoCIII strongly predicts coronary events in diabetic patients independently of other lipids and may be an atherogenic remnant of triglyceride-rich VLDL metabolism.
The antioxidant activity of lemon balm ( Melissa officinalis ) essential oil (LBEO) on 2,2-diphenyl-1-picrylhydrazyl (DPPH) radicals and its hypoglycaemic effect in db / db mice were investigated. LBEO scavenged 97 % of DPPH radicals at a 270-fold dilution. Mice administered LBEO (0·015 mg/d) for 6 weeks showed significantly reduced blood glucose (65 %; P < 0·05) and TAG concentrations, improved glucose tolerance, as assessed by an oral glucose tolerance test, and significantly higher serum i
Olfactory receptors (ORs) are present in tissues outside the olfactory system; however, the function of these receptors remains relatively unknown. Here, we determined that olfactory receptor 544 (Olfr544) is highly expressed in the liver and adipose tissue of mice and regulates cellular energy metabolism and obesity. Azelaic acid (AzA), an Olfr544 ligand, specifically induced PKA-dependent lipolysis in adipocytes and promoted fatty acid oxidation (FAO) and ketogenesis in liver, thus shifting th
AX is a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
In this study, we confirmed that ursolic acid, a plant triterpenoid, activates peroxisome proliferator-activated receptor (PPAR)-α in vitro. Surface plasmon resonance and time-resolved fluorescence resonance energy transfer analyses do not show direct binding of ursolic acid to the ligand-binding domain of PPAR-α; however, ursolic acid enhances the binding of PPAR-α to the peroxisome proliferator response element in PPAR-α-responsive genes, alters the expression of key genes in lipid metabolism,
We investigated hypocholesterolemic mechanisms of linalool, an aromatic anti-oxidative monoterpene, which is abundant in teas and essential oils. Oral administration of linalool to mice for 6 weeks significantly lowered total and low-density lipoprotein cholesterol concentrations, and HMG-CoA reductase protein expression (-46%; P<0.05) by both transcriptional and posttranscriptional mechanisms. Linalool suppressed the gene expression of HMG-CoA reductase by reducing the binding of SREBP-2 to its
Metallothioneins (MTs) are small, cysteine-rich zinc binding proteins that are powerful antioxidants. In this study, we investigated the interaction between zinc, MTs, and other components of the antioxidant defense system in HepG2 cells. Cells were preincubated with zinc and then exposed to sodium nitroprusside (SNP), a nitric oxide (NO) donor. Both zinc pretreatment and SNP exposure separately induced transcription of MT genes (MT1A, MT2A, MT1E, MT1X), as measured using real time-polymerase ch
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