# Effects of Yomogi Tea on Lipid Metabolism in Renal Tubular HK-2 Cells

**Authors:** Wei Qin, Hsin-Jung Ho, Xun-Zhi Wu, Miki Eguchi, Manami Uchita, Minato Takeuchi, Shu-Ping Hui

PMC · DOI: 10.3390/foods14223817 · 2025-11-07

## TL;DR

Yomogi tea reduces lipid accumulation and lipotoxicity in kidney cells, suggesting it could help manage metabolic disorders like diabetic nephropathy.

## Contribution

This study demonstrates yomogi tea's novel regulatory effects on lipid metabolism and lipotoxicity in renal tubular cells.

## Key findings

- YL and YP significantly reduced intracellular triglyceride and free fatty acid levels in HK-2 cells.
- Yomogi tea downregulated FAS mRNA and upregulated ATGL mRNA, suggesting regulation of lipid metabolism.
- Treatment reduced lipid droplet size and neutral lipid content, potentially mitigating lipotoxic effects.

## Abstract

Excessive accumulation of lipid droplets (LDs), their dynamics, and lipotoxicity are critical factors in the progression of metabolic disorders, including diabetic nephropathy. This study investigates the effects of yomogi tea (Mugwort tea), specifically its leaf infusion (YL) and powdered infusion (YP), on lipid metabolism in human kidney proximal tubular epithelial HK-2 cells under lipotoxic conditions induced by palmitic acid (PA). Both YL and YP significantly reduced intracellular triglyceride (TG) and free fatty acid (FFA) levels, with YP showing a trend toward greater efficacy. Mechanistic analysis revealed that yomogi tea regulates lipid metabolism by significantly downregulating mRNA expression of FAS and upregulating that of the lipolytic ATGL, while SCD-1 mRNA expression remained largely unchanged. Furthermore, yomogi tea reduced LD size and neutral lipid content, potentially enhancing lipid hydrolysis efficiency and mitigating lipotoxic effects. These findings highlight the potential of yomogi tea as a natural agent for regulating lipid metabolism and reducing lipotoxicity, offering promise for managing lipid metabolism-related disorders.

## Linked entities

- **Genes:** FAS (Fas cell surface death receptor) [NCBI Gene 355], PNPLA2 (patatin like domain 2, triacylglycerol lipase) [NCBI Gene 57104], SCD (stearoyl-CoA desaturase) [NCBI Gene 6319]
- **Chemicals:** palmitic acid (PubChem CID 985), triglyceride (PubChem CID 5460048)
- **Diseases:** diabetic nephropathy (MONDO:0005016)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** PNPLA2 (patatin like domain 2, triacylglycerol lipase) [NCBI Gene 57104] {aka 1110001C14Rik, ATGL, FP17548, PEDF-R, TTS-2.2, TTS2}, SCD (stearoyl-CoA desaturase) [NCBI Gene 6319] {aka FADS5, MSTP008, SCD1, SCDOS, hSCD1}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}
- **Diseases:** diabetic nephropathy (MESH:D003928), metabolic disorders (MESH:D008659)
- **Chemicals:** YL (-), PA (MESH:D019308), Lipid (MESH:D008055), FFA (MESH:D005230), TG (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12651026/full.md

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Source: https://tomesphere.com/paper/PMC12651026