# The Antioxidant Quercetin Affects Mitochondrial Function and Inhibits the Differentiation of Human Preadipocytes

**Authors:** Agnieszka Dziewońska, Anna Gruca, Anna Polus, Bogdan Solnica, Joanna Góralska

PMC · DOI: 10.3390/molecules31040725 · 2026-02-20

## TL;DR

Quercetin, an antioxidant, inhibits fat cell development and affects mitochondria, suggesting potential for obesity prevention.

## Contribution

The study reveals quercetin's novel impact on mitochondrial function and preadipocyte differentiation.

## Key findings

- Quercetin inhibits differentiation of human preadipocytes and reduces fat accumulation.
- Quercetin alters mitochondrial biogenesis and uncoupling, increasing mitochondrial membrane potential.
- Quercetin decreases routine respiration and related respiratory control ratios in preadipocytes.

## Abstract

Obesity is associated with numerous pathological processes in the body, including inflammation, oxidative stress, and consequently, mitochondrial dysfunction. In recent years, research in anti-obesity therapy has also focused on the function of adipocytes and the inhibition of adipogenesis. In this study, we investigated the effect of the well-known flavonoid quercetin on mitochondrial function, apoptosis and differentiation of human preadipocytes. The Chub-S7 cell line model was used in the in vitro studies. Mitochondrial function was measured by oxygen consumption rates, intracellular ATP content, mitochondrial membrane potential, apoptosis assay (Annexin-5, caspase-9 activity), and ROS generation. Chub-S7 cell differentiation was assessed by Oil Red O staining. The results showed that the quercetin inhibited differentiation of human Chub-S7 preadipocytes and reduced fat accumulation in lipid droplets. Additionally, quercetin influenced mitochondrial biogenesis and mitochondrial uncoupling by changes in mitochondrial respiratory states and also increased mitochondrial membrane potential. Quercetin decreased routine respiration, R/E and netROUTINE control ratio. Our results demonstrate that quercetin is a dietary component that may modulate mitochondrial bioenergetics and inhibit adipogenesis. If these results were confirmed in in vivo studies, quercetin could be considered a factor used to prevent obesity.

## Linked entities

- **Chemicals:** quercetin (PubChem CID 5280343)
- **Diseases:** obesity (MONDO:0011122)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** CASP9 (caspase 9) [NCBI Gene 426970] {aka caspase-9}, CASP9 (caspase 9) [NCBI Gene 842] {aka APAF-3, APAF3, ICE-LAP6, MCH6, PPP1R56}, ANXA5 (annexin A5) [NCBI Gene 308] {aka ANX5, CPB-I, ENX2, HEL-S-7, PP4, RPRGL3}
- **Diseases:** insulin resistance (MESH:D007333), cytotoxic (MESH:D064420), weight loss (MESH:D015431), hypertension (MESH:D006973), necrosis (MESH:D009336), breast cancer (MESH:D001943), adipose tissue dysfunction (MESH:D018205), type 2 diabetes (MESH:D003924), coronary artery ease (MESH:D003324), diabetic (MESH:D003920), cancer (MESH:D009369), metabolic syndrome (MESH:D024821), injury to (MESH:D014947), inflammation (MESH:D007249), mitochondrial dysfunction (MESH:D028361), dyslipidemia (MESH:D050171), metabolic disorders (MESH:D008659), Obesity (MESH:D009765), weight gain (MESH:D015430), stroke (MESH:D020521)
- **Chemicals:** carbonylcyanide (MESH:C100076), IBMX (MESH:D015056), dexamethasone (MESH:D003907), selenium (MESH:D012643), R (MESH:D001120), fatty acid (MESH:D005227), DMEM (-), H2O2 (MESH:D006861), Hepes (MESH:D006531), JC-1 (MESH:C068624), TG (MESH:D013866), proton (MESH:D011522), triiodothyronine (MESH:D014284), PBS (MESH:D007854), flavones (MESH:D047309), oligomycin (MESH:D009840), ROS (MESH:D017382), flavonoid (MESH:D005419), rotenone (MESH:D012402), luciferin (MESH:D000090562), ATP (MESH:D000255), Polyphenols (MESH:D059808), antimycin A (MESH:D000968), paraformaldehyde (MESH:C003043), Lipid (MESH:D008055), EDTA (MESH:D004492), CCCP (MESH:D002258), 3,5,7,3',4'-pentahydroxyflavone (MESH:D011794), 2',7'-dichlorodihydrofluorescein diacetate (MESH:C110400), triglyceride (MESH:D014280), ADP (MESH:D000244), D-luciferin (MESH:C532924), fat (MESH:D005223), Oxygen (MESH:D010100), PI (MESH:D010716), isopropanol (MESH:D019840), d-biotin (MESH:D001710), DTT (MESH:D004229), blood sugar (MESH:D001786), NaOH (MESH:D012972), FCCP (MESH:D002259), water (MESH:D014867), dichlorofluorescein (MESH:C037631), Oil Red O (MESH:C011049), free fatty acids (MESH:D005230), 2',7'-dichlorofluorescein diacetate (MESH:C029569)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]
- **Cell lines:** Chub-S7 — Homo sapiens (Human), Transformed cell line (CVCL_0239), C57BL/6J — Mus musculus (Mouse), Transformed cell line (CVCL_C0MW), 3T3-L1 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0123), MCF-7 — Homo sapiens (Human), Invasive breast carcinoma of no special type, Cancer cell line (CVCL_0031)

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12943750/full.md

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Source: https://tomesphere.com/paper/PMC12943750