Strenuous Exercise and Quercetin Supplementation Differentially Alter Lipid Metabolism in C57BL/6J Mice

Halleh Shafiy; Badia Nourti; Mahdi Garelnabi

doi:10.12997/jla.2026.15.3.519

. 2026 May 13;15(3):519–532. doi: 10.12997/jla.2026.15.3.519

Strenuous Exercise and Quercetin Supplementation Differentially Alter Lipid Metabolism in C57BL/6J Mice

Halleh Shafiy ¹, Badia Nourti ¹, Mahdi Garelnabi ^1,^✉

PMCID: PMC13620183 PMID: 42812474

Abstract

Objective

While moderate exercise improves lipid profiles, strenuous activity can increase oxidative stress, highlighting the potential role of antioxidants. Quercetin, a polyphenol with both antioxidant and lipid-regulating effects, may counteract exercise-induced oxidative damage and influence cholesterol metabolism. This study investigates whether combining strenuous exercise with quercetin supplementation produces distinct effects on lipoprotein remodeling, offering insights into integrative approaches for reducing cardiovascular disease risk.

Methods

Forty C57BL/6 LDLr+/+ mice were randomly assigned to 4 groups (n=10): control with no exercise or quercetin (C), quercetin supplementation without exercise (Q), exercise without quercetin (E), and combined exercise with quercetin (EQ). All groups received a high-fat diet consisting of 42% fat and 1.5% cholesterol, formulated without added antioxidants. After 2 months, the mice were euthanized, and liver tissues were collected for gene expression analysis of ATP-binding cassette transporter A1 (ABCA1), proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTL) 3, ANGPTL4, peroxisome proliferator-activated receptor (PPAR) γ, apolipoprotein (APO) CIII, and APO A5 using quantitative real-time polymerase chain reaction.

Results

EQ produced the most pronounced alterations in metabolic markers and lipid-regulating genes. Both Q and EQ groups showed significantly elevated total cholesterol, high-density lipoprotein, triglycerides, and glucose compared with controls, while all treated groups exhibited reduced plasma lipase levels (p<0.05). EQ induced a significant downregulation of ABCA1 and PPARγ (p<0.05). PCSK9 messenger RNA expression rose in Q and EQ, reaching significance only in EQ, and adiponectin levels were significantly elevated in both E and EQ (p<0.05).

Conclusion

Hepatic lipoprotein expression was modulated by the combined effects of quercetin supplementation and exercise. The observed reductions in ABCA1 and PCSK9 expressions may reflect a feedback response to enhanced clearance of circulating cholesterol.

Keywords: Quercetin, Exercise, Lipoproteins, Atherosclerosis, Cardiovascular disease

INTRODUCTION

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, underscoring the urgent need for preventive strategies that go beyond pharmacological interventions.¹,²,³ Among lifestyle-based approaches, physical activity represents one of the most potent modulators of cardiovascular health. Large-scale epidemiological studies and clinical trials have consistently shown that regular exercise lowers the incidence and progression of CVD by attenuating major risk factors such as hypertension, insulin resistance, obesity, and dyslipidemia.⁴,⁵,⁶,⁷,⁸,⁹ Mechanistically, exercise enhances vascular homeostasis, improves endothelial function, and promotes favorable alterations in lipoprotein metabolism. In preclinical models, exercise training reduces atherosclerotic plaque burden and shifts lipoprotein profiles toward a less atherogenic distribution, in part through enhanced reverse cholesterol transport, increased antioxidant enzyme activity, and suppression of systemic inflammation.¹⁰

Despite these benefits, the cardiometabolic effects of exercise are not uniform across all intensities or durations. Moderate physical activity is generally associated with improvements in lipid profiles, including reductions in low-density lipoprotein cholesterol (LDL-C) and elevations in high-density lipoprotein cholesterol (HDL-C), changes that contribute to a protective cardiovascular phenotype.¹¹ In contrast, strenuous or prolonged exercise can present a paradox: while it improves aerobic capacity and metabolic efficiency, it may simultaneously induce oxidative stress through the excessive generation of reactive oxygen species (ROS). These ROS can impair endothelial function, promote lipid peroxidation, and alter lipoprotein metabolism in complex ways that may both attenuate and exacerbate atherogenic processes.¹² This duality highlights the importance of understanding exercise intensity–dependent effects on lipid metabolism and cardiovascular risk.

Parallel to the role of exercise, dietary antioxidants have drawn considerable interest for their capacity to mitigate oxidative stress, one of the central mechanisms driving lipid peroxidation and atherosclerosis progression. Antioxidants function primarily by neutralizing ROS, thereby stabilizing lipids, protecting cellular membranes, and preserving endothelial integrity.⁹ α-Tocopherol (vitamin E), a lipid-soluble antioxidant found abundantly in plant oils, nuts, seeds, and leafy vegetables, has been extensively studied in both humans and animal models. However, despite its theoretical benefits, clinical evidence suggests that α-tocopherol provides limited additional protection when combined with exercise, raising questions about the effectiveness of conventional antioxidant supplementation in this context.⁹,¹³

In recent years, attention has turned toward polyphenolic compounds such as quercetin, a flavonoid abundant in fruits and vegetables and noted for its antioxidant and anti-inflammatory properties. Beyond classical free-radical scavenging, quercetin modulates key pathways relevant to lipid regulation, including chelation of oxidized iron that drives lipid peroxidation and modulation of hepatic enzymes, ATP-binding cassette transporters, and peroxisome proliferator-activated receptors (PPARs) involved in lipid synthesis, catabolism, and cholesterol efflux.¹⁴,¹⁵,¹⁶,¹⁷ These diverse mechanisms suggest that quercetin may influence lipoprotein remodeling more comprehensively than traditional antioxidants.

Despite substantial evidence that both strenuous exercise and dietary antioxidants independently affect lipid metabolism, their combined effects remain poorly understood. Strenuous exercise elevates oxidative stress and alters lipoprotein dynamics, while quercetin may buffer oxidative damage and shift lipid-regulating pathways. Yet it is unclear whether these processes interact synergistically to enhance lipid regulation, counteract one another by blunting adaptive responses, or operate through distinct mechanisms. Clarifying these interactions is essential for understanding how quercetin shapes lipoprotein subclass remodeling under physiological stress and how such changes might influence atherosclerosis risk.

On this basis, we hypothesized that combining quercetin supplementation with strenuous exercise would synergistically alter lipid metabolism and the hepatic expression of genes regulating lipoprotein synthesis and clearance.

MATERIALS AND METHODS

1. Animals

All animal experiments were conducted in accordance with the Public Health Service Policy on the Use of Laboratory Animals and complied with the U.S. National Institutes of Health Guide for the Care and Use of Laboratory Animals. The experimental protocol was further reviewed and approved by the Institutional Animal Care and Use Committee (IACUC) at the University of Massachusetts Lowell, titled “Benefits of exercise and flavonoids supplement in cardiovascular disease” (IACUC protocol #11-06-04-Gar).

All animals were fed a high-fat diet containing 1.5% cholesterol as part of a 42% fat diet without antioxidants (Cat.: TD.110489; Harlan Laboratories). Animals were exposed and acclimatized to the housing facility prior to the start of the experiment.

2. Materials

Quercetin was purchased from Cayman Chemicals. Gene expression reagents SYBR^® Green Supermixes, SsoAdvanced™ and EvaGreen were purchased from Bio-Rad Laboratories, Inc. Primers were designed and purchased along with TRIzol^® from Life Technologies. All other chemicals and reagents were purchased from Sigma-Aldrich Chemical Co.

3. Animals and experimental design

Forty C57BL/6J 4-week-old male mice were obtained from Jackson Laboratory. Mice were housed under standard laboratory conditions (12-hour light/dark cycle, controlled temperature and humidity, ad libitum access to food and water) and allowed to acclimate for 1 week prior to the study. Animals were randomly assigned to 4 experimental groups (n=10 per group): control (C; no exercise, no quercetin), quercetin only (Q; no exercise, quercetin), exercise only (E; exercise, no quercetin), and exercise plus quercetin (EQ; exercise, quercetin).

A group size of 10 mice was chosen to balance statistical power with ethical use of animals. Previous studies examining the effects of polyphenol supplementation and/or exercise on lipoprotein metabolism and oxidative stress in mice have typically used 8–12 animals per group to detect biologically meaningful differences in lipid profiles and related biomarkers. On this basis, 10 mice per group was considered sufficient to capture expected variability in lipoprotein subclasses and oxidative measures, while allowing for limited attrition over the course of the exercise and supplementation protocol.

4. Quercetin supplementation

Mice in the Q and EQ groups received 100 μg of quercetin dissolved in water containing 1% sodium lauryl sulfate (SLS). Controls not on quercetin received only SLS. The solution (100 μL) was administered orally using a pipette while mice were gently restrained in an upright position. Supplementation was provided once daily, 5 days per week, for 2 months. Administration occurred 30 minutes prior to exercise in the EQ group.

Quercetin dose justification

Mice received 100 µg of quercetin per day, corresponding to approximately 4 mg/kg/day for an adult mouse weighing 25 g. This dose was selected to provide a physiologically relevant, sub-pharmacologic exposure while remaining well below levels commonly used in rodent studies (25–100 mg/kg/day) that have demonstrated metabolic effects without overt toxicity.¹⁸ Based on standard body surface area-based allometric scaling (Km mouse=3, Km human=37), this regimen translates to a human equivalent dose of ~0.32 mg/kg, or ~19 mg/day for a 60-kg adult¹⁹ which lies within the range achievable by dietary intake and low-dose supplementation. Thus, the chosen dose is sufficient to engage quercetin’s proposed antioxidant and lipid-modulating pathways while preserving translational relevance to habitual human exposure.

5. Exercise protocol

Mice, assigned to the E and EQ groups, performed treadmill running (Columbus Instruments) for 30 minutes per day at a constant speed of 30 m/min. Exercise was conducted 5 days per week for 2 months. Control animals (C and Q groups) were handled similarly to minimize nonspecific stress effects.

6. Animal sacrifice and tissue collection

At the conclusion of the experimental period, mice were fasted overnight with free access to water prior to sacrifice. Animals were anesthetized with an intraperitoneal injection of ketamine (100 mg/kg) and xylazine (10 mg/kg) to ensure deep anesthesia, and the absence of reflex responses was confirmed prior to tissue collection. Terminal blood samples were obtained via cardiac puncture, followed by exsanguination. Subsequently, euthanasia was completed by cervical dislocation in accordance with the recommendations of the American Veterinary Medical Association (AVMA) Guidelines for the Euthanasia of Animals.

Following sacrifice, liver, heart, skeletal muscle, brain, and adipose tissues were rapidly excised, rinsed in ice-cold phosphate-buffered saline (PBS), and blotted dry. Portions of each tissue were either snap-frozen in liquid nitrogen and stored at −80°C for molecular analyses or fixed in 10% neutral buffered formalin for histological examination. Plasma was isolated from whole blood by centrifugation at 3,000 × g for 15 minutes at 4°C and stored at −80°C until biochemical assays were performed.

All procedures were conducted in compliance with the U.S. Public Health Service Policy on Humane Care and Use of Laboratory Animals and were approved by the IACUC of The University of Massachusetts Lowell. Efforts were made to minimize animal suffering and to use the minimum number of animals required to achieve statistical significance.

7. Plasma lipids and glucose measurements

Ethylenediaminetetraacetic acid (EDTA) Plasma samples were analyzed to quantify low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), and glucose concentrations. Measurements were performed using standardized enzymatic reagents and calibration standards obtained from Medica Corporation. All assays were conducted on a Medica EasyRA clinical chemistry autoanalyzer (Medica Corporation), following the manufacturer’s recommended protocols to ensure accuracy, precision, and reproducibility of lipid and metabolic assessments.

8. Plasma lipase measurements

Lipase activity in EDTA plasma samples was measured using a commercially available enzyme-linked immunosorbent assay kit (Abcam). The assay was performed strictly according to the manufacturer’s protocol to ensure consistency, accuracy, and reproducibility of the measurements, the assay was conducted using BioTek Microplate Reader (Agilent).

9. Quantitative real-time polymerase chain reaction (qPCR)

Liver tissue samples were collected immediately after sacrifice, rinsed briefly in ice-cold PBS to remove excess blood, and homogenized in TRIzol reagent (Invitrogen) using a motorized tissue homogenizer under RNase-free conditions. Homogenization was performed on ice to minimize RNA degradation. Total RNA was then extracted according to the manufacturer’s instructions.

RNA concentration and purity were determined spectrophotometrically by measuring absorbance at 260/280 nm, and integrity was confirmed by agarose gel electrophoresis. Between 10 and 100 ng of high-quality RNA was reverse transcribed into complementary DNA (cDNA) using a BioRad High-Capacity cDNA Reverse Transcription Kit.

One-twentieth of the synthesized cDNA was subsequently used as template for qPCR amplification. Reactions were performed with the SYBR^® Green on a Bio-Rad iCycler iQ5 Multicolor Real-Time PCR Detection System iQ5 Optical Module. Cycling conditions included an initial denaturation step, followed by 40 amplification cycles of denaturation, annealing, and extension. Melt-curve analysis was carried out at the end of each run to confirm the specificity of amplification products.

Relative messenger RNA (mRNA) expression levels were quantified using the comparative threshold cycle (ΔΔCt) method, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) serving as the internal reference gene. Primer specificity was validated by single-peak melting curves, and amplification efficiencies were verified to fall within the acceptable range (90–110%). Each reaction was performed in triplicate, and no-template controls were included to rule out contamination.

10. Statistical analysis for gene expression data

Gene expression data were analyzed following normalization to housekeeping genes (GAPDH). Relative transcript abundance was calculated using the ΔΔCt method, and results were expressed as fold change relative to control groups. Normalization and fold-change calculations were performed using Bio-Rad iCycler iQ5 Manager.

Data were evaluated for normality using the Shapiro Wilk test and for homogeneity of variance using Levene’s test. For normally distributed data, differences between groups were assessed using 1- or 2-way analysis of variance, as appropriate, followed by Tukey’s post hoc test for multiple comparisons.

All statistical analyses were performed using SPSS 20 software (IBM Corp.). Data are presented as mean ± standard error of the mean unless otherwise stated. A threshold of p<0.05 was considered statistically significant.

RESULTS

Plasma lipid and glucose levels, presented in Fig. 1, showed changes in response to exercise and quercetin intake. TC was significantly higher in the Q and EQ groups compared to the control. Notably, these 2 groups also exhibited elevated levels of HDL, triglycerides (TG), and glucose relative to the control.

Lipase enzyme levels were significantly decreased (p<0.05) in all groups compared to the control (Fig. 2).

The EQ treatment group demonstrated a pronounced downregulation of ATP-binding cassette transporter A1 (ABCA1) gene expression relative to the control group (p<0.05). ABCA1 plays a critical role in cholesterol efflux and HDL biogenesis, and its suppression in the EQ group may indicate impaired lipid export from hepatocytes. In comparison, the Q and E groups also exhibited reductions in ABCA1 expression, but these changes were modest and did not reach statistical significance, suggesting that the combined treatment (EQ) exerted a stronger suppressive effect than either agent alone (Fig. 3).

Fig. 3 — ABCA1, ATP-binding cassette transporter A1; mRNA, messenger RNA.

^*p<0.05 calculated by analysis of variance.

As illustrated in Fig. 4, the expression pattern of PPARγ showed significantly reduced mRNA levels in both the E and EQ groups when compared to controls (p<0.05). Given that PPARγ is a nuclear receptor involved in regulating adipogenesis, insulin sensitivity, and lipid metabolism, this downregulation implies that E and EQ treatments may dampen transcriptional activity linked to lipid storage and glucose utilization.

Apolipoprotein (APO) CIII was significantly upregulated in the Q and EQ groups relative to the control (Fig. 5), while APO A5 was significantly downregulated in the same groups (Fig. 6). APO CIII is known to inhibit TG clearance, whereas APO A5 facilitates TG hydrolysis. The opposing regulation of these apolipoproteins suggests a shift toward impaired TG metabolism and clearance, particularly in the EQ group, which may contribute to dyslipidemic changes.

Fig. 6 — APO A5, apolipoprotein A5; mRNA, messenger RNA.

^*p<0.05 calculated by analysis of variance.

Angiopoietin-like protein 3 (ANGPTL3; Fig. 7) expression was elevated in the EQ group, whereas angiopoietin-like protein 4 (ANGPTL4; Fig. 8) was significantly suppressed relative to the control group. Both proteins play key roles in modulating lipoprotein lipase (LPL) activity, with ANGPTL3 acting as an inhibitor and ANGPTL4 providing context-dependent regulation. The concurrent upregulation of ANGPTL3 and downregulation of ANGPTL4 in the EQ group points toward a net inhibitory effect on LPL activity, which could exacerbate hypertriglyceridemia.

Apolipoprotein analysis further highlighted divergent regulatory effects of the treatments. The angiopoietin-like proteins exhibited a similar pattern of opposing regulation.

The regulation of proprotein convertase subtilisin/kexin type 9 (PCSK9) (Fig. 9) revealed a complex and somewhat paradoxical outcome. At the transcriptional level, PCSK9 mRNA expression increased in both the Q and EQ groups, with the increase reaching statistical significance only in the EQ group (p<0.05).

Finally, adiponectin mRNA levels in adipose significantly increased in E and EQ (p<0.05) compared to the control or the quercetin only groups (Fig. 10).

Together, these findings reveal a consistent pattern in which the EQ treatment group demonstrates the most pronounced and often adverse alterations in lipid-related gene and protein expression. The downregulation of ABCA1 and PPARγ, along with the opposing regulation of APO CIII/APO A5 and ANGPTL3/ANGPTL4, indicates a coordinated shift toward reduced lipid clearance, impaired cholesterol efflux, and disrupted TG metabolism. The paradoxical regulation of PCSK9 at the mRNA and protein levels further underscores the complexity of post-transcriptional control in hepatic lipid pathways.

In summary, the EQ combination appears to exert synergistic but detrimental effects on hepatic lipid homeostasis, amplifying disruptions in lipid metabolism responses beyond those observed with E or Q treatments alone.

DISCUSSION

In this study, we demonstrate that quercetin supplementation and strenuous exercise, particularly when administered concurrently over a two-month period, exert significant and unexpectedly adverse effects on lipid and glucose metabolism. While each intervention alone produced measurable metabolic changes, the combined treatment (EQ) consistently elicited the most detrimental outcomes, including elevations in plasma cholesterol, HDL-C, TG, and glucose. These systemic responses were accompanied by reduced lipase activity and a coordinated dysregulation of key genes governing lipid transport, efflux, and TG hydrolysis. Together, these findings indicate that quercetin profoundly modifies exercise-induced metabolic adaptations in directions that impair lipid handling rather than improve it.¹⁸,¹⁹,²⁰,²¹,²²

The observed lipid-raising effects of quercetin both alone and in combination with exercise contrast with numerous reports describing quercetin as lipid-lowering, anti-oxidative, and insulin-sensitizing.²² Prior studies have shown that quercetin upregulates ABCA1 and promotes cholesterol efflux in macrophages, whereas aerobic exercise reliably enhances ABCA1 expression and improves plasma lipid profiles.²³,²⁴ Contrary to these findings, our combined EQ intervention markedly reduced ABCA1 expression and resulted in higher circulating lipid levels after 2 months of treatment.

Similar discrepancies emerged across the TG-regulatory network. Whereas APO CIII upregulation and APO A5 suppression are consistent with classical models of impaired TG clearance, the pattern of ANGPTL3 and ANGPTL4 expression did not fully align with established mechanisms of LPL inhibition.²⁵ The transcriptional upregulation of PCSK9 in the Q and EQ groups also mirrors findings from exercise-based studies, yet the marked reduction in PCSK9 protein in EQ animals suggests altered post-transcriptional or secretory regulation.²⁶,²⁷ Furthermore, although adiponectin expression increased in exercise-treated groups, this response did not translate into improved lipid or glucose handling, diverging from the authors’ previous findings in LDL receptor deficient models.²⁸ Overall, these inconsistencies emphasize that the metabolic effects of quercetin are highly context-dependent and substantially modified by concurrent physiological stressors.

Several interacting mechanisms may account for the paradoxical rise in plasma lipids in the EQ group and the broader maladaptive metabolic profile observed. The downregulation of ABCA1 and PPARγ suggests reduced cholesterol efflux and diminished lipid storage capacity, favoring the accumulation of circulating cholesterol and TG. The combined upregulation of APO CIII and ANGPTL3, together with the suppression of APO A5 and ANGPTL4, creates a strongly inhibitory milieu for LPL. This regulatory pattern is consistent with reduced lipase activity and elevated plasma TG. Increased PCSK9 transcription implies enhanced LDL receptor degradation and impaired hepatic LDL uptake. The observed reduction in PCSK9 protein in EQ animals may reflect quercetin-driven changes in secretory pathways, further destabilizing LDL-C homeostasis. Although adiponectin expression rose in E and EQ animals, this adaptive response was insufficient to counteract broader metabolic disturbances, particularly in TG and glucose homeostasis. The unexpected lipid-elevating effects of combined quercetin and strenuous exercise likely arise from cross-interference between quercetin’s molecular targets and exercise-induced adaptive pathways: Antioxidant suppression of exercise-generated ROS, which normally function as essential signaling intermediates for upregulating lipid-handling genes, may prevent beneficial metabolic remodeling.²⁹,³⁰,³¹,³²,³³

Long-term negative feedback, such as suppression of ABCA1 after extended cholesterol efflux, may explain the divergence from short-term studies reporting increased ABCA1 expression.

Collectively, these mechanisms illustrate how 2 individually beneficial interventions can interact in ways that reverse or negate expected metabolic improvements.

Finally, Quercetin bioavailability is typically low, but the presence of SLS often used to enhance solubility can substantially alter intestinal absorption dynamics. SLS may increase quercetin uptake in a non-physiological manner, disrupt intestinal epithelial integrity, alter lipid micelle formation and transporter interactions, and modify hepatic first-pass metabolism.³⁴ Enhanced or erratic absorption could exaggerate systemic quercetin exposure, leading to effects on PCSK9, and TG-regulatory pathways. The interplay of altered gut permeability and exaggerated quercetin delivery may help explain the stronger dyslipidemia response in the EQ group.³⁵,³⁶

Several limitations warrant consideration. First, the 2-month treatment duration may have activated chronic feedback pathways that differ from those observed in short-term studies. Second, rodent models may not fully recapitulate human metabolic responses, particularly regarding nutraceutical-exercise interactions. Third, additional proteomic and functional assays are required for confirmation. Additionally, the strenuous exercise protocol may elicit stress responses that are not comparable to moderate or recreational exercise in humans. Finally, the study was conducted under a single dietary regimen, and metabolic responses may differ under varying nutritional conditions.

In conclusion, strenuous exercise alone produced metabolic responses consistent with established lipid-regulatory adaptations, whereas the addition of quercetin substantially altered these trajectories and often in maladaptive directions. The combined intervention resulted in impaired lipid clearance, suppressed LPL activity, reduced cholesterol efflux capacity, and disrupted TG metabolism. These findings highlight the potential risks associated with combining bioactive flavonoid supplementation with intensive exercise without a clear mechanistic understanding of their interaction. Further investigation is needed to elucidate the molecular basis of this antagonistic interaction. Protein-level validation, enzyme activity assays, dose-response studies, and evaluations across diverse dietary or disease backgrounds will be essential. Given the widespread use of quercetin as a nutraceutical, understanding its interaction with exercise holds significant implications for metabolic health and cardiovascular risk management.

Footnotes

Funding: This work was supported by seed grants from the University of Massachusetts Lowell (Garelnabi). The funding source had no role in the design and content of the paper, the approval of the manuscript; or the decision to submit the manuscript for publication.

Conflict of Interest: The authors have no conflicts of interest to declare.

Data Availability Statement: The datasets generated and/or analyzed during the current study are not publicly available because they are still being used for ongoing research by the investigators, but are available from the corresponding author on reasonable request.

Author Contributions:

Conceptualization: Garelnabi M.
Formal analysis: Shafiy H.
Funding acquisition: Garelnabi M.
Investigation: Shafiy H, Garelnabi M.
Methodology: Shafiy H.
Writing - original draft: Nourti B, Garelnabi M.
Writing - review & editing: Nourti B, Garelnabi M.

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[B33] 33.Punch E, Klein J, Diaba-Nuhoho P, Morawietz H, Garelnabi M. Effects of PCSK9 targeting: alleviating oxidation, inflammation, and atherosclerosis. J Am Heart Assoc. 2022;11:e023328. doi: 10.1161/JAHA.121.023328. [DOI] [PMC free article] [PubMed] [Google Scholar]

[B34] 34.Katsarou A, Davoy E, Xenos K, Armenaka M, Theoharides TC. Effect of an antioxidant (quercetin) on sodium-lauryl-sulfate-induced skin irritation. Contact Dermat. 2000;42:85–89. doi: 10.1034/j.1600-0536.2000.042002085.x. [DOI] [PubMed] [Google Scholar]

[B35] 35.Ergin AD, Bayindir ZS, Gumustas M, Ozcelikay AT, Yuksel N. A new strategy for enhancing S-Adenosyl-L-Methionine (SAMe) oral bioavailability: Preparation of SAMe loaded inulin nanoparticles for colon targeting with in vivo validation. Int J Biol Macromol. 2025;289:138818. doi: 10.1016/j.ijbiomac.2024.138818. [DOI] [PubMed] [Google Scholar]

[B36] 36.Amara J, Itani T, Hajal J, Bakhos JJ, Saliba Y, Aboushanab SA, et al. Circadian rhythm perturbation aggravates gut microbiota dysbiosis in dextran sulfate sodium-induced colitis in mice. Nutrients. 2024;16:247. doi: 10.3390/nu16020247. [DOI] [PMC free article] [PubMed] [Google Scholar]

PERMALINK

Strenuous Exercise and Quercetin Supplementation Differentially Alter Lipid Metabolism in C57BL/6J Mice

Halleh Shafiy

Badia Nourti

Mahdi Garelnabi