Effects Of Dietary Quercetin Research Articles

Effect of dietary quercetin on growth performance, blood parameters and testicular development of Hu sheep in summer

Effect of dietary quercetin on growth performance, blood parameters and testicular development of Hu sheep in summer

The combined analysis of transcriptomics and metabolomics reveals the mechanisms by which dietary quercetin regulates growth and immunity in Penaeus vannamei

As a potent antioxidant, the flavonoid compound quercetin (QUE) has been widely used in the farming of aquatic animals. However, there are fewer reports of the beneficial effects, especially in improving immunity of Penaeus vannamei by QUE. The aim of this study was to investigate the effects of dietary QUE on growth, apoptosis, antioxidant and immunity of P. vannamei. It also explored the potential mechanisms of QUE in improving the growth and immunity of P. vannamei. P. vannamei were fed diets with QUE for 60 days. The results revealed that QUE (0.5 or 1.0 g/kg) ameliorated the growth, and the expressions of genes related to apoptosis, antioxidant, and immunity. The differentially expressed genes (DEGs) and differential metabolites (DMs) obtained through transcriptomics and metabolomics, respectively, enriched in pathways related to nutritional metabolism such as lipid metabolism, amino acid metabolism, and carbohydrate metabolism. After QUE addition, especially at 0.5 g/kg, DEGs were enriched into the functions of response to stimulus and antioxidant activity, and the pathways of HIF-1 signaling pathway, C-type lectin receptor signaling pathway, Toll-like receptor signaling pathway, and FoxO signaling pathway. In conclusion, dietary QUE can ameliorate growth, apoptosis, antioxidant and immunity of P. vannamei, the appropriate addition amount was 0.5 g/kg rather than 1.0 g/kg. Regulations of QUE on nutrient metabolism and immune-related pathways, and bioactive metabolites, were important factors for improving the aforementioned abilities in P. vannamei.

Effects of dietary quercetin on growth, antioxidant capacity, immune response and immune-related gene expression in snakehead fish, Channa argus

The present study aimed to evaluate the effects of quercetin-supplemented in diet on growth, antioxidant capacity and immune response and immune-related gene expression of Channa argus (C. argus) (initial weight, 24.50 ± 0.24 g). A basal diet was supplemented with quercetin at 0, 150, 300 or 450 mg kg−1 and feed to C. argus 56 days. Weight gain (WG) and specific growth rate (SGR) were significantly increased (P < .05), and feed conversion ratio (FCR) were significantly decreased (P < .05) with the increase of dietary quercetin levels from 0 to 450 mg kg−1. Supplemented quercetin (150, 300 or 450 mg kg−1) significantly enhanced (P < .05) serum or tissues superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (T-AOC), glutathione S-transferase (GST), glutathione peroxidase (GSH-Px), lysozyme (LZM) activity and complement 3 (C3), complement 4 (C4), immunoglobulin M (IgM) concentration. Meanwhile, quercetin administration significantly up-regulated (P < .05) the expression of immune-related cytokines (interleukin-1β[IL-1β], tumor necrosis factor-α[TNF-α], interleukin-8[IL-8], interleukin-10[IL-10]) in liver, spleen, kidney and intestine of C. argus. These results indicated that dietary supplement quercetin could enhance growth, antioxidant capacity, immune response and regulated immune-related genes expression of C. argus, with greatest effects in C. argus given 300 mg kg−1 quercetin for 56 days.

Effects of dietary quercetin on the innate immune response and resistance to white spot syndrome virus in Procambarusclarkii

In recent years, the use of natural products with immune-stimulating and antimicrobial properties has attracted increasing attention in aquaculture researches. In our study, the effect of diet supplemented with quercetin, a flavonoid commonly found in some types of plants substance on the innate immune response and disease resistance in crayfish (Procambarus clarkii) against white spot syndrome virus (WSSV) is reported. It was found that dietary 40 mg/kg quercetin significantly reduced the mortality of crayfish and WSSV copy number after WSSV challenge. Dietary quercetin increased catalase (CAT), and lysozyme (LZM) activity in crayfish. Dietary quercetin increased the expression of NF-κB, anti-lipopolysaccharide factor (ALF) and toll-like receptor (TLR) genes in crayfish. The apoptosis rate of hemocyte was increased by quercetin supplement in crayfish. Our results suggest that dietary quercetin may affect the innate immunity of crayfish and protect crayfish from WSSV infection.

Effects of dietary quercetin on the antioxidative status and cecal microbiota in broiler chickens fed with oxidized oil

This study was conducted to evaluate the effects of quercetin on the antioxidant ability, intestinal barrier functions, and cecal microbiota in broiler chickens fed with oxidized soya oil. Four hundred eighty male Arbor Acres broilers were randomly assigned to 5 treatments, each involving 8 cages (12 birds per cage). The treatment groups were as follows: the control group, birds fed with basal diets containing oxidized oil, and birds fed with basal diets containing oxidized oil and supplemented with 200 ppm of quercetin, 400 ppm of quercetin, and 800 ppm of quercetin. The results showed that dietary supplementation with quercetin at a dose of 400 ppm or 800 ppm alleviated the increased serum malondialdehyde (MDA) level induced by oxidized oil on day 11 (P = 0.005) and reversed the increased MDA level in the mucosa on day 11 (P = 0.021). Quercetin significantly upregulated the transcription of nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream genes such as catalase (P < 0.001), superoxide dismutase 1 (P < 0.001), glutathione peroxidase 2 (P = 0.018), heme oxygenase-1 (HO-1) (P = 0.0), and thioredoxin (P = 0.002) and reversed the mRNA expression of HO-1 (P = 0.007) in the ileal mucosa. Tight junction protein 1 was only downregulated by oxidized oil (P = 0.013). In addition, quercetin (800 ppm) alleviated the decreased mRNA expression of mucin 2 (MUC2), which contributed to the intestinal chemical barrier (P = 0.039). The supplemental dose of 400 ppm of quercetin was able to promote Lactobacillus in the cecum, which enhanced the gastrointestinal tract health. In summary, these results indicated that quercetin ameliorated the oxidized oil–induced oxidative stress by upregulating the transcription of Nrf2 and its downstream genes to restore redox balance and reinforced the intestinal barrier via higher expression and secretion of MUC2 and facilitating the growth of Lactobacillus in the cecum. Therefore, quercetin could be a potential feed additive that can be applied in poultry production for amelioration of oxidative stress caused by oxidized oil and preventing the potential invasion of exogenous pathogens.

The Effect of Dietary Quercetin on the Glutathione Redox System and Small Intestinal Functionality of Weaned Piglets.

Quercetin has been shown to alleviate mucosal damage and modulate the glutathione (GSH) redox system in the colon of rodents. In the current study, we assessed whether quercetin was able to mitigate small intestinal dysfunction in weaned pigs. Here, 224 weaned piglets were fed a diet containing quercetin at either 0, 100, 300, or 900 mg/kg diet until d14 post-weaning, followed by a common basal diet until d42. Eight animals per treatment were sampled at d5 and d14 post-weaning. In these animals, the small intestinal histomorphology, barrier function, and protein abundance of occludin, caspase-3, and proliferating cell nuclear antigen were assessed. None of these parameters were affected, and neither did quercetin improve performance up to d42 post-weaning. The GSH redox system was evaluated in blood, small intestinal mucosa, and liver. Quercetin did not affect the glutathione peroxidase, glutathione reductase, and glutamate–cysteine ligase activity in these tissues. In contrast, the hepatic glutathione transferase (GST) activity was significantly increased by quercetin supplementation at d5 post-weaning of 100, 300, and 900 mg/kg. Importantly, d5 was characterized by a more oxidized GSH redox status. To conclude, dietary quercetin had little effect on the small intestine, but did upregulate hepatic GST in the occurrence of redox disturbance.

Effects of dietary quercetin on female fertility in mice: implication of transglutaminase 2.

Use of the dietary supplement quercetin is on the rise. Because previous studies imply an inhibitory effect of quercetin on male fertility, we explored the effects of this flavonoid on fertility in female mice. Birth outcomes, and ovarian morphology in 4-week-old offspring, were assessed in mice receiving dietary quercetin (5mgkg-1day-1) for 9 months during two breeding periods: from 2 to 6 months (prime reproductive age) and 8 to11 months of age. Quercetin increased birth spacing, leading to a 60% reduction in the number of litters, but enhanced folliculogenesis in ovaries of female offspring. While in young females quercetin caused an almost 70% increase in litter size, in older animals this effect was reversed. Consistent with the inhibitory activity of quercetin on the enzyme transglutaminase 2 (TG2), genetic ablation of TG2 in mice mirrors the effects of quercetin on birth outcomes and follicular development. Further, TG2-null mice lack responsiveness to quercetin ingestion. Our study shows for the first time that dietary quercetin can cause reduced reproductive potential in female mice and implies that TG2 may regulate ovarian ageing.

Effect of dietary quercetin on brain quercetin levels and the expression of antioxidant and Alzheimer's disease relevant genes in mice

The aim of the present feeding trial was to investigate the effect of the dietary flavonol quercetin on brain quercetin concentration and the expression of antioxidant and Alzheimer's disease relevant genes in mouse brain. Laboratory mice were fed control and quercetin-enriched diets (2 mg/g diet) for 6 weeks. Dietary quercetin supplementation significantly increased the levels of quercetin and its methylated metabolite isorhamnetin in plasma and brain. However, quercetin and isorhamnetin levels in the brain were manifold lower as compared to the plasma. Both mRNA and activity levels of alpha- and beta-secretase in cortex remained unchanged by the dietary quercetin supplementation. Furthermore dietary quercetin did not affect brain mRNA levels of neprilysin, heme oxygenase-1 and gamma-glutamylcysteine synthetase. Taken together, a short term dietary treatment with quercetin increased quercetin and isorhamnetin levels in the brain but had no effect on mRNA levels of antioxidant and Alzheimer's disease relevant genes in mouse brain.

Effect of dietary quercetin and sphingomyelin on intestinal nutrient absorption and animal growth

Research on cancer and other conditions has shown flavonoids and sphingolipids to be food components capable of exerting chemoprotective action. Nevertheless, little is known about their effects on healthy individuals and their potential usefulness as therapeutic agents. The present study examined the possible action of a dietary flavonoid, quercetin, and a sphingolipid, sphingomyelin, as functional foods in healthy animals. In particular, the effect on animal growth of supplementing a conventional diet with one or other of these substances (0.5 % quercetin and 0.05 % sphingomyelin) was considered. Possible action affecting intestinal physiology was also analysed by measuring the uptake of sugar and dipeptide, mediated by the Na(+)-dependent sugar transporter SGLT1 and the dipeptide Na(+)/H(+) exchanger PEPT1 respectively, and the activity of related intestinal enzymes such as sucrase, maltase and aminopeptidase N. Both substances seemed to modify small intestinal activity in healthy mice, altering intestinal enzymatic activity and nutrient uptake. These effects observed in the small intestine did not impair normal development of the animals, as no differences in serum biochemical parameters or in organ and body weights were found. The findings should help in elucidating the mechanisms of action of these food components with a view to their possible use in the prevention of certain pathological conditions.

Effect of dietary quercetin on oxidative DNA damage in healthy human subjects

The effect of dietary intake of flavonols (predominantly quercetin) on oxidative DNA damage was studied in thirty-six healthy human subjects (sixteen men, twenty women). The study was a randomised crossover study, comprising two 14 d treatments of either a low-flavonol (LF) or high-flavonol (HF) diet with a 14 d wash-out period between treatments. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion (Allium cepa) cake (containing 89.7 mg quercetin) and one 300 ml cup of black tea (containing 1.4 mg quercetin) daily during the HF dietary treatment. A 7 d food diary was kept during each dietary period and blood samples were taken after each dietary treatment. Products of oxidative damage to DNA bases were measured in DNA from leucocytes. The study had more than 95% power to detect a change of 20% in DNA damage products Plasma vitamin C and plasma quercetin concentrations were also measured. No significant differences in intake of macronutrients or assessed micronutrients, measured DNA base damage products, or plasma vitamin C were found between the HF and LF dietary treatments. The plasma quercetin concentration was significantly higher after the HF dietary treatment period (228.5 (SEM 34.7) nmol/l) than after the LF dietary treatment period (less than the limit of detection, i.e. <66.2 nmol/l). These findings do not support the hypothesis that dietary quercetin intake substantially affects oxidative DNA damage in leucocytes.

Quercetin enhances pretumorous lesions in the NMU model of rat pancreatic carcinogenesis

The effect of dietary quercetin (Q) was evaluated in rats treated with nitrosomethylurea (NMU). Pancreatic nodules and focal acinar cell hyperplasias were observed in groups treated with NMU (87%) and Q-NMU (100%). Although rats with dysplastic foci (27%) were found in the NMU-treated group, Q-NMU treatment resulted in a significantly higher number of rats with dysplastic foci (73%). Furthermore, carcinomas in situ (12%) and one microcarcinoma (4%) were found in these animals. Mitosis was significantly increased and apoptosis was diminished in focal acinar cell hyperplasias of the Q-NMU group. Our present results support a promoting and progressing effect of quercetin in the NMU model of rat pancreatic carcinogenesis.

The effect of dietary quercetin and rutin on AOM‐induced acute colonic epithelial abnormalities in mice fed a high‐fat diet

Dietary quercetin (QU) and rutin (RU), phenolic flavonoids found in many fruits and vegetables, when fed to mice on a low-fat diet successfully modified the response to azoxymethanol (AOM) by initially inhibiting hyperproliferation and the formation of foci of dysplasia (FADs) and ultimately reducing tumor incidence (Carcinogenesis 12, 1193-1196, 1991). In this study, we tested the efficacy of QU and RU when a high-fat diet was presented. An AIN 76A diet made with 20% corn oil (CO) was supplemented with QU (0.5%, 2.0%, or 5.0%) and RU (2.0% or 4.0%). These five diets, as well as a 5.0% and a 20.0% CO diet, were fed to a group of CF1 female mice for nine weeks. Both QU and RU showed nonsignificant dose-related trends toward normalization of the AOM-induced upward extension of S phase cells. Examination of 500 microns of serially sectioned distal colon revealed that 29% of mice fed the 20% CO control diet were free of FADs. Among the mice fed QU, regardless of dose, > 80% were free of FADs. When the three groups fed QU were pooled and compared with the control 20% CO-fed mice, the degree of protection was significant (p < 0.01). Mice fed RU expressed a level of protection that bordered on the significant (p < 0.08). These data suggest that, regardless of the fat content of the diet, QU and RU are capable of modifying or inhibiting events in the development of chemically induced colonic neoplasia.

Effects of dietary quercetin on serum lipids.

(1983). Effects of Dietary Quercetin on Serum Lipids. Agricultural and Biological Chemistry: Vol. 47, No. 9, pp. 2119-2120.