Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western‐style diet in C57/BL6J mice

Kobori, Masuko; Masumoto, Shuji; Akimoto, Yukari; Oike, Hideaki

doi:10.1002/mnfr.201000392

Cited by 229 publications

(202 citation statements)

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“…We have chosen the db/db mouse as a model of diabetes because it reliably reflects the development of insulin resistance towards progressive β-cell failure with hyperglycemia as found in human NIDDM. Based on the results from the present study in db/db mice and previous studies in other animal models of obesity [28,29], we conclude that the effects of quercetin are not anti-adipogenic. Rosiglitazone, a member of the thiazolidinediones and a well-established insulin-sensitizing drug, is known to increase body weight [34].…”

Section: Discussionsupporting

confidence: 66%

“…Present data suggests that the type of adipose tissue has an impact on adipokine secretion and insulin sensitivity and thus might be more relevant than total body weight or total body fat mass. Although oral quercetin supplementation may exert antidiabetic effects by increasing plasma adiponectin concentrations in high fat diet-fed rats [21,36] and mice [28] the same dose was ineffective in inducing adiponectin mRNA and plasma concentrations in db/db mice after 4 weeks of treatment. Obesity and insulin resistance both have a mild chronic inflammation in common, often accompanied by elevated TNF-α secretion from adipose tissue.…”

Section: Discussionmentioning

confidence: 97%

“…In vitro studies in 3T3-L1 preadipocytes have indicated anti-adipogenic effects of the flavonol quercetin, suggesting inhibition of differentiation [26,27] and TG accumulation [27]. Oral quercetin supplementation has also been shown to reduce visceral adipose tissue in C56BL/6J mice and obese Zucker rats fed a high-fat/high-sucrose diet for 20 [28] and 10 weeks [29], respectively. However, in the present study, 4 weeks of oral quercetin supplementation in db/db mice had no effect on body weight and rather increased periuterine adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

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Oral Quercetin Supplementation Lowers Plasma sICAM-1 Concentrations in Female db/db Mice

Wein

Schrader²,

Rimbach³

et al. 2013

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Background: Flavonoids are documented for their potential anti-adipogenic, anti-inflammatory and anti-diabetic effects. Quercetin, one of the most abundant flavonoids in edible plants, was investigated for these effects in a diabetic mouse model (db/db, leptin receptor mutation) exerting early relevant clinical signs of non-insulin dependent diabetes mellitus, such as hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypoadiponectinemia and obesity. Materials & Methods: Female db/db mice (n = 24) were fed a flavonoid-poor maintenance diet without (C) or with the addition of quercetin (0.3 g/kg diet, Q) or rosiglitazone (4 mg/kg diet, TZD). Food and water were freely available during the 4 week feeding period. Thereafter, blood samples (fasted) were analyzed for glucose, insulin, triacylglycerols, non-esterified fatty acids, cholesterol, adiponectin and soluble intercellular adhesion molecule-1 (sICAM-1). Adiponectin mRNA levels were measured in adipose tissue. Furthermore, sICAM-1 release was investigated using tumor necrosis factor alpha stimulated EAhy926 cells. Results: Only TZD treatment reduced fasted plasma glucose, triacylglycerols and cholesterol and increased plasma adiponectin concentrations compared to groups C and Q. Adiponectin mRNA levels after quercetin treatment were not different from TZD-treatment or controls. Only quercetin treatment reduced sICAM-1 release in vitro and in vivo. Conclusions: Quercetin effectively reduced sICAM-1 release in the progressive diabetic state, revealing its anti-inflammatory potential in vivo.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Oral Quercetin Supplementation Lowers Plasma sICAM-1 Concentrations in Female db/db Mice

Wein

Schrader²,

Rimbach³

et al. 2013

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“…Stewart et al (2008) found no changes in adiposity among mice fed on a high-fat diet supplemented with 0.8 % of quercetin (which led to a dose of approximately 30 mg/kg body weight/day) for 3 or 8 weeks. By contrast, Kobori et al (2011) observed a significant decrease in visceral fat (-15.5 %) in mice fed a Western diet supplemented with 0.5 % quercetin for 20 weeks. More recently, Jung et al (2013) have found a significant reduction in epididymal adipose tissue in mice fed a diet supplemented with 0.025 % for 9 weeks.…”

Section: Controlmentioning

confidence: 75%

Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation

et al. 2013

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Quercetin exhibits a wide range of biological functions. The first aim of the present work was to analyze the effects of quercetin on fat accumulation in adipose tissue and glycemic control in rats. Any potential involvement of muscle fatty acid oxidation in its effect on glycemic control was also assessed. Animals were fed a high-fat high-sucrose diet either supplemented with quercetin (30 mg/kg body weight/day), or not supplemented, for 6 weeks. One week before killing, a glucose tolerance test was carried out. Muscle triacylglycerol content, serum glucose, insulin, fructosamine and free fatty acids were measured, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. The activities of lipogenic enzymes and lipoprotein lipase in adipose tissue, carnitine palmitoyl transferase-1b (CPT-1b) and citrate synthase in skeletal muscle, and the expression of several genes, ACO, CD36, CPT-1b, PPAR-a, PGC-1a, UCP 3 , TFAM and COX-2 in skeletal muscle were analyzed. Quercetin caused no significant reduction in body weight or adipose tissue sizes. However, fructosamine, basal glucose and insulin, and consequently HOMA-IR, were significantly reduced by quercetin. No changes were observed in the activity of lipogenic enzymes and lipoprotein lipase. Muscle triacylglycerol content was similar in both experimental groups. The expression of ACO, CD36, CPT-1b, PPAR-a, PGC-1a, UCP 3 , TFAM and COX-2 remained unchanged. It can be concluded that quercetin is more effective as an anti-diabetic than as an anti-obesity biomolecule. The improvement in insulin resistance induced by this flavonoid is not mediated by a delipidating effect in skeletal muscle.

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“…Other rodent studies with quercetin supplementation that investigated lipid lowering effects showed reduction in body weight, serum lipid levels, hepatic lipid accumulation, and/or white adipose tissue mass. However, these effects were not seen in all studies and were sometimes conflicting (de Boer et al 2006;Hoek-van den Hil et al 2013;Jung et al 2013;Kobori et al 2011;Odbayar et al 2006;Stewart et al 2009;Wein et al 2010). It is not clear which combination of factors, like dose of quercetin, dietary en% of fat or duration causes these effects on lipids.…”

Section: Introductionmentioning

confidence: 95%

Quercetin decreases high-fat diet induced body weight gain and accumulation of hepatic and circulating lipids in mice

et al. 2014

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Dietary flavonoids may protect against cardiovascular diseases (CVD). Increased circulating lipid levels and hepatic lipid accumulation are known risk factors for CVD. The aim of this study was to investigate the effects and underlying molecular mechanisms of the flavonoid quercetin on hepatic lipid metabolism in mice with high-fat diet induced body weight gain and hepatic lipid accumulation. Adult male mice received a 40 energy% high-fat diet without or with supplementation of 0.33 % (w/w) quercetin for 12 weeks. Body weight gain was 29 % lower in quercetin fed mice (p \ 0.01), while the energy intake was not significantly different. Quercetin supplementation lowered hepatic lipid accumulation to 29 % of the amount present in the control mice (p \ 0.01).1 H nuclear magnetic resonance serum lipid profiling revealed that the supplementation significantly lowered serum lipid levels. Global gene expression profiling of liver showed that cytochrome P450 2b (Cyp2b) genes, key target genes of the transcription factor constitutive androstane receptor (Car; official symbol Nr1i3), were downregulated. Quercetin decreased high-fat diet induced body weight gain, hepatic lipid accumulation and serum lipid levels. This was accompanied by regulation of cytochrome P450 2b genes in liver, which are possibly under transcriptional control of CAR. The quercetin effects are likely dependent on the fat content of the diet.

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Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western‐style diet in C57/BL6J mice

Cited by 229 publications

References 53 publications

Oral Quercetin Supplementation Lowers Plasma sICAM-1 Concentrations in Female db/db Mice

Oral Quercetin Supplementation Lowers Plasma sICAM-1 Concentrations in Female db/db Mice

Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation

Quercetin decreases high-fat diet induced body weight gain and accumulation of hepatic and circulating lipids in mice

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