Direct comparison of metabolic health effects of the flavonoids quercetin, hesperetin, epicatechin, apigenin and anthocyanins in high-fat-diet-fed mice

Hil, E.F. Hoek–van den; Schothorst, Evert M. van; Stelt, Inge van der; Swarts, Hans J. M.; Vliet, Marjanne van; Amolo, Tom; Vervoort, Jacques; Venema, D.P.; Hollman, P.C.H.; Rietjens, Ivonne M.C.M.; Keijer, Jaap

doi:10.1007/s12263-015-0469-z

Cited by 82 publications

(58 citation statements)

References 33 publications

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“…Although the body weight gain was lower in the EC supplemented HFD mice, this reduction per se seems improbable to account for the observed major improvement of systemic insulin sensitivity. In mice fed a HFD similar to that the used in our current study, but receiving 16 times higher EC, the decrease in body weight gain was partial and of similar magnitude [29]. This suggests that at 20 mg/kg body weight/d, dietary EC may have already reached the maximum potential benefit on HFD-induced mouse body weight gain, and that higher EC consumption may have limited benefits.…”

Section: Discussionmentioning

confidence: 53%

(-)-Epicatechin improves insulin sensitivity in high fat diet-fed mice

Cremonini

Bettaieb

Haj

et al. 2016

Archives of Biochemistry and Biophysics

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Obesity constitutes a major public health concern, being frequently associated with type 2 diabetes (T2D). Evidence from studies in humans and experimental animals suggest that consumption of the flavan-3-ol (−)-epicatechin (EC) and of EC-rich foods may improve insulin sensitivity. To further understand the potential benefits of dietary EC consumption on insulin resistance, this study investigated the capacity of EC supplementation to prevent high fat diet (HFD)-induced insulin resistance in mice. To assess the underlying mechanisms, the effects of HFD and EC consumption on the activation of the insulin cascade and of its negative modulators were evaluated. HFD consumption for 15 w caused obesity and insulin resistance in C57BL/6J mice as evidenced by high fasted and fed plasma glucose and insulin levels, and impaired ITT and GTT tests. This was associated with alterations in the activation of components of the insulin-triggered signaling cascade (insulin receptor, IRS1, ERK1/2, Akt) in adipose and liver tissues. EC supplementation prevented/ameliorated all these parameters. EC acted improving insulin sensitivity in the HFD-fed mice in part through a downregulation of the inhibitory molecules JNK, IKK, PKC and protein tyrosine phosphatase 1B (PTP1B). Thus, the above results suggest that consumption of EC-rich foods could constitute a dietary strategy to mitigate obesity-associated insulin resistance.

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Section: Discussionmentioning

confidence: 53%

(-)-Epicatechin improves insulin sensitivity in high fat diet-fed mice

Cremonini

Bettaieb

Haj

et al. 2016

Archives of Biochemistry and Biophysics

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“…One persistently up-regulated gene, Cyp2b9, displays the most dramatic increase in response to HF diet. This gene encodes for a cytochrome P450, which previously has been shown to be strongly up-regulated by HF diet and important for regulating lipid homeostasis (35,36).…”

Section: Resultsmentioning

confidence: 99%

Persistent Chromatin Modifications Induced by High Fat Diet*

Leung

Trac

et al. 2016

Journal of Biological Chemistry

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Obesity is a highly heritable complex disease that results from the interaction of multiple genetic and environmental factors. Formerly obese individuals are susceptible to metabolic disorders later in life, even after lifestyle changes are made to mitigate the obese state. This is reminiscent of the metabolic memory phenomenon originally observed for persistent complications in diabetic patients, despite subsequent glycemic control. Epigenetic modifications represent a potential mediator of this observed memory. We previously demonstrated that a high fat diet leads to changes in chromatin accessibility in the mouse liver. The regions of greatest chromatin changes in accessibility are largely strain-dependent, indicating a genetic component in diet-induced chromatin alterations. We have now examined the persistence of diet-induced chromatin accessibility changes upon diet reversal in two strains of mice. We find that a substantial fraction of loci that undergo chromatin accessibility changes with a high fat diet remains in the remodeled state after diet reversal in C57BL/6J mice. In contrast, the vast majority of dietinduced chromatin accessibility changes in A/J mice are transient. Our data also indicate that the persistent chromatin accessibility changes observed in C57BL/6J mice are associated with specific transcription factors and histone post-translational modifications. The persistent loci identified here are likely to be contributing to the overall phenotype and are attractive targets for therapeutic intervention.Obesity and related metabolic diseases result from both genetic and environmental factors, such as exercise and diet. However, the molecular mechanisms that contribute to disease progression remain unclear. Intriguingly, previously obese individuals have increased mortality compared with normal individuals, despite therapeutic intervention (1). This is reminiscent of "metabolic memory," a phenomenon originally described in diabetic patients in which micro-and macrovascular complications develop long after blood glucose is normalized (2-4). It has been hypothesized that epigenetic modifications, such as alterations to the chromatin and non-sequence changes to DNA, including DNA methylation, can contribute to this "metabolic memory" (5-7).It is now well established that epigenetic modifications can contribute to disease progression (8). One manner by which external environmental factors can influence molecular pathways is through alterations to chromatin. It has been shown that high fat (HF) 2 diet leads to chromatin accessibility changes in the liver tissue of mice (9). Intriguingly, the genomic loci with the greatest degree of diet-induced chromatin accessibility changes are largely strain-specific, indicating a role for genetics in this response (9). Previous studies examining diet-induced metabolic dysfunctions have shown that mice that transition from HF to diets that are low in fats do not completely revert to the same state as mice only maintained on low fat diets (10). The data indicate th...

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“…Accumulating evidence has shown that psychological stress may correlate with the increasing incidence of metabolic syndrome, inflammation, and NAFLD [41, 42]. However, previous studies mostly concentrated on the effect of chronic stress on obesity or metabolic syndrome combined with a high-fat diet [43, 44].…”

Section: Discussionmentioning

confidence: 99%

Effect of traditional Chinese medicine formula Sinisan on chronic restraint stress-induced nonalcoholic fatty liver disease: a rat study

Cheng

Wang

et al. 2017

BMC Complement Altern Med

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BackgroundNonalcoholic fatty liver disease (NAFLD) represents one of the most common forms of liver disease worldwide, and it is always regarded as a consequence of a sedentary, food-abundant lifestyle, sitting for an extended time, and a low physical activity level, which often coincide with chronic and long-lasting psychological stress. A Chinese medicine Sinisan (SNS) may be a potential formula for treating this kind of disease.MethodsIn this study, a long-term chronic restraint stress protocol was used to investigate the mechanism underlying stress-induced NALFD. To investigate the effect of SNS treatment on stress-induced NAFLD, we measured the liver and serum values of total cholesterol (TC), triglyceride (TG), liver free fatty acids (FFA), low-density lipoprotein, superoxide dismutase, tumor necrosis factor-α, malondialdehyde, interleukin (IL)-6, and serum values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase. Results are shown as a mean ± standard deviation. Significant differences between the groups were evaluated using the Student t-test. For multiple comparisons, one-way analysis of variance (ANOVA) was used. If the results of ANOVA indicated significant differences, post hoc analysis was performed with the Tukey test or Dunnett test, and p < 0.05 was considered statistically significant.ResultsLong-term chronic stress led to steatosis and non-alcoholic steatohepatitis. Additionally, SNS treatment significantly increased body weight gain (p < 0.01) and sucrose preference (p < 0.001), and it reduced the liver values of TC, TG, and FFA (p < 0.05). SNS also reduced the serum values of AST and ALT (p < 0.001), and the liver value of IL-6 (p < 0.01).ConclusionsThis study’s results demonstrate that psychological stress may be a significant risk factor of NAFLD. Furthermore, the traditional Chinese medicine formula SNS may have some beneficial effect in antagonizing psychological stress and stress-related NAFLD.

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Direct comparison of metabolic health effects of the flavonoids quercetin, hesperetin, epicatechin, apigenin and anthocyanins in high-fat-diet-fed mice

Cited by 82 publications

References 33 publications

(-)-Epicatechin improves insulin sensitivity in high fat diet-fed mice

(-)-Epicatechin improves insulin sensitivity in high fat diet-fed mice

Persistent Chromatin Modifications Induced by High Fat Diet*

Effect of traditional Chinese medicine formula Sinisan on chronic restraint stress-induced nonalcoholic fatty liver disease: a rat study

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