Dietary broccoli protects against fatty liver development but not against progression of liver cancer in mice pretreated with diethylnitrosamine

Chen, Yung Ju; Myracle, Angela D.; Wallig, Matthew A.; Jeffery, Elizabeth H.

doi:10.1016/j.jff.2016.03.028

Cited by 17 publications

(13 citation statements)

References 26 publications

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“…SFN has drawn considerable attention due to its roles in controlling energy balance and metabolism . Previous articles report that sustained treatment of diet‐induced obese mice or rats with SFN lessens the development of fatty liver . In this study, we document that SFN improves mitochondrial function and elevate mitochondrial biogenesis, reducing lipid content in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 53%

Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro

Lei

Tian

Teng

et al. 2019

Molecular Nutrition Food Res

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Scope Sulforaphane (SFN) is reported to reduce the accumulation of lipids. However, the underling mechanism remains unclear. In this study, the potential of SFN to improve lipid metabolism is investigated through altering mitochondrial function and biogenesis‐related mechanisms. Methods and Results The abnormal lipid metabolism model was established both in HHL‐5 cells and in rats by feeding a high‐fat diet (HFD) for 10 weeks. The current findings suggest that SFN alleviates the swelling of mitochondria and stimulates mitochondrial biogenesis. The reduced expression of NRF1 and TFAM, were reversed by SFN. SFN increases the levels of antioxidant compounds via nuclear factor erythroid‐2‐related factor (Nrf2) activation. Furthermore, SFN improves multiple mitochondrial bioactivities, such as mitochondrial membrane potential, ATP, and the electron transfer chain based on PGC‐1α pathway. SFN also activates lipolysis by transcriptionally upregulating adipose triglyceride lipase (ATGL) and hormone‐sensitive lipase (HSL). Conclusions SFN enhances utilization of lipids via both the PGC‐ 1α‐dependent promotion of mitochondrial biogenesis and Nrf2 dependent improvement of mitochondrial function.

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Section: Discussionmentioning

confidence: 53%

Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro

Lei

Tian

Teng

et al. 2019

Molecular Nutrition Food Res

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“…A subsequent study from the same group again showed that broccoli attenuated the NAFLD effects of the Western diet (94). However, in the second mouse study, the broccoli did not slow down hepatocarcinogenesis, but mice were induced with diethylnitrosamine at a younger age (2 wk) and before the administration of broccoli and the Western diet (4 wk to 7 mo) (94). Based on these studies, broccoli can attenuate the effects of NAFLD in mouse models, minimizing the risk that they develop liver adenomas, but not necessarily alter the course of hepatocarcinogenesis.…”

mentioning

confidence: 92%

“…In this study, mice were started on a Western diet and 10% broccoli at 5 wk before induction with diethylnitrosamine at 6 wk (93). A subsequent study from the same group again showed that broccoli attenuated the NAFLD effects of the Western diet (94). However, in the second mouse study, the broccoli did not slow down hepatocarcinogenesis, but mice were induced with diethylnitrosamine at a younger age (2 wk) and before the administration of broccoli and the Western diet (4 wk to 7 mo) (94).…”

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confidence: 98%

Nutritional Approaches to Achieve Weight Loss in Nonalcoholic Fatty Liver Disease

Hsu

Ness

Kowdley

2017

Advances in Nutrition

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Nonalcoholic fatty liver disease (NAFLD) can range in spectrum from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH), which is characterized by lipotoxicity, hepatocellular ballooning, and inflammation and can progress to cirrhosis. Weight loss is the cornerstone treatment for NAFLD and NASH. Various randomized controlled trials have shown that weight loss of $5-10% leads to significant improvements in hepatic steatosis. Diets high in sodium and fructose have been implicated in the pathogenesis of NAFLD. Although some clinical studies suggest that an isocaloric high-fructose diet does not worsen NAFLD, these clinical studies are often short in duration. More recently, the Dietary Approaches to Stop Hypertension diet, a sodium-restricted diet, has been associated with less prevalence of NAFLD and has been shown to improve NAFLD. In addition, the Mediterranean diet has been promising in improving hepatic steatosis, and a larger randomized controlled trial is currently enrolling subjects. For those who are unable to pursue weight loss through dietary approaches, bariatric surgery has been shown to improve hepatic steatosis and steatohepatitis. This method has been variable in improving hepatic fibrosis. In conclusion, weight loss is crucial to the improvement of NAFLD and NASH, and patients should attempt various diets in an attempt to achieve weight loss. Adv Nutr 2017;8:253-65.

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“…Previous studies have indicated that SFN has many biological properties, including anti-oxidant, anti-inflammatory, and anti-bacterial effects [11,12]. SFN has been found to act as a tumor suppressor in many different cancers during cancer progression, including oral, breast, liver, colon, and prostate cancers [13][14][15][16]. In addition, it has been demonstrated that SFN has the ability to prevent carcinogen-induced initiation of oral cancer [14].…”

Section: Introductionmentioning

confidence: 99%

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Chen

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Sulforaphane (SFN) is known for its potent bioactive properties, such as anti-inflammatory and anti-tumor effects. However, its anti-tumor effect on pancreatic cancer is still poorly understood. In the present study, we explored the therapeutic potential of SFN for pancreatic cancer and disclosed the underlying mechanism. Methods: Panc-1 and MiaPaca-2 cell lines were used in vitro. The biological function of SFN in pancreatic cancer was measured using EdU staining, colony formation, apoptosis, migration and invasion assays. Reactive oxygen species (ROS) production was measured using 2’-7’-Dichlorofluorescein diacetate (DCF-DA) fluorometric analysis. Western blotting and immunofluorescence were used to measure the protein levels of p-AMPK and epithelial-mesenchymal transition (EMT) pathway-related proteins, and cellular translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Nude mice and transgenic pancreatic cancer mouse model were used to measure the therapeutic potential of SFN on pancreatic cancer. Results: SFN can inhibit pancreatic cancer cell growth， promote apoptosis, curb colony formation and temper the migratory and invasion ability of pancreatic cancer cells. Mechanistically, excessive ROS production induced by SFN activated AMPK signaling and promoted the translocation of Nrf2, resulting in cell viability inhibition of pancreatic cancer. Pretreatment with compound C, a small molecular inhibitor of AMPK signaling, reversed the subcellular translocation of Nrf2 and rescued cell invasion ability. With nude mice and pancreatic cancer transgenic mouse, we identified SFN could inhibit tumor progression, with smaller tumor size and slower tumor progression in SFN treatment group. Conclusion: Our study not only elucidates the mechanism of SFN-induced inhibition of pancreatic cancer in both normal and high glucose condition, but also testifies the dual-role of ROS in pancreatic cancer progression. Collectively, our research suggests that SFN may serve as a potential therapeutic choice for pancreatic cancer.

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Dietary broccoli protects against fatty liver development but not against progression of liver cancer in mice pretreated with diethylnitrosamine

Cited by 17 publications

References 26 publications

Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro

Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro

Nutritional Approaches to Achieve Weight Loss in Nonalcoholic Fatty Liver Disease

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

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