TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Li, Li; Chen, Jing; Ni, Yinxing; Feng, Xiaochi; Zhao, Zhigang; Wang, Peijian; Sun, Jing; Yu, Hao; Yan, Zhencheng; Liu, Daoyan; Nilius, Bernd; Zhu, Zhiming

doi:10.1007/s00424-012-1078-y

Cited by 66 publications

(66 citation statements)

References 25 publications

(29 reference statements)

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“…A previous study also showed that dietary capsaicin significantly decreased triglyceride levels in the plasma and/or liver, as well as the expression of inflammatory adipocytokine genes (e.g., monocyte chemoattractant protein-1 and interleukin-6) and macrophage infiltration [11]. The capsaicin-induced TRPV1 activation promoted lipolysis of visceral fat, and reduced triglyceride level via upregulation of hepatic uncoupling protein 2 (UCP2) [51]. …”

Section: Discussionmentioning

confidence: 99%

Capsaicin Supplementation Reduces Physical Fatigue and Improves Exercise Performance in Mice

et al. 2016

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Chili pepper is used as a food, seasoning and has been revered for its medicinal and health claims. It is very popular and is the most common spice worldwide. Capsaicin (CAP) is a major pungent and bioactive phytochemical in chili peppers. CAP has been shown to improve mitochondrial biogenesis and adenosine triphosphate (ATP) production. However, there is limited evidence around the effects of CAP on physical fatigue and exercise performance. The purpose of this study was to evaluate the potential beneficial effects of CAP on anti-fatigue and ergogenic functions following physiological challenge. Female Institute of Cancer Research (ICR) mice from four groups (n = 8 per group) were orally administered CAP for 4 weeks at 0, 205, 410, and 1025 mg/kg/day, which were respectively designated the vehicle, CAP-1X, CAP-2X, and CAP-5X groups. The anti-fatigue activity and exercise performance was evaluated using forelimb grip strength, exhaustive swimming time, and levels of serum lactate, ammonia, glucose, BUN (blood urea nitrogen) and creatine kinase (CK) after a 15-min swimming exercise. The grip strength and exhaustive swimming time of the CAP-5X group were significantly higher than other groups. CAP supplementation dose-dependently reduced serum lactate, ammonia, BUN and CK levels, and increased glucose concentration after the 15-min swimming test. In addition, CAP also increased hepatic glycogen content, an important energy source for exercise. The possible mechanism was relevant to energy homeostasis and the physiological modulations by CAP supplementation. Therefore, our results suggest that CAP supplementation may have a wide spectrum of bioactivities for promoting health, performance improvement and fatigue amelioration.

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Section: Discussionmentioning

confidence: 99%

Capsaicin Supplementation Reduces Physical Fatigue and Improves Exercise Performance in Mice

et al. 2016

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“…Recently, Li et al reported that transient receptor potential vanilloid 1 (TRPV1) activation by capsaicin reduced lipid accumulation and TG levels in mice, and chronic dietary capsaicin increased the hepatic uncoupling protein 2 expression. 26) As an alternative mechanism it would be interesting to test whether eugenol activates TRPV1 cation channel in hepatocytes, because eugenol belongs to a vanilloid compound and natural congener of capsaicin. TRPV1 is affiliated to the family of nonselective cation channels that display high Ca 2+ permeability.…”

Section: Discussionmentioning

confidence: 99%

Eugenol Ameliorates Hepatic Steatosis and Fibrosis by Down-Regulating SREBP1 Gene Expression <i>via</i> AMPK-mTOR-p70S6K Signaling Pathway

Kim

Jeong

et al. 2014

Biological & Pharmaceutical Bulletin

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Beneficial effect of eugenol on fatty liver was examined in hepatocytes and liver tissue of high fat diet (HFD)-fed C57BL/6J mice. To induce a fatty liver, palmitic acid or isolated hepatocytes from HFD-fed Sprague-Dawley (SD) rats were used in vitro studies, and C57BL/6J mice were fed HFD for 10 weeks. Lipid contents were markedly decreased when hepatocytes were treated with eugenol for up to 24 h. Gene expressions of sterol regulatory element binding protein 1 (SREBP1) and its target enzymes were suppressed but those of lipolysis-related proteins were increased. As a regulatory kinase for lipogenic transcriptional factors, the AMP-activated protein kinase (AMPK) signaling pathway was examined. Protein expressions of phosphorylated Ca 2 -calmodulin dependent protein kinase kinase (CAMKK), AMPK and acetyl-CoA carboxylase (ACC) were significantly increased and those of phosphorylated mammalian target of rapamycin (mTOR) and p70S6K were suppressed when the hepatocytes were treated with eugenol at up to 100 µM. These effects were all reversed in the presence of specific inhibitors of CAMKK, AMPK or mTOR. In vivo studies, hepatic triglyceride (TG) levels and steatosis score were decreased by 45% and 72%, respectively, in eugenoltreated mice. Gene expressions of fibrosis marker protein such as α-smooth muscle actin (α-SMA), collagen type I (Col-I) and plasminogen activator inhibitor-1 (PAI-1) were also significantly reduced by 36%, 63% and 40% in eugenol-treated mice. In summary, eugenol may represent a potential intervention in populations at high risk for fatty liver.Key words eugenol; fatty liver; fibrosis; AMP-activated protein kinase; sterol regulatory element binding protein Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver ailment worldwide.1) While hepatic steatosis is often asymptomatic, it can progress to non-alcoholic steatohepatitis (NASH). If untreated, NASH can progress to cirrhosis and increased risk of early mortality.2) Obesity and insulin resistance, as seen in type 2 diabetes mellitus (T2DM), and hypertriglyceridemia are well-documented risk factors for NAFLD.3) These factors are key targets for prevention and therapy of NAFLD tends to focus on addressing the obesity or insulin resistance rather than NAFLD itself. NAFLD in the hepatic steatosis (HS) phase can be reversed by lifestyle modification, while NASH is more difficult to treat. Thus, preventing the progression of HS to NASH is of primary importance. Lifestyle recommendations for NAFLD are generally limited to losing weight through energy restriction and/or increasing physical activity, which is often to fail to hold on to them. With this notion, phytochemicals obtained from medicinal plants or foods are attracting alternative options for the treatment of NAFLD and prevention to progress to NASH.

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“…Furthermore, appropriate amounts of dietary capsaicin have beneficial effects on obesity and NAFLD[63,64]. A survey indicated that dietary capsaicin could reduce lipid accumulation and triglyceride levels in mice fed with a high-fat diet by up-regulating the levels of uncoupling protein 2 (UCP2)[64].…”

Section: Role Of Autophagy Induced By Traditional Chinese Herbal Extrmentioning

confidence: 99%

“…A survey indicated that dietary capsaicin could reduce lipid accumulation and triglyceride levels in mice fed with a high-fat diet by up-regulating the levels of uncoupling protein 2 (UCP2)[64]. UCP2 was thought to play an important role in mitochondrial lipolysis and oxidative stress.…”

Section: Role Of Autophagy Induced By Traditional Chinese Herbal Extrmentioning

confidence: 99%

Traditional Chinese herbal extracts inducing autophagy as a novel approach in therapy of nonalcoholic fatty liver disease

Liu¹,

Liao²,

Li³

2017

WJG

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Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases around the world due to the modern sedentary and food-abundant lifestyle, which is characterized by excessive fat accumulation in the liver related with causes other than alcohol abuse. It is widely acknowledged that insulin resistance, dysfunctional lipid metabolism, endoplasmic reticulum stress, oxidative stress, inflammation, and apoptosis/necrosis may all contribute to NAFLD. Autophagy is a protective self-digestion of intracellular organelles, including lipid droplets (lipophagy), in response to stress to maintain homeostasis. Lipophagy is another pathway for lipid degradation besides lipolysis. It is reported that impaired autophagy also contributes to NAFLD. Some studies have suggested that the histological characteristics of NAFLD (steatosis, lobular inflammation, and peri-sinusoid fibrosis) might be improved by treatment with traditional Chinese herbal extracts, while autophagy may be induced. This review will provide insights into the characteristics of autophagy in NAFLD and the related role/mechanisms of autophagy induced by traditional Chinese herbal extracts such as resveratrol, Lycium barbarum polysaccharides, dioscin, bergamot polyphenol fraction, capsaicin, and garlic-derived S-allylmercaptocysteine, which may inhibit the progression of NAFLD. Regulation of autophagy/lipophagy with traditional Chinese herbal extracts may be a novel approach for treating NAFLD, and the molecular mechanisms should be elucidated further in the near future.

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TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Cited by 66 publications

References 25 publications

Capsaicin Supplementation Reduces Physical Fatigue and Improves Exercise Performance in Mice

Capsaicin Supplementation Reduces Physical Fatigue and Improves Exercise Performance in Mice

Eugenol Ameliorates Hepatic Steatosis and Fibrosis by Down-Regulating SREBP1 Gene Expression <i>via</i> AMPK-mTOR-p70S6K Signaling Pathway

Traditional Chinese herbal extracts inducing autophagy as a novel approach in therapy of nonalcoholic fatty liver disease

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