Coffee consumption delays the hepatitis and suppresses the inflammation related gene expression in the Long-Evans Cinnamon rat

Katayama, Masafumi; Donai, Kenichiro; Sakakibara, Hiroyuki; Ohtomo, Yukiko; Miyagawa, Makoto; Kuroda, Kensuke; Kodama, Hiroko; Suzuki, Kazufumi; Kasai, Noriyuki; Nishimori, Katsuhiko; Uchida, Takafumi; Watanabe, Kouichi; Aso, Hisashi; Isogai, Emiko; Sone, Hirohito; Fukuda, T.

doi:10.1016/j.clnu.2013.05.006

Cited by 18 publications

(15 citation statements)

References 38 publications

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“…The effects seem to be most pronounced in liver, which is in accordance with the consistent epidemiological data on the association of reduced risk of liver cancers with coffee intake [17,[34][35][36]. In several rat models of hepatic injury, disease progression is halted, and induction of inflammatory markers, such as IL-6, TNF-␣ (where TNF is tumor necrosis factor), IFN-␥, and tumor growth factor ␤, is inhibited by the administration of coffee [90,92,93]. Similar findings have been observed by administration of isolated caffeine, where hepatic fibrosis and inflammation was reduced in rats with chemically induced cirrhosis [94], while Furtado et al [95] found decreased hepatic injury and inflammation of both coffee and caffeine, but not by decaffeinated coffee.…”

Section: Inflammationsupporting

confidence: 85%

Coffee and cancer risk, epidemiological evidence, and molecular mechanisms

Bøhn

Blomhoff

Paur

2013

Molecular Nutrition Food Res

141

105

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Although early studies suggested that coffee consumption might increase risk of some cancers, more comprehensive epidemiological and experimental data now generally indicate either neutral or beneficial effects. In this review, we summarize the current evidence for associations between breast, prostate, colorectal, and liver cancers and the consumption of coffee, and discuss the experimental evidence for potential chemopreventive mechanisms of coffee and coffee constituents. The epidemiological evidence consistently indicates that coffee protects against liver cancer, and also point toward protective effects for risk of colorectal cancers (with relative risks of 0.50 (95% CI: 0.42-0.59) and 0.83 (95% CI: 0.75-0.92), respectively, in the most recent meta-analyses). There seems to be no association between the overall risk of breast and prostate cancer and coffee intake. However, for subgroups such as postmenopausal breast cancers, advanced prostate cancers, and breast and prostate cancer survivors, an inverse association with coffee intake is indicated. Potential mechanisms for chemopreventive effects of coffee phytochemicals includes inhibition of oxidative stress and oxidative damage, regulation of DNA repair, phase II enzymatic activity, apoptosis, inflammation, as well as having antiproliferative, antiangiogenetic effects and antimetastatic effects. The experimental evidence for effects of coffee and coffee constituents on each of these processes is discussed.

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Section: Inflammationsupporting

confidence: 85%

Coffee and cancer risk, epidemiological evidence, and molecular mechanisms

Bøhn

Blomhoff

Paur

2013

Molecular Nutrition Food Res

141

105

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“…97 Ten studies on whole coffee consumption in relation to hepatic carcinogenesis were conducted, [99][100][101][102] of which six specifically looked into tumor morphology. [103][104][105][106][107][108] Only Hasegawa et al found no difference in the frequency and location of diethylnitrosamine-induced tumors in coffeetreated rats. 103 All other studies found either reduced tumor frequency or size upon coffee consumption in rats with endogenously or exogenously induced carcinogenesis.…”

Section: Hepatocellular Carcinomamentioning

confidence: 96%

“…103 All other studies found either reduced tumor frequency or size upon coffee consumption in rats with endogenously or exogenously induced carcinogenesis. [104][105][106][107][108] Furtado et al identified higher expression of proapoptotic Bax proteins in rats treated with instant coffee or caffeine, suggesting apoptosis-mediated protection against liver carcinogenesis. 107 This apoptosis-mediated hypothesis was supported by a preceding in vivo/in vitro study on rats implanted with a hepatoma cell line treated with instant CC.…”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

Potential Mechanisms Underlying the Role of Coffee in Liver Health

2018

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Coffee, the most consumed hot beverage worldwide, is composed of many substances, of which polyphenols, caffeine, and diterpenoids are well studied. Evidence on potential effects of coffee on human health has been accumulating over the past decades. Specifically, coffee has been postulated to be hepatoprotective in several epidemiological and clinical studies. Several underlying molecular mechanisms as to why coffee influences liver health have been proposed. In this review, the authors summarized the evidence on potential mechanisms by which coffee affects liver steatosis, fibrosis, and hepatic carcinogenesis. The experimental models reviewed almost unanimously supported the theorem that coffee indeed may benefit the liver. Either whole coffee or its specific compounds appeared to decrease fatty acid synthesis (involved in steatogenesis), hepatic stellate activation (involved in fibrogenesis), and hepatic inflammation. Moreover, coffee was found to induce apoptosis and increased hepatic antioxidant capacity, which are involved in carcinogenesis.

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“…Additionally, NAC, a prodrug to cysteine and therefore a precursor for glutathione, reduced liver copper and overall liver damage mainly due to metal chelation rather than ROS scavenging (Kitamura et al, 2005). Additionally, fermented brown rice (Shibata et al, 2006) and coffee (Katayama et al, 2014) were tested to reduce liver damage in LEC rats. Both treatment options were able to prolong survival.…”

Section: Copper Toxicity In Age-related Diseases and Wilson Diseasementioning

confidence: 99%

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

Giorgi

Marchi

Simões

et al. 2018

International Review of Cell and Molecular Biology

281

162

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Aging has been linked to several degenerative processes that, through the accumulation of molecular and cellular damage, can progressively lead to cell dysfunction and organ failure. Human aging is linked with a higher risk for individuals to develop cancer, neurodegenerative, cardiovascular, and metabolic disorders. The understanding of the molecular basis of aging and associated diseases has been one major challenge of scientific research over the last decades. Mitochondria, the center of oxidative metabolism and principal site of reactive oxygen species (ROS) production, are crucial both in health and in pathogenesis of many diseases. Redox signaling is important for the modulation of cell functions and several studies indicate a dual role for ROS in cell physiology. In fact, high concentrations of ROS are pathogenic and can cause severe damage to cell and organelle membranes, DNA, and proteins. On the other hand, moderate amounts of ROS are essential for the maintenance of several biological processes, including gene expression. In this review, we provide an update regarding the key roles of ROS-mitochondria cross talk in different fundamental physiological or pathological situations accompanying aging and highlighting that mitochondrial ROS may be a decisive target in clinical practice.

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Coffee consumption delays the hepatitis and suppresses the inflammation related gene expression in the Long-Evans Cinnamon rat

Cited by 18 publications

References 38 publications

Coffee and cancer risk, epidemiological evidence, and molecular mechanisms

Coffee and cancer risk, epidemiological evidence, and molecular mechanisms

Potential Mechanisms Underlying the Role of Coffee in Liver Health

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

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