In vitro studies on the inhibition of colon cancer by butyrate and carnitine

Roy, Marie‐Josée; Dionne, Serge; Marx, George; Qureshi, Ijaz A.; Sarma, D.S.R.; Lévy, Émile; Seidman, Ernest G.

doi:10.1016/j.nut.2009.04.008

Cited by 52 publications

(45 citation statements)

References 50 publications

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“…Litvak et al [33] employed flow cytometric methods similar to those of the current study and reported a significant increase in apoptosis in butyrate-treated Caco-2 cells [33]. This is further supported by the findings of Roy et al [34], who demonstrated that Caco-2 cells treated with butyrate induced a 65.7% increase in apoptosis compared to negative controls, as detected by flow cytometry and further confirmed by ELISA [33,34]. In the current study, lower concentrations of lauric acid (0.3 m M ) also induced cell death compared to controls but not to butyrate.…”

Section: Discussionsupporting

confidence: 87%

Induction of Apoptosis by the Medium-Chain Length Fatty Acid Lauric Acid in Colon Cancer Cells due to Induction of Oxidative Stress

Fauser

Matthews²,

Cummins³

et al. 2013

Chemotherapy

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Background: Fatty acids are classified as short-chain (SCFA), medium-chain (MCFA) or long-chain and hold promise as adjunctive chemotherapeutic agents for the treatment of colorectal cancer. The antineoplastic potential of MCFA remains underexplored; accordingly, we compared the MCFA lauric acid (C12:0) to the SCFA butyrate (C4:0) in terms of their capacity to induce apoptosis, modify glutathione (GSH) levels, generate reactive oxygen species (ROS), and modify phases of the cell cycle in Caco-2 and IEC-6 intestinal cell lines. Methods: Caco-2 and IEC-6 cells were treated with lauric acid, butyrate, or vehicle controls. Apoptosis, ROS, and cell cycle analysis were determined by flow cytometry. GSH availability was assessed by enzymology. Results: Lauric acid induced apoptosis in Caco-2 (p < 0.05) and IEC-6 cells (p < 0.05) compared to butyrate. In Caco-2 cells, lauric acid reduced GSH availability and generated ROS compared to butyrate (p < 0.05). Lauric acid reduced Caco-2 and IEC-6 cells in G0/G1and arrested cells in the S and G2/M phases. Lauric acid induced apoptosis in IEC-6 cells compared to butyrate (p < 0.05). Butyrate protected IEC-6 cells from ROS-induced damage, whereas lauric acid induced high levels of ROS compared to butyrate. Conclusion: Compared to butyrate, lauric acid displayed preferential antineoplastic properties, including induction of apoptosis in a CRC cell line.

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Section: Discussionsupporting

confidence: 87%

Induction of Apoptosis by the Medium-Chain Length Fatty Acid Lauric Acid in Colon Cancer Cells due to Induction of Oxidative Stress

Fauser

Matthews²,

Cummins³

et al. 2013

Chemotherapy

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“…However, there are conflicting reports between the in vivo and in vitro effectiveness of FA in the treatment of CRC. 55,65 The in vitro concentrations of butyrate, for example, required for the induction of apoptosis, are in the physiologically normal concentration of 5 mM. As this SCFA has a short half life, oral administration as an adjunctive chemotherapeutic agent may not be feasible.…”

Section: Long Chain Fatty Acids (Lcfa)mentioning

confidence: 99%

“…As this SCFA has a short half life, oral administration as an adjunctive chemotherapeutic agent may not be feasible. 65 Therefore, with increasing advances in identification of molecular bio-markers of CRC, administration of FA at apoptosis-inducing concentrations may be plausible, with the use of targeted therapies, such as liposomes or nanoparticles. 9,82,97 Furthermore, in order to identify the FA with the greatest potential as a CRC chemotherapeutic agent, standardization of the following determinants would be advantageous.…”

Section: Long Chain Fatty Acids (Lcfa)mentioning

confidence: 99%

Fatty acids as potential adjunctive colorectal chemotherapeutic agents

Fauser¹,

Prisciandaro²,

Cummins³

et al. 2011

Cancer Biology & Therapy

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“…Acetate is important for lowering the pH of the intestine, thereby inhibiting enteropathogenic bacteria (16,17). Butyrate is the preferred energy source for colonocytes, and studies have shown that butyrate can act as an anticarcinogenic agent through selective induction of apoptosis in colon cancer cells (39,52,54). With respect to inflammatory bowel diseases, butyrate is important because it stimulates an anti-inflammatory state in the colon by downregulation of proinflammatory cytokine production (62).…”

mentioning

confidence: 99%

In Vitro Fermentation of Sugar Beet Arabino-Oligosaccharides by Fecal Microbiota Obtained from Patients with Ulcerative Colitis To Selectively Stimulate the Growth of Bifidobacterium spp. and Lactobacillus spp

Vigsnæs

Holck

Meyer

et al. 2011

Appl Environ Microbiol

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The potential prebiotic properties of arabino-oligosaccharides (AOS) derived from sugar beet pulp was studied using mixed cultures of human fecal bacteria from patients with ulcerative colitis (UC), in remission or with active disease, and in healthy controls. These results were compared to those for fructo-oligosaccharides (FOS), which are known to have a prebiotic effect. Fermentation studies were carried out using a small-scale static batch system, and changes in the fecal microbial communities and metabolites were monitored after 24 h by quantitative real-time PCR and short-chain fatty acid analysis. With a few minor exceptions, AOS affected the communities similarly to what was seen for FOS. Quantitative real-time PCR revealed thatBifidobacteriumspp. andLactobacillusspp. were selectively increased after fermentation of AOS or FOS by fecal microbiota derived from UC patients. The stimulation of growth ofLactobacillusspp. andBifidobacteriumspp. was accompanied by a high production of acetate and hence a decrease of pH. The fermentation of AOS may help improve the inflammatory conditions in UC patients through stimulation of bacteria eliciting anti-inflammatory responses and through production of acetate. AOS may therefore represent a new prebiotic candidate for reduction of the risk of flare-ups in UC patients. However, human trials are needed to confirm a health-promoting effect.

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In vitro studies on the inhibition of colon cancer by butyrate and carnitine

Cited by 52 publications

References 50 publications

Induction of Apoptosis by the Medium-Chain Length Fatty Acid Lauric Acid in Colon Cancer Cells due to Induction of Oxidative Stress

Induction of Apoptosis by the Medium-Chain Length Fatty Acid Lauric Acid in Colon Cancer Cells due to Induction of Oxidative Stress

Fatty acids as potential adjunctive colorectal chemotherapeutic agents

In Vitro Fermentation of Sugar Beet Arabino-Oligosaccharides by Fecal Microbiota Obtained from Patients with Ulcerative Colitis To Selectively Stimulate the Growth of Bifidobacterium spp. and Lactobacillus spp

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