Microbiota source impact in vitro metabolite colonic production and anti-proliferative effect of spent coffee grounds on human colon cancer cells (HT-29)

- Colonic spent coffee metabolism differed between lean and overweight microbiota.
- Overweight/hgf-NDSCG displayed cytostatic and cytotoxic effects on HT-29.
- Lean/hgf-NDSCG induced HT-29 cell apoptosis by reducing oxidative stress.
- Additional studies are needed to demonstrate cause/effect relationships.

Human gut flora-mediated non-digestible fraction of spent coffee grounds (hgf-NDSCG) was evaluated for its chemopreventive effect and molecular mechanisms involved on human colon adenocarcinoma HT-29 cell survival using two different microbiota source [lean (L) and overweight (OW)]. The source of human gut flora (hgf) (L or OW) affected the pH of hgf-NDSCG only minimally, but linearly reduced those of hgf-inulin. The variability between lean and overweight microbiota was characterized by the metabolism and/or bioaccessibility of different phenolic metabolites, their intermediate and end products as well as by variable time courses. Apoptosis of colon cancer HT-29 cells depended on the microbiota source with the lean microbiota expressing a low lethal concentration 50 (LC50/L-hgf-NDSCG = 13.5%). We demonstrate that NDSCG and its colonic metabolite from lean microbiota induced HT-29 cell apoptosis by reducing catalase and 8-iso-prostaglandin F2α as biomarkers of in vivo oxidative stress as the primary mechanism underlying its overall chemoprotection against colon cancer.

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