Bile salts and proinflammatory cytokines inhibit MCT1-mediated cellular uptake of butyrate and interfere with its antiproliferative properties.

Butyrate (BT) is important in the prevention and inhibition of colorectal cancer (CRC). Inflammatory bowel disease, a risk factor for CRC, is associated with higher levels of proinflammatory cytokines and bile acids. The aim of this work was to investigate the interaction of these compounds in inhibiting BT uptake by Caco-2 cells, as a mechanism contributing to the link between IBD and CRC.

Microbiota-derived butyrate regulates intestinal inflammation: Focus on inflammatory bowel disease.

Inflammatory bowel disease (IBD) refers to a group of heterogeneous disorders associated with chronic inflammation of the gut, having a high rate of incidence in the world. In the present review, we will discuss the link between the short-chain fatty acids, especially butyrate (BT), produced by bacterial fermentation of dietary fiber, and IBD development. Current knowledge supports an anti-inflammatory role for BT and suggests that BT insufficiency may be involved in the pathogenesis of IBD.

The Effect of Inflammatory Status on Butyrate and Folate Uptake by Tumoral (Caco-2) and Non-Tumoral (IEC-6) Intestinal Epithelial Cells.

Objective: Colorectal cancer (CRC) is the second leading cause of cancer death in occidental countries. Chronic inflammatory bowel disease (crohn's disease and ulcerative colitis) is associated with an increased risk for CRC development. The aim of this work was to investigate the relationship between inflammatory status and absorption of nutrients with a role in CRC pathogenesis.

The effect of oxidative stress upon the intestinal uptake of folic acid: in vitro studies with Caco-2 cells.

Folic acid (FA) is a vitamin essential for normal cellular functions, growth, and development. Because humans cannot synthesize this micronutrient, it must be obtained from dietary sources through intestinal absorption. The intestinal tract is a major target for oxidative stress.