4.6 Review

Molecular Mechanisms Triggered by Bile Acids on Intestinal Ca2+ Absorption

Journal

CURRENT MEDICINAL CHEMISTRY
Volume 25, Issue 18, Pages 2122-2132

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929867324666171116125131

Keywords

Bile acids; intestinal Ca2+ absorption; NaDOC; UDCA; LCA; oxidative stress; autophagy; nitrosative stress; apoptosis

Funding

  1. CONICET (PIP)
  2. SECYT (UNC), Argentina

Ask authors/readers for more resources

Background: Bile acids (BAs) are among the main components of bile. Lately, they are also considered important signaling molecules, not only by regulating their own synthesis, but also having a role in several metabolic diseases. Objective: In this review we focus on the effect of sodium deoxycholate (NaDOC), ursodeoxycholic (UDCA) and litocholic (LCA) acids and their combination upon the intestinal Ca2+ absorption. To make clear the actions of those BAs on this physiological process, an overview of current information about the mechanisms by which the intestinal Ca2+ occurs is described. Methods: The PubMed database was searched until 2017, using the keywords bile acids, NaDOC, UDCA and LCA and redox state, apoptosis, autophagy and intestinal Ca2+ absorption. Results: The modulation of redox state, apoptosis and autophagy are mechanisms that are involved in the action of BAs on intestinal Ca2+ absorption. Although the mechanisms are still not completely understood, we provide the latest knowledge regarding the effect of BAs on intestinal Ca2+ absorption. Conclusion: The response of the intestine to absorb Ca2+ is affected by BAs, but it is different according to the type and dose of BA. When there is a single administration, NaDOC has an inhibitory effect, UDCA is an stimulator whereas LCA does not have any influence. However, the combination of BAs modifies the response. Either UDCA or LCA protects the intestine against the oxidative injury caused by NaDOC by blocking the oxidative/nitrosative stress, apoptosis and autophagy.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available