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Modified Citrus Pectin


Daniel
(@daniel)
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Modified Citrus Pectin it is often promoted as a supplement that helps against metastasis. Many years ago, I did believe in this. However, during the recent years, I came to the conclusion that the science behind this claim is very limited, and it seems to come from a limited group of scientist and MDs.

Today, I indeed came across a letter that helps bring more clarity on this subject, a letter that I would like to share here:

Letter by Leffler Regarding Article, “Modified Citrus Pectin Prevents Blood-Brain Barrier Disruption in Mouse Subarachnoid Hemorrhage by Inhibiting Galectin-3”

To the Editor:
I read with great interest the recent article by Nishikawa et al1 entitled “Modified Citrus Pectin Prevents Blood-Brain Barrier Disruption in Mouse Subarachnoid Hemorrhage by Inhibiting Galectin-3.” As the title indicates the authors found potential effects of intracerebroventricular injection of modified citrus pectin (MCP) on preventing blood-brain barrier disruption after subarachnoid hemorrhage in mice and suggested this may be due to inhibition of galectin-3.

The suggested role of galectin-3 rests on the assumption from previous publications that MCP is a good specific galectin-3 inhibitor. However, we found that it is not.2,3 A number of modified citrus pectins, including Pectasol-C used in this study, were tested in a solution assay and found to be at best very weak inhibitors of galectin-3 and definitely not specific. Instead, MCP and other plant polysaccharides may have other effects unrelated to galectin-3, as found for example, in cells not expressing galectin-3,4 and perhaps some of the effects suggested by Shao et al5 in their letter.

The fact that R-galectin-3 blocked the neuroprotective effects of MCP does not prove that MCP acts via galectin-3. There may be independent counteracting effects, and R-galectin-3 alone increased the injury (Figure 5C).1 Some previous studies have suggested an interaction of MCP or similar saccharides with galectin-3 at surfaces, but do not show that the biological effects of these saccharides are due to inhibition of galectin-3, as discussed in detail in reference.2

The authors shall be commended for a cautious discussion of the data, and also state well in the Discussion that “MCP’s galectin-3–unrelated action cannot be excluded” and that “further studies are needed to elucidate the role and mechanisms of galectin-3 in SAH.”

Like Nishikawa et al,1 many articles state that MCP or similar saccharides act as galectin-3 inhibitors by only referring to other studies (eg, reference 13–15 and 27 in reference1) showing biological effects of MCP assumed, but not proven, to be due to inhibition of galectin-3. However, galectin-3 is not a typical signaling molecule but is fairly abundantly expressed and take part in many regulatory functions both extra and intracellularly.3 Consequently, there are ample opportunities for extraneous complex saccharides like MCP to affect the level or localization of galectin-3 by indirect mechanisms, just as they could affect a number of other molecules, possibly with useful and interesting effects. Therefore, previous, current, and new data on MCP need to be interpreted without the assumption that it is a specific or pharmacological galectin-3 inhibitor, as this is not experimentally justified.2

Hakon Leffler, MD, PhD
Department of Laboratory Medicine
Lund University
Sweden

https://www.ahajournals.org/doi/10.1161/STROKEAHA.119.024744

Indeed, the main mechanism claimed to be behind the anti-cancer effects of MCP is galectin-3 inhibition, and the above scientist and MD indicates that MCP does a poor job at inhibiting galectin-3.

 


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