Beta-glucuronidase: Friend or foe?

Author: Christine Stewart

January 2021

Depiction of the assumed biological unit of human beta-glucuronidase (Wikipedia)


Beta-glucuronidase is a bacterial enzyme which can limit the excretion of compounds from the body such as medications, hormones, neurotransmitters and environmental toxins1 by reversing a detoxification process known as glucuronidation.


What is glucuronidation?

Glucuronidation is a well-described phase II metabolic pathway that occurs predominantly in the liver and involves the transfer of glucuronic acid or GlcUA (a sugar molecule) on to the compound marked for excretion2,3. Glucuronidation generally makes compounds more water-soluble allowing them to be more easily excreted via the urine or bile. 


Gut bacteria and glucuronidation

Beta-glucuronidase is a specialised enzyme produced by some gut bacteria that breaks the tight glycosilic bonds between the deactivated compound and glucuronic acid. These sugar scavenging bacteria do this in order to use the glucuronic acid sugar as a fuel source.

Once the glucuronic acid has been removed, the original molecule (previously marked for excretion) can be reabsorbed through the epithelial layer back into the body2.



For example, it has been suggested that high beta-glucuronidase potential in the microbiome may increase the toxicity of certain medications.  A recent study4 identified 100 medications which could be reactivated by microbial beta-glucuronidase ranging from opioids, estrogens, NSAIDs, benzodiazepines, antihypertensives and antidiabetic medications.

This recycling of compounds is not always bad as some beneficial compounds such as serotonin and vitamin D  can also undergo glucuronidation5. This suggests that for some patients maintaining an adequate level of beta-glucuronidase activity in their gut could be clinically beneficial to ensure optimal salvaging of these important compounds from the bile.

Taken together this highlights the need to consider the microbiome’s beta-glucuronidase potential within the context of the patient’s exposure to certain compounds as well as their presenting symptoms to identify if reducing beta-glucuronidase activity is required.


How prebiotic fibre may reduce beta-glucuronidase activity

Glucomannan is a type of prebiotic fibre which has been shown to reduce faecal beta-glucuronidase activity6. A double-blind, placebo-controlled trial found that supplementing a typical low fibre Taiwanese diet with 4.5g glucomannan per day for 4 weeks resulted in a 31.5% reduction in faecal beta-glucuronidase activity. The proposed mechanism for this was the prebiotic effect of glucomannan which was supported by a preliminary assessment of the microbiome which showed that the glucomannan intervention was associated with increased abundances of Bifidobacterium and Lactobacillus species. More research is needed to confirm whether other prebiotic fibres would have a similar impact.


Where can glucomannan be found?

Glucomannan can be found in konjac root and konjac based foods such as low-calorie noodles and pasta (see Fig 1). These products tend to contain around 5% konjac flour – indicating that a 100g serve would contain an ‘active dose’ of 5g of glucomannan. Some soups list konjac noodles in their ingredients list (around 15-20%). Therefore, a 400g serve would essentially provide 3 – 4g glucomannan.


Figure 1. Bowl of cooked Konjac noodles


Understanding your patients beta-glucuronidase potential within their microbiome can reveal their bodies ability to balance the excretion of potentially harmful compounds with the recovery of beneficial compounds.

Looking for more exclusive practitioner resources? Find clinical reference guides, video tutorials and more on the clinical resources page.

About the author


Christine Stewart

Christine is a Nutritionist, Registered Nurse and Clinical Application Specialist at Microba. Christine has a passion for obesity-related chronic disease prevention and furthering our understanding of the association between the microbiome and metabolic disease.


1) Pellock SJ, Redinbo MR. Glucuronides in the gut: Sugar-driven symbioses between microbe and host. The Journal of Biological Chemistry. 2017; 292, 8569-8576. doi: 10.1074/jbc.R116.767434


2) Chackalamannil S, Rotella D, Ward WE. Comprehensive Medicinal Chemistry III. 3rd Amsterdam: Elsevier; 2017

3) Claus, S., Guillou, H. & Ellero-Simatos, S. The gut microbiota: a major player in the toxicity of environmental pollutants?. npj Biofilms Microbiomes 2, 16003 (2016). 


4) Elmassry MM, Kim S, Busby B (2021) Predicting drug-metagenome interactions: Variation in the microbial β-glucuronidase level in the human gut metagenomes. PLoS ONE 16(1): e0244876.


5) Walsh J, Olavarria-Ramirez L, Lach G, Boehme M, Dinan TG, Cryan JF, Griffin BT, Hyland NP, Clarke Impact of host and environmental factors on β-glucuronidase enzymatic activity: implications for gastrointestinal serotonin. Am J Phys. 2020; 318(4): 816-26


6) Gao C, Liao MZ, Han LW, Thummel KE, Mao Q. Hepatic Transport of 25-Hydroxyvitamin D3 Conjugates: A Mechanism of 25-Hydroxyvitamin D3 Delivery to the Intestinal Tract. Drug Metab Dispos. 2018;46(5):581-591. doi:10.1124/dmd.117.078881


7) Wu WT, Cheng HC, Chen HL. Ameliorative effects of konjac glucomannan on human faecal β-glucuronidase activity, secondary bile acid levels and faecal water toxicity towards Caco-2 cells. Br J Nutr. 2011 Feb;105(4):593-600. doi: 1017/S0007114510004009.