IngredientesGlucuronolactone is a naturally occurring cyclic ester of D-glucuronic acid, with the molecular formula C₆H₈O₆ and a molecular weight of 176.12 g/mol. Its International Nonproprietary Name (INN) is Glucurolactone, and it is registered in the NIH PubChem database under CID 92283 and CAS number 32449-92-6. Its IUPAC name is (2R)-2-[(2S,3R,4S)-3,4-dihydroxy-5-oxooxolan-2-yl]-2-hydroxyacetaldehyde.
Common synonyms and alternate names include: D-Glucurono-6,3-lactone, D-Glucurono-3,6-lactone, D-glucurono-gamma-lactone (d-glucurono-γ-lactone), Glucurone, D-Glucurolactone, Glucuronic acid lactone, and D-Glucurone. Glucuronolactone is a white solid odorless compound, soluble in hot and cold water. Its melting point ranges from 176 to 178 °C. The compound can exist in a monocyclic aldehyde form or in a bicyclic hemiacetal (lactol) form.
Glucuronolactone functions as a human and animal metabolite derived from glucose metabolism in the liver, playing a vital role in phase II detoxification by facilitating the conjugation and elimination of toxins, drugs, and carcinogens through glucuronidation. Glucuronolactone is also found in many plant gums. In plants, it is present in various gums and exudates, such as gum arabic and other polysaccharide-rich secretions from tree barks. It can be found as part of plant gums, although in limited bioavailability, because it is combined with other carbohydrates in the form of polymers.
Wine is the richest natural food source of this compound, with concentrations around 20 mg/L. The glucuronolactone intake via normal food is small (1–2 mg/day), and it is naturally produced in the body as a metabolite of glucose and is a component of fibrous connective tissue. In an average diet, glucuronolactone intake through food sources is estimated to be very low (1.2 mg/day).
Glucuronolactone is commercially available in several forms, including as an ingredient in energy drinks, standalone dietary supplement powders and capsules, and pre-workout formulations. Glucuronolactone is an ingredient used in some energy drinks, often in unnaturally high doses. One 250 ml can of Red Bull contains about 600 mg glucuronolactone. The synthetically produced form used in commercial products is chemically identical to the endogenous molecule.
Historically, glucuronolactone has been used as a hepatoprotective agent to alleviate liver metabolism burdens, supporting the detoxification of chemicals such as drugs and metabolic waste. Glucuronolactone is approved in China and Japan as an over-the-counter "hepatoprotectant," though there is a conspicuous lack of systematic reviews on this use. This approval reflects a long-standing practice in East Asian medicine and pharmacology of utilizing the compound in tablet form for liver support indications. According to The Merck Index, glucuronolactone is used as a detoxicant.
In Chinese clinical comparative research, glucuronolactone tablets were used as an active control comparator in studies examining the clinical efficacy of herbal preparations in preventing drug-induced liver injury (DILI) caused by anti-tuberculosis drugs. This context confirms that glucuronolactone has an established clinical profile for liver-protective indications in China, where it is prescribed or sold as a reference standard hepatoprotective agent rather than merely a supplement additive.
Energy drinks became increasingly popular since the late 1990s. Manufacturers claimed these drinks improve physical endurance, reaction speed, and concentration. The main ingredients of energy drinks are caffeine, sugar, taurine, and glucuronolactone. The formulation approach combined these ingredients on the premise that synergistic interaction would produce greater effect than any single ingredient alone. According to manufacturers, the stimulating effects of these drinks are due to interaction between the various ingredients.
Glucuronolactone is a naturally occurring lactone that is produced by the liver during the metabolism of glucose. It is a metabolite of glucose. Biochemically, D-glucurono-3,6-lactone is a molecule with the formula C₆H₈O₆. The biochemical precursor of glucuronolactone is glucuronic acid, which is involved in liver metabolism and the glucuronidation process.
Orally administered glucuronolactone is completely absorbed, hydrolyzed, and excreted in urine as glucuronic acid, xylitol, and L-xylulose. Glucuronolactone is converted to glucuronic acid when it enters the body through oral intake. Studies have found that glucuronic acid is involved in glucose metabolism and is the direct precursor of ascorbic acid formation in organisms. Both -CHO and -COOH groups exist in the molecule of glucuronic acid, which can react with toxic metabolites, such as -OH, -CH₂OH, and -SH groups, in the body to form non-toxic or low-toxic compounds excreted in urine and bile.
Glucuronolactone plays a key role in detoxification processes within the body, primarily through its conversion to glucuronic acid, which serves as the activated donor in glucuronidation — a phase II metabolic reaction that conjugates toxins, drugs, and endogenous compounds with glucuronic acid to enhance their water solubility and facilitate excretion via urine or bile. This pathway is essential for eliminating xenobiotics and maintaining homeostasis, with glucuronidation accounting for a significant portion of hepatic metabolism in mammals.
A key metabolic product of glucuronolactone breakdown is D-glucaro-1,4-lactone. Approximately 25% of glucuronolactone is quickly converted to it. This compound is a potent inhibitor of beta-glucuronidase, an enzyme dominantly produced by gut bacteria. Gut bacteria that produce beta-glucuronidase can break down complex carbohydrates; however, this enzyme also reverses the glucuronidation process, which slows detoxification. Its levels rise with exposure to chemical and environmental pollutants, such as tobacco smoke and heavy metals. By inhibiting beta-glucuronidase via its metabolite, glucuronolactone may help preserve the integrity of the glucuronidation pathway.
Glucuronolactone serves as a major structural component of connective tissues and collagen, contributing to tissue integrity and repair processes. In biological systems, glucuronolactone is rapidly converted to D-glucuronic acid, which is essential for the biosynthesis of glycosaminoglycans and proteoglycans found in extracellular matrices. Glycosaminoglycans (GAGs) are unbranched, polysaccharide chains which, with the exception of hyaluronan (HA), are highly sulfated and constitute the glucidic moieties of proteoglycan macromolecules. Depending on monosaccharide composition and protein linkage region, as well as sulfation pattern and degree, GAGs can be grouped into four subfamilies: chondroitin/dermatan sulfate, heparan sulfate/heparin, hyaluronan, and keratan sulfate. GAGs contribute to proteoglycan native folding and functions, as well as to tissue and organ behavior. In fact, GAGs are involved in stabilization of the fibrillar extracellular matrix, control of hydration, regulation of tissue and organism development by controlling cell cycle, cell behavior, and differentiation.
In non-human mammals capable of de novo vitamin C synthesis, glucuronolactone acts as a precursor in the ascorbic acid biosynthetic pathway; it equilibrates with glucuronic acid, which undergoes reduction at the C-1 position to form L-gulonic acid and subsequently L-gulonolactone, the immediate precursor to L-ascorbic acid via oxidation by gulonolactone oxidase. Humans lack this terminal enzyme and thus cannot synthesize vitamin C from glucuronolactone.
Glucuronolactone is attributed a possible detoxifying function and a positive effect in the reduction of oxidative stress and inflammation through the attenuation of hepatic fibrosis, thus increasing the antioxidant capacity of the organism. More recent animal research has proposed molecular signaling pathways. Glucuronolactone alleviates weaning stress-induced intestinal oxidative stress and inflammatory responses partly through activating the Nrf2-Akt signaling pathway to suppress the transcriptional activity of FOXO1, while also inhibiting the activation of the TLR4-MAPK signaling pathway.
Studies have investigated whether energy drinks improve cognitive performance and which ingredients are responsible, through literature searches covering the period from 1997 to 2006 based on Medline searches using the term "energy drink." Focused and sustained attention improved significantly, as did reaction speed in all sorts of reaction-time tasks. However, the findings suggest that most of the effects of energy drinks on cognitive performance are related mainly to the presence of caffeine, and that further investigation is needed into the effects of the lesser known ingredients of energy drinks (taurine, glucuronolactone) to obtain a better understanding of possible interactions.
One clinical study examined the combination of glucuronolactone with caffeine and taurine. The findings indicated that the mixture of three key ingredients of Red Bull Energy Drink — caffeine, taurine, and glucuronolactone — had positive effects upon human mental performance and mood. Mood was assessed by the "Basler-Befindlichkeitsbogen" questionnaire, a standard test for evaluation of feelings of well-being. Measurements were made at night, prior to and starting one hour after consumption of energy drink ingredients or placebo. At the end of the experiment, P300 latency and motor reaction time were significantly longer compared with baseline measurements in the placebo group, but were unchanged in the energy drink group. In the test system for evaluating feelings of well-being, total scores, vitality scores, and social extrovertedness scores were significantly decreased in the placebo group but not in the energy drink group.
Evidence quality assessment: Unfounded claims that glucuronolactone can be used to reduce "brain fog" are based on research conducted on energy drinks that contain other active ingredients that have been shown to improve cognitive function, such as caffeine. All published clinical studies on cognitive effects used combination products; no adequately controlled study has isolated the contribution of glucuronolactone alone from other co-ingredients. The evidence for a specific cognitive effect of glucuronolactone as an individual ingredient must therefore be considered unverified and currently unsupported at the clinical level.
A double-blind study administered 500 mL of a glucose-based "energy" drink versus a control without the active ingredients (caffeine, taurine, glucuronolactone) to 11 sleepy participants driving an interactive real-car driving simulator. Lane drifting and a secondary task (reaction time) were measured for two hours post-treatment. The energy drink significantly improved both indices, particularly for the first hour. Again, this study used a combination product, making it impossible to attribute the observed effects specifically to glucuronolactone.
In an earlier animal study, 100 mg glucuronolactone per kg body weight or other sugars were injected into rats three times a day. After glucuronolactone administration, positive effects on swimming performance, blood sugar, and liver glycogen levels were observed, which were not observed after treatment with the other sugars. However, similar observations have been made in other studies after injection of glucose and galactose, suggesting that these effects are based on the known ergogenic effects of carbohydrates in general.
Although manufacturers of energy drinks claim that these beverages are beneficial in that they can boost energy, physical performance, and improve cognitive performance, there is insufficient scientific evidence to support these claims. Hardly any studies have been found that examined glucuronolactone as a single substance.
Evidence quality assessment: Physical performance evidence for glucuronolactone as a standalone ingredient consists primarily of older animal/injection studies and human studies using combination beverages. No rigorous, placebo-controlled clinical trial has established a specific ergogenic effect attributable to glucuronolactone alone. Evidence is therefore classified as preliminary and insufficient.
D-Glucuronolactone (DGL), described as a hepatoprotective compound widely used in clinical and energy products, has been evaluated in animal feeding trials. Serum analysis in animal studies showed decreased activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase, and reduced low-density lipoprotein cholesterol, total cholesterol, and triacylglycerols. Histologically, high-dose DGL alleviated liver lesions in the animal model.
DGL has been extensively employed in clinical settings in some regions for managing liver disorders, ranging from chronic and acute hepatitis to cirrhosis and other liver diseases. As noted above, glucuronolactone is approved in China and Japan as an over-the-counter "hepatoprotectant," though there is a conspicuous lack of systematic reviews on this use.
Evidence quality assessment: Hepatoprotective use is supported by regulatory approval in two major Asian jurisdictions and by mechanistic plausibility through the glucuronidation pathway. However, no published systematic review or large, well-controlled randomized clinical trial from peer-reviewed English-language literature was identified to robustly confirm efficacy in humans with liver disease. The clinical evidence base for this application is limited and largely unreviewed in the Western literature.
Recent animal research has investigated glucuronolactone's effects on gut health at the molecular level. In a 2025 pig study, glucuronolactone increased average daily gain, average daily feed intake, and final body weight of piglets, while reducing the diarrhea rate. Glucuronolactone is described as a glucose metabolite with antioxidant activity. The study used 24 weaned piglets randomly assigned to two groups, with one group receiving a basal diet and the other receiving an experimental diet supplemented with 200 mg/kg of glucuronolactone.
Additional mechanistic research published in 2026 investigated glucuronolactone against mycotoxin-induced gut injury. Glucuronolactone as a natural metabolite of glucose was shown to increase Lactobacillus amylovorus abundance and luminal indole-3-acetic acid (IAA) level to activate AHR (aryl hydrocarbon receptor) signaling. In a piglet model, glucuronolactone effectively alleviated mycotoxin-induced intestinal injury and inflammation. Transcriptomic analysis revealed that glucuronolactone promotes mucin sulfation, a critical process for fortifying the intestinal mucus barrier. Microbiome and metabolomics analyses uncovered that glucuronolactone increased probiotic Lactobacillus amylovorus abundance and luminal indole-3-acetic acid level, thereby facilitating mucin sulfation.
Evidence quality assessment: Gut health evidence is entirely from animal models (piglets) and in vitro work at this time. The pathways identified are mechanistically coherent, but no human clinical data exist for this indication.
In animal studies, antioxidant indices revealed elevated catalase and superoxide dismutase (SOD) activities in serum and intestine, coupled with reduced malondialdehyde, following DGL supplementation. DGL also suppressed inflammatory cytokines (TNF-α, IL-1β, IL-10) in liver and intestine. Challenge tests with Aeromonas hydrophila confirmed enhanced disease resistance in DGL-supplemented animals. Glucuronolactone has been shown to effectively alleviate oxidative stress and cellular apoptosis induced by mycotoxin ochratoxin A in animal models.
Evidence quality assessment: Antioxidant and immune effects are supported by animal and in vitro data only. No controlled human studies have been published demonstrating these effects in clinical populations.
Since glucuronolactone is not approved by the FDA for any condition, there is no official dose. Users and supplement manufacturers have established unofficial doses based on trial and error.
Available supplement product forms include capsules, standalone powder, and as a component of pre-formulated energy drink powders and ready-to-drink beverages.
Taurine and D-glucuronolactone occur as natural ingredients in food and are normal human metabolites. However, they are also used at much higher levels in energy drinks. EFSA's Panel on Food Additives and Nutrient Sources concluded that exposure to taurine and D-glucuronolactone through regular consumption of energy drinks was not of safety concern.
Based on a NOAEL of D-glucurono-γ-lactone of 1,000 mg/kg body weight per day, EFSA concluded that exposure to D-glucurono-γ-lactone as an individual ingredient at the levels presently used in "energy drinks" and at the intake levels presented in the EFSA opinion is of no safety concern.
When taken by mouth, glucuronolactone is likely safe when used in food amounts. There is not enough reliable information to know if glucuronolactone is safe when taken by mouth in higher amounts.
Data with regard to possible acute toxicity of glucuronolactone are not available so far, and hardly any studies have been found that examined glucuronolactone as a single substance.
Risk characterization by estimating the margin of safety (MOS) suggests that the consumption of a high volume of energy drinks (up to 500 mL) reduces the MOS. Individuals weighing 60 and 80 kg would only present an MOS ≥ 100 when their consumption of energy drinks with 2,400 mg of D-glucuronolactone/L is limited to 250 mL. This finding raises concern for individuals who habitually consume large or multiple servings of high-glucuronolactone beverages.
The European Food Safety Authority (EFSA) concluded that it is unlikely that glucurono-γ-lactone would have any interaction with caffeine, taurine, alcohol, or the effects of exercise. The EFSA Panel also concluded, based on the available data, that additive interactions between taurine and caffeine on diuretic effects are unlikely.
A single oral dose of 1.5 g/kg of glucuronolactone in rats significantly prolonged whole blood clotting times for 6 days. This preclinical finding has not been replicated in human clinical studies, but suggests a theoretical interaction with anticoagulant medications that has not been adequately investigated.
Decreases in noradrenaline, serotonin, and dopamine levels indicating neurochemical alterations and neurotoxic effects on subchronic drug administration have been suggested in animal models. The combination of taurine, gluconolactone, and glucuronolactone caused more noticeable changes in neurotransmitter levels than individual compounds. These findings are from young rat models treated for 21 days and have not been confirmed in human clinical trials.
Because exposure to D-glucuronolactone and taurine has raised safety concerns, especially in high and chronic consumption scenarios, individual initiatives have been launched in different countries, such as Germany and Denmark, promoting the standardization of energy drinks with maximum glucuronolactone contents at 2,400 mg/L. Regulatory bodies have not established safety profiles specific to children, pregnant women, or individuals with hepatic impairment consuming supplemental glucuronolactone at doses above typical food intake levels.
Glucuronolactone has a well-established safety record and is already approved for use in functional foods, beverages, and dietary supplements across key global markets. In the United States, it is present in the NIH Dietary Supplement Label Database as a declared ingredient in dietary supplement products. In the European Union, EFSA has reviewed its safety as a constituent of energy drinks. In China and Japan, it is approved as an over-the-counter hepatoprotectant.
Condiciones de salud que Glucuronolactona puede ayudar a apoyar.
Glucuronolactone is a naturally occurring compound from glucose metabolism commonly included in energy drinks alongside caffeine and taurine for athletic performance. While human-specific RCT evidence for glucuronolactone alone is limited, the combination with caffeine and taurine in energy drink RCTs shows consistent exercise performance improvements.
Sistemas corporales que Glucuronolactona puede ayudar a apoyar.
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