Guanidinoacetic Acid Consumption via Regular Diet in Adults

Ostojić, Sergej M.; Štajer, Valdemar; Rátgéber, László; Betlehem, József; Ács, Pongrác

doi:10.1159/000520550

Cited by 4 publications

(4 citation statements)

References 6 publications

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“…[ 12 ]). In addition, GAA could be obtained by a regular diet [ 13 , 14 ] and gut microbiota [ 15 ], yet these pathways contribute marginally to the total daily turnover of GAA.…”

Section: Gaa Physiology Biomolecular Interactions and Pathwaysmentioning

confidence: 99%

Safety of Dietary Guanidinoacetic Acid: A Villain of a Good Guy?

Ostojić

2021

Nutrients

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Guanidinoacetic acid (GAA) is a natural amino acid derivative that is well-recognized for its central role in the biosynthesis of creatine, an essential compound involved in cellular energy metabolism. GAA (also known as glycocyamine or betacyamine) has been investigated as an energy-boosting dietary supplement in humans for more than 70 years. GAA is suggested to effectively increase low levels of tissue creatine and improve clinical features of cardiometabolic and neurological diseases, with GAA often outcompeting traditional bioenergetics agents in maintaining ATP status during stress. This perhaps happens due to a favorable delivery of GAA through specific membrane transporters (such as SLC6A6 and SLC6A13), previously dismissed as un-targetable carriers by other therapeutics, including creatine. The promising effects of dietary GAA might be countered by side-effects and possible toxicity. Animal studies reported neurotoxic and pro-oxidant effects of GAA accumulation, with exogenous GAA also appearing to increase methylation demand and circulating homocysteine, implying a possible metabolic burden of GAA intervention. This mini-review summarizes GAA toxicity evidence in human nutrition and outlines functional GAA safety through benefit-risk assessment and multi-criteria decision analysis.

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“…[ 12 ]). In addition, GAA could be obtained by a regular diet [ 13 , 14 ] and gut microbiota [ 15 ], yet these pathways contribute marginally to the total daily turnover of GAA.…”

Section: Gaa Physiology Biomolecular Interactions and Pathwaysmentioning

confidence: 99%

Safety of Dietary Guanidinoacetic Acid: A Villain of a Good Guy?

Ostojić

2021

Nutrients

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“…Meatbased products contain the highest relative amount of GAA (~50 mg per kg), followed by a dairy group (~0.3 mg per kg), and plant-based foods (~1 μg per kg), suggesting relatively low dietary exposure to exogenous GAA in omnivores, and even lower in vegans/vegetarians. We recently confirmed this hypothesis in a population-based study in U.S. adults, where the mean dietary intake of GAA was ~10 mg per day (Ostojic et al, 2022), with men consuming more GAA than women (12 vs. 8 mg/day). A small amount of GAA provided via regular diet implies that de novo synthesis of GAA from glycine and L-arginine likely provides a larger part of this compound (Figure 1).…”

Section: Ie Tary Intak E Of G a Amentioning

confidence: 56%

Guanidinoacetic acid in human nutrition: Beyond creatine synthesis

Ostojić

Jorga²

2023

Food Science & Nutrition

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Guanidinoacetic acid (GAA) is a nutrient that has been used in human nutrition since the early 1950s. Recommended for its role in creatine biosynthesis, GAA demonstrated beneficial energy‐boosting effects in various clinical conditions. Dietary GAA has also been suggested to trigger several creatine‐independent mechanisms. Besides acting as a direct precursor of high‐energy phosphagen creatine, dietary GAA is suggested to reduce blood glucose concentration by acting as an insulinotropic food compound, spare amino acid arginine for other metabolic purposes (including protein synthesis), modulate taste, and perhaps alter methylation and fat deposition in various organs including the liver. GAA as a food component can have several important metabolic roles beyond creatine biosynthesis; future studies are highly warranted to address GAA overall role in human nutrition.

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“…This may explain why the endogenous creatine synthesis was more strongly associated with urinary guanidinoacetate excretion as compared to plasma guanidinoacetate. It should be noted that guanidinoacetate dietary intake may also contribute to circulating guanidinoacetate concentrations and urinary guanidinoacetate excretion, although a recent study in NHANES reported that food-driven guanidinoacetate appears to provide approximately 0.5% of the creatine homeostatic load in a regular diet, so that this contribution is likely limited (Ostojic et al 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Creatine homeostasis and the kidney: comparison between kidney transplant recipients and healthy controls

Post,

Groothof,

Kremer

et al. 2024

Amino Acids

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Creatine is a natural nitrogenous organic acid that is integral to energy metabolism and crucial for proper cell functioning. The kidneys are involved in the first step of creatine production. With kidney transplantation being the gold-standard treatment for end-stage kidney disease, kidney transplant recipients (KTR) may be at risk of impaired creatine synthesis. We aimed to compare creatine homeostasis between KTR and controls. Plasma and urine concentrations of arginine, glycine, guanidinoacetate, creatine and creatinine were measured in 553 KTR and 168 healthy controls. Creatine intake was assessed using food frequency questionnaires. Iothalamate-measured GFR data were available in subsets of 157 KTR and 167 controls. KTR and controls had comparable body weight, height and creatine intake (all P > 0.05). However, the total creatine pool was 14% lower in KTR as compared to controls (651 ± 178 vs. 753 ± 239 mmol, P < 0.001). The endogenous creatine synthesis rate was 22% lower in KTR as compared to controls (7.8 ± 3.0 vs. 10.0 ± 4.1 mmol per day, P < 0.001). Despite lower GFR, the plasma guanidinoacetate and creatine concentrations were 21% and 41% lower in KTR as compared to controls (both P < 0.001). Urinary excretion of guanidinoacetate and creatine were 66% and 59% lower in KTR as compared to controls (both P < 0.001). In KTR, but not in controls, a higher measured GFR was associated with a higher endogenous creatine synthesis rate (std. beta: 0.21, 95% CI: 0.08; 0.33; P = 0.002), as well as a higher total creatine pool (std. beta: 0.22, 95% CI: 0.11; 0.33; P < 0.001). These associations were fully mediated (93% and 95%; P < 0.001) by urinary guanidinoacetate excretion which is consistent with production of the creatine precursor guanidinoacetate as rate-limiting factor. Our findings highlight that KTR have a disturbed creatine homeostasis as compared to controls. Given the direct relationship of measured GFR with endogenous creatine synthesis rate and the total creatine pool, creatine supplementation might be beneficial in KTR with low kidney function.Trial registration ID: NCT02811835.Trial registration URL: https://clinicaltrials.gov/ct2/show/NCT02811835.

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Guanidinoacetic Acid Consumption via Regular Diet in Adults

Cited by 4 publications

References 6 publications

Safety of Dietary Guanidinoacetic Acid: A Villain of a Good Guy?

Safety of Dietary Guanidinoacetic Acid: A Villain of a Good Guy?

Guanidinoacetic acid in human nutrition: Beyond creatine synthesis

Creatine homeostasis and the kidney: comparison between kidney transplant recipients and healthy controls

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