Potential Toxicity of Chronic Creatine Supplementation in Mice

Wang, Lin; Shuhua, Xiao; Li, Yujuan; Wang, Lu; Che, Baoquan; Zhao, Xuan; Deng, Yulin

doi:10.1109/icbbe.2009.5163209

Cited by 1 publication

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References 18 publications

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“…Subsequently, cytotoxic compounds are produced [ 21 , 68 ]. The accumulation of those compounds in mice was found as a result of high concentrations of methylamine and enhanced activity of SSAO [ 21 , 69 ]. Poortmans et al studied 21 g/day of creatine monohydrate oral supplementation in 20 healthy male individuals and revealed that high dose loading of creatine in a short period of time increased excreted levels of methylamine and formaldehyde, 9.2-fold and 4.5-fold in the urine, respectively.…”

Section: Role Of Semicarbazide-sensitive Amine Oxidase In Creatinementioning

confidence: 99%

Beneficial Impact of Semicarbazide-Sensitive Amine Oxidase Inhibition on the Potential Cytotoxicity of Creatine Supplementation in Type 2 Diabetes Mellitus

2020

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Creatine supplementation of the population with type 2 diabetes mellitus (T2DM) combined with an exercise program is known to be a possible therapy adjuvant with hypoglycemic effects. However, excessive administration of creatine leads to the production of methylamine which is deaminated by the enzyme semicarbazide-sensitive amine oxidase (SSAO) and as a result, cytotoxic compounds are produced. SSAO activity and reaction products are increased in the serum of T2DM patients. Creatine supplementation by diabetics will further augment the activity of SSAO. The current review aims to find a feasible way to ameliorate T2DM for patients who exercise and desire to consume creatine. Several natural agents present in food which are involved in the regulation of SSAO activity directly or indirectly are reviewed. Particularly, zinc-α2-glycoprotein (ZAG), zinc (Zn), copper (Cu), histamine/histidine, caffeine, iron (Fe), and vitamin D are discussed. Inhibiting SSAO activity by natural agents might reduce the potential adverse effects of creatine metabolism in population of T2DM.

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