Glycine Abstracts 4

Glycine Therapy in the Myopathies

         (1934) Download

Treatment of Gastric Hemorrhage

         (Andresen 1927) Download

Myasthenia Gravis

         (Boothby 1934) Download

Muscular Dystrophy

         (Reinhold, Clark et al. 1934) Download

Determinants of aspirin metabolism in healthy men and women: effects of dietary inducers of UDP-glucuronosyltransferases

         (Navarro, Saracino et al. 2011) Download

BACKGROUND/AIMS: Interindividual variation in aspirin (ASA) metabolism is attributed to concomitant use of drugs or alcohol, urine pH, ethnicity, sex, and genetic variants in UDP-glucuronosyltransferases (UGT). Little is known about the effects of diet. METHODS: We evaluated cross-sectionally whether urinary excretion of ASA and its metabolites [salicylic acid (SA), salicyluric acid (SUA) phenolic glucuronide (SUAPG), salicylic acid acyl glucuronide (SAAG) and salicylic acid phenolic glucuronide (SAPG)] differed by UGT1A6 genotype and dietary factors shown to induce UGT. Following oral treatment with 650 mg ASA, urine was collected over 8 h in 264 men and 264 women (21-45 years old). RESULTS: There were statistically significant differences in metabolites excreted between sexes and ethnicities. Men excreted more SUA; women more ASA (p = 0.03), SA, SAAG and SAPG (p </= 0.001 for all). Compared to Caucasians, Asians excreted more ASA, SA and SAAG, and less SUA and SUAPG (p </= 0.03 for all); African-Americans excreted more SAAG and SAPG and less SUA (p </= 0.04). There was no effect of UGT1A6 genotypes. Increased ASA and decreased SUAPG excretion was observed with increased servings of vegetables (p = 0.008), specifically crucifers (p = 0.05). CONCLUSION: Diet may influence the pharmacokinetics of ASA, but effects may be through modulation of glycine conjugation rather than glucuronidation.

Uric acid transport and disease

         (So and Thorens 2010) Download

Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.


References

(1934). "Glycine Therapy in the Myopathies." JAMA 115: 2001. [PMID:

Andresen, A. F. R. (1927). "Treatment of Gastric Hemorrhage." JAMA 89: 1397. [PMID:

Boothby, W. M. (1934). "Myasthenia Gravis." JAMA 102: 259. [PMID:

Navarro, S. L., M. R. Saracino, et al. (2011). "Determinants of aspirin metabolism in healthy men and women: effects of dietary inducers of UDP-glucuronosyltransferases." J Nutrigenet Nutrigenomics 4(2): 110-8. [PMID: 21625173]

Reinhold, J. G., J. H. Clark, et al. (1934). "Muscular Dystrophy." JAMA 102: 261. [PMID:

So, A. and B. Thorens (2010). "Uric acid transport and disease." J Clin Invest 120(6): 1791-9. [PMID: 20516647]