In man, physiological amounts of vitamin B12 (cyanocobalamin) are absorbed by the intrinsic factor mediated mechanism exclusively in the ileum. Human faeces contain appreciable quantities of vitamin B12 or vitamin B12-like material presumably produced by bacteria in the colon, but this is unavailable to the non-coprophagic individual. However, the human small intestine also often harbours a considerable microflora and this is even more extensive in apparently healthy southern Indian subjects. We now show that at least two groups of organisms in the small bowel, Pseudomonas and Klebsiella sp., may synthesise significant amounts of the vitamin.
Six normal untrained men were studied during the intravenous infusion of a balanced amino acid mixture (approximately --1 for 3 h) at rest and after a leg resistance exercise routine to test the influence of exercise on the regulation of muscle protein kinetics by hyperaminoacidemia. Leg muscle protein kinetics and transport of selected amino acids (alanine, phenylalanine, leucine, and lysine) were isotopically determined using a model based on arteriovenous blood samples and muscle biopsy. The intravenous amino acid infusion resulted in comparable increases in arterial amino acid concentrations at rest and after exercise, whereas leg blood flow was 64 +/- 5% greater after exercise than at rest. During hyperaminoacidemia, the increases in amino acid transport above basal were 30-100% greater after exercise than at rest. Increases in muscle protein synthesis were also greater after exercise than at rest (291 +/- 42% vs. 141 +/- 45%). Muscle protein breakdown was not significantly affected by hyperminoacidemia either at rest or after exercise. We conclude that the stimulatory effect of exogenous amino acids on muscle protein synthesis is enhanced by prior exercise, perhaps in part because of enhanced blood flow. Our results imply that protein intake immediately after exercise may be more anabolic than when ingested at some later time.
Two severe disorders, both quite well described, are associated with defects in purine metabolism: Lesch-Nyhan syndrome and severe combined immunodeficiency disease (SCID) . Lesch-Nyhan syndrome results from the loss of a functional HGPRT gene. The disorder is inherited as a sex-linked trait, with the HGPRT gene on the X chromosome (Xq26–). Patients with this defect exhibit not only severe symptoms of gout but also a severe malfunction of the nervous system. In the most serious cases, patients resort to self-mutilation. Death usually occurs before patients reach their 20th year.