Herein we have described the biochemical characterization of human GntK, an enzyme flagged in two network gap filling analyses of Recon 1 and employed constraint based network analysis to assess how gluconate might impact human metabolism. The results advance knowledge of the biochemical properties of isoform I of human GntK and suggest that considerable perturbation of metabolic Estazolam pathways associated with the HMS result given that gluconate degradation follows similar routes in humans as reported in vertebrates. Furthermore, these data serve to highlight an overlooked carbon flux pathway into the HMS in humans which could be of significance given the pathways central anabolic role and importance in combating oxidative stress. Finally the results demonstrate the application of human metabolic 5HPP-33 models to assess metabolic phenotypes and how these can be put into context with existing biological data to advance functional genomic hypotheses. Cellular cardiomyoplasty has emerged as a potential therapeutic strategy for patients with acute myocardial infarction. MI results in loss of cardiomyocytes, ventricular remodeling, scar formation, fibrosis and subsequently heart failure. The ultimate goal of any regenerative therapy for ischemic myocardium is to regenerate lost cardiomyocytes and facilitate cardiovascular neovascularization, in order to lead to clinical improvement in cardiac functions. An array of adult stem cell types including skeletal myoblasts, bone marrow derived stem cells, endothelial progenitor as well as cardiac stem cells have been shown to lead to functional benefit in animal models of infarction, but clinical trials have generated mixed results. Hence, a search for a novel stem cell type that is capable of restoring cardiac function is of paramount importance. Mesenchymal stem cells due to their characteristic properties such as ease of isolation, extensive ex vivo expansion capacity and multi-lineage differentiation potential are considered to be one of the potential stem cells for cardiac repair and regeneration after MI in both experimental animals, and clinical studies. Although originally identified in bone marrow, MSC have also been isolated from many adult organs as well as fetal-stage tissues.