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Jun 2023
S. Prakasha Gowda A.Corresponding author
Insulin is a frequent peptide hormone addition in serum-free mammalian cell culture media. It contributes in a variety of biological functions, including as promoting cell proliferation, cell cycle progression, and glucose uptake. However, it is unknown how stable insulin is under in vitro cell culture media treatment conditions. The instability of insulin in aqueous solutions has caused a number of issues, necessitating the development of new therapeutic strategies that can keep insulin stable and functioning. Such choices are required to accommodate updated insulin delivery guidelines as well as the storage and transportation of insulin. To preserve structural and functional integrity, protein medicines are frequently stabilized with antioxidants in aqueous solutions. In the present study, the effects of the antioxidants disodium ethylenediaminetetraacetic acid dihydrate (EDTA) and sodium selenite (Se) and their ability to scavenge free radicals on insulin stability in the medium Dulbecco's Modified Eagle Medium (DMEM) and Roswell Park Memorial Institute (RPMI) were examined. To investigate the stability of human recombinant insulin, in vitro serum-free DMEM and RPMI media were utilized for 5 days at 37˚C containing different EDTA and Se concentrations. Reversed phase high performance liquid chromatography (RP-HPLC) was used to detect and quantify insulin. Sodium dodecyl sulfate polyacrylamide gel (SDS-PAGE) electrophoresis was used to assess conformational stability. The results demonstrated that, when EDTA and Se were added separately to DMEM and RPMI media, insulin stability was improved compared to when neither compound was added.
Oct 2014 DOI 10.14302/issn.2374-9431.jbd-13-212
Ahmad Sliem HamdyCorresponding author
Biochemistry and internal Medicine*, Basic oral and medical sciences, College of dentistry, Qassim University, Saudi Arabia
Diabetes mellitus type 2 (DMT2) is a complex polygenic disorder. DMT2 is a result of insulin resistance and destruction of pancreatic β-cell or dysfunction. Therefore, glucose builds up in the bloodstream, leading to nerve damage, blindness, organ failures and sometimes death. Recently, some recently discovered genes play a key role in regulating the sensitivity to insulin. Scientists have long known that the disease often runs in families, and other genetic links. Human genetic discoveries will keep improving our knowledge about diabetes for many years to come. Varieties of prospective diabetic researches were developed to diagnose and control DMT2. Researchers spent thousands of millions of dollars to address DMT2. Pioneers of advanced biotechnology developed bioinformatics tools that changed the course of research about the role of metabolomics in DMT2. It will facilitate the identification of possible causes of DMT2 in genome studies. The present article aimed at reviewing the research studies per training to metabolomics and bioinformatics in genome studies in relation to DMT2.
Sep 2013 DOI 10.14302/issn.2374-9431.jbd-13-218
Oxenkrug GregoryCorresponding author
Psychiatry and Inflammation Program, Department of Psychiatry, Tufts University School of Medicine and Tufts Medical Center, Boston MA, USA.
The increased association between depression and diabetes mellitus is generally acknowledged. Recent studies suggest that depression leads to diabetes.However, the underlying molecular mechanisms for this association remain unclear.Literature and our data indicate that inflammatory and/or stress factors in depression up-regulate tryptophan (TRP) conversion into kynurenine (KYN), a substrate for nicotinamide adenine dinucleotide (NAD) biosynthesis. Deficiency of vitamin B6, a co-factor of the key enzymes of KYN – NAD pathway, shunts KYN metabolism from formation of NAD towards production of xanthurenic (XA) and kynurenic (KYNA) acids. Human and experimental studies reveal that XA, KYNA and their metabolites interfere with production, release and biological activity of insulin. We propose that inflammation- and/or stress-induced up-regulation of TRP – KYN metabolism in combination with vitamin B6 deficiency is one of the mechanisms mediating increased risk of diabetes in depression. Consequently, monitoring formation of diabetogenic KYN derivatives might help to identify subjects-at-risk for the development of diabetes. Pharmacological down-regulation of the TRP – KYN – NAD pathway and maintenance of adequate vitamin B6 status might help to prevent the development of diabetes in depression and other conditions associated with inflammation/stress–induced excessive production of KYN and vitamin B6 deficiency, e.g., obesity, cardiovascular diseases, aging, menopause, pregnancy, and hepatitis C virus infection.