Bioinformatics of Metabolomics in Diabetes Mellitus Type 2

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. DOI : 10.14302/issn.2374-9431.jbd-13-212 Corresponding author: Prof. Hamdy Sliem, , email: hamdy.sliem@yahoo.com


Introduction
Proteomics 2012 discussed a variety of proteomic and bioinformatic sciences ranging from computation methods, intracellular organelle proteomics, cellular proteomics, to clinical biological fluids/tissue proteomics and provided an excellent pathway for an effective multidisciplinary interactions in the control of diabetes [1].Omics methods such as proteomics and metabolomics, if used concurrently, can complement each other and provide an unbiased confirmation of biologically relevant signal pathways [2].
Globally, diabetes is one of the most common non-communicable metabolic disorders. It is the fourth or fifth leading cause of death in most high-income countries and there is substantial evidence to show that it is epidemic in many low-and middle-income countries.
DM is a complex metabolic disease marked by the uncoupling of blood glucose levels and insulin secretion with causing abnormal glycemic stages. Complications from diabetes, such as coronary artery and peripheral vascular disease, stroke, diabetic neuropathy, amputations, renal failure and blindness are resulting in increasing disability, reduced life expectancy and enormous health costs for virtually every society [3].The complications guided to molecular investigations to study genes that are involved with both diseases and sets genes driving each illness separately. The identification of these different genetic backgrounds discloses a molecular link between DM and complications. DMT2 is marked by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. In addition, the loss of insulin secretion may be attributed to loss of function in individual cells and loss of β-cell mass [4].
Abnormalities of metabolism ( and their encoded proteins, and the acquired metabolic macromolecules [12].

β-cell insulin secretion
The endocrine pancreas comprises the islets of Advanced studies ensured that insulin secretion capacity reflects β cell activity. Therefore, it is an early and sensitive biomarker for β -cell activity. Many transcriptional factors control the development of βcells and expression of many genes leading to impaired insulin secretion such as hepatocyte nuclear factor-4α, -1α, -1β (HNF-4α, -1α, -1β), insulin promoter factor-1 α (IPF-1α), and NEUROD1 [16].   abnormalities are known to cause insulin deficiency, insulin resistance and diabetes mellitus. From a population based epidemiologic study, it was found that mtDNA quantity was decreased in the peripheral blood of diabetic subjects, and also in those subjects who will convert to diabetes mellitus within 2 years [28][29][30].

3-Vitamin D and metabolomics in DMT2
It is virtual that, genes encoding proteins  Vitamin D may not be effective enough to improve insulin resistance and related morbidities. Therefore, they should ideally receive further nutritional support according to their genotype [41].

-Oxidative Stress
Oxidative stress may contribute to the development of DM. mainly, oxidative stress is due to variation in the genes coding these enzymes endogenous antioxidants including antioxidant enzymes e.g. superoxide dismutase, catalase, glutathione peroxidase, paraoxanase, and glutathione S -transferase.
Many recent nutrigenetics studies highlighted relation of interactions between diet, genetic variation in antioxidant enzymes, and oxidative stress [42][43].

Conclusion:
Genome-wide association data mining for identifying novel DMT2 genes are involved in the crosstalk between insulin signaling systems and metabolomics especially potential risk factors. The data from the Genome project can be utilized to identify novel DMT2 genes involved in the cross-linkages between insulin signaling systems and metabolomics.