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Study of Protein Biomarkers of Diabetes Mellitus Type 2 and Therapy with Vitamin B1.

Riaz S - J Diabetes Res (2015)

Bottom Line: In the present research work, the levels of protein biomarkers specific to diabetes mellitus type 2 in the Pakistani population using proteomic technology have been identified and characterized and effect of high dose thiamine has been seen on the levels of these marker proteins.Some proteins were up- and downregulated in diabetic samples as compared to control and decreased after thiamine therapy, while other protein markers did not show a significant change after the thiamine therapy.The effect of high dose thiamine on the levels of these identified protein biomarkers in the human urine has also been observed.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Molecular Genetics, University of the Punjab, Lahore 54590, Pakistan.

ABSTRACT
In the present research work, the levels of protein biomarkers specific to diabetes mellitus type 2 in the Pakistani population using proteomic technology have been identified and characterized and effect of high dose thiamine has been seen on the levels of these marker proteins. Diabetic patients and normal healthy controls were recruited from the Sheikh Zayed Hospital, Lahore, Pakistan. Total biochemical assays and proteins were estimated by modern proteomic techniques. Some proteins were up- and downregulated in diabetic samples as compared to control and decreased after thiamine therapy, while other protein markers did not show a significant change after the thiamine therapy. The effect of high dose thiamine on the levels of these identified protein biomarkers in the human urine has also been observed. Assessment of the levels of these biomarkers will be helpful in not only early diagnosis but also prognosis of diabetes mellitus type 2.

No MeSH data available.


Related in: MedlinePlus

Insulin signal transduction pathway in skeletal muscle (adapted from [9]).
© Copyright Policy - open-access
Related In: Results  -  Collection


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fig4: Insulin signal transduction pathway in skeletal muscle (adapted from [9]).

Mentions: The molecular mechanism of insulin resistance can be explained briefly as levels of insulin receptors and tyrosine kinase activity in skeletal muscles are reduced. These alterations are most likely to cause hyperinsulinemia. Therefore, postreceptor defects play the important and dominant role in insulin resistance. Polymorphism in insulin receptor substrates (IRS) may also be linked with intolerance of glucose, which raised the possibility that polymorphism in different postreceptors molecules combined and created a state of insulin resistance. The pathogenesis of insulin resistance is focused on signaling defect of a phosphatidylinositol-3-kinase (PI-3 kinase). Among other abnormalities, it also lowers the translocation of GLUT4 to the membrane of plasma. The insulin receptor has tyrosine kinase activity which has intrinsic property. These may interact with the proteins of IRS. Many docking proteins bind to these proteins and stimulated the metabolic action of insulin and PI-3-kinase pathway. As a result, insulin gives rise to elevation in glucose transport via PI-3-kinase pathway and stimulates the translocation of intracellular vesicles which has glucose transporters as GLUT4 to the plasma membrane as shown in Figure 4. There are some pathways of insulin signal transduction which are not resistant to effect of insulin like the cell growth/differentiation and mitogenic activated protein (MAP) kinase pathways. As a result, hyperinsulinemia elevated the insulin action through these pathways and accelerated the diabetes and other conditions like atherosclerosis. Free fatty acids can impair the utilization of glucose in the muscles. It also promotes the production of glucose by the liver and impairs the function of beta-cells in the case of obese type 2 DM [9].


Study of Protein Biomarkers of Diabetes Mellitus Type 2 and Therapy with Vitamin B1.

Riaz S - J Diabetes Res (2015)

Insulin signal transduction pathway in skeletal muscle (adapted from [9]).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4530253&req=5

fig4: Insulin signal transduction pathway in skeletal muscle (adapted from [9]).
Mentions: The molecular mechanism of insulin resistance can be explained briefly as levels of insulin receptors and tyrosine kinase activity in skeletal muscles are reduced. These alterations are most likely to cause hyperinsulinemia. Therefore, postreceptor defects play the important and dominant role in insulin resistance. Polymorphism in insulin receptor substrates (IRS) may also be linked with intolerance of glucose, which raised the possibility that polymorphism in different postreceptors molecules combined and created a state of insulin resistance. The pathogenesis of insulin resistance is focused on signaling defect of a phosphatidylinositol-3-kinase (PI-3 kinase). Among other abnormalities, it also lowers the translocation of GLUT4 to the membrane of plasma. The insulin receptor has tyrosine kinase activity which has intrinsic property. These may interact with the proteins of IRS. Many docking proteins bind to these proteins and stimulated the metabolic action of insulin and PI-3-kinase pathway. As a result, insulin gives rise to elevation in glucose transport via PI-3-kinase pathway and stimulates the translocation of intracellular vesicles which has glucose transporters as GLUT4 to the plasma membrane as shown in Figure 4. There are some pathways of insulin signal transduction which are not resistant to effect of insulin like the cell growth/differentiation and mitogenic activated protein (MAP) kinase pathways. As a result, hyperinsulinemia elevated the insulin action through these pathways and accelerated the diabetes and other conditions like atherosclerosis. Free fatty acids can impair the utilization of glucose in the muscles. It also promotes the production of glucose by the liver and impairs the function of beta-cells in the case of obese type 2 DM [9].

Bottom Line: In the present research work, the levels of protein biomarkers specific to diabetes mellitus type 2 in the Pakistani population using proteomic technology have been identified and characterized and effect of high dose thiamine has been seen on the levels of these marker proteins.Some proteins were up- and downregulated in diabetic samples as compared to control and decreased after thiamine therapy, while other protein markers did not show a significant change after the thiamine therapy.The effect of high dose thiamine on the levels of these identified protein biomarkers in the human urine has also been observed.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Molecular Genetics, University of the Punjab, Lahore 54590, Pakistan.

ABSTRACT
In the present research work, the levels of protein biomarkers specific to diabetes mellitus type 2 in the Pakistani population using proteomic technology have been identified and characterized and effect of high dose thiamine has been seen on the levels of these marker proteins. Diabetic patients and normal healthy controls were recruited from the Sheikh Zayed Hospital, Lahore, Pakistan. Total biochemical assays and proteins were estimated by modern proteomic techniques. Some proteins were up- and downregulated in diabetic samples as compared to control and decreased after thiamine therapy, while other protein markers did not show a significant change after the thiamine therapy. The effect of high dose thiamine on the levels of these identified protein biomarkers in the human urine has also been observed. Assessment of the levels of these biomarkers will be helpful in not only early diagnosis but also prognosis of diabetes mellitus type 2.

No MeSH data available.


Related in: MedlinePlus