Predict Diabetes Mellitus Using Machine Learning Algorithms

Diabetes mellitus has become a very frequent disease that affects totally different organs of human body. Diabetes cause diverge depending on genetic, family history, health and environmental factors. Diabetes mellitus refers to a gaggle of diseases that affect how your body uses blood glucose. The underlying reason behind diabetes varies by type. But, despite what kind of diabetes you’ve got, it will cause excess sugar in your blood. Diabetes will be of two types, they are Type1 Diabetes and Type2 Diabetes. Early prediction will help in society a lot. It will provides the humanlife in safe way. The aim of this analysis is to develop a system that predicts the diabetes with a better accuracy. Parameters used to predict the type of Diabetes Mellitus are Glucose, Pregnancies, skin thickness, Blood pressure, Insulin, BMI, Diabetes pedigree function, age and upshot. In this we are with different machine learning algorithms, namely SVM, ANN, Decision tree, Logistic regression and Farthest first to predict the accuracy. Our experimental results show that farthest first attain superior correctness compare to dissimilar machine learning techniques.

Reno-Protective Effect of GLP-1 Receptor Agonists in Type1 Diabetes: Dual Action on TRPC6 and NADPH Oxidases

Diabetic kidney disease (DKD), a serious diabetic complication, results in podocyte loss and proteinuria through NADPH oxidases (NOX)-mediated ROS production. DUOX1 and 2 are NOX enzymes that require calcium for their activation which enters renal cells through the pivotal TRPC channels. Hypoglycemic drugs such as liraglutide can interfere with this deleterious mechanism imparting reno-protection. Herein, we aim to investigate the reno-protective effect of GLP1 receptor agonist (GLP1-RA), via its effect on TRPC6 and NADPH oxidases. To achieve our aim, control or STZ-induced T1DM Sprague–Dawley rats were used. Rats were treated with liraglutide, metformin, or their combination. Functional, histological, and molecular parameters of the kidneys were assessed. Our results show that treatment with liraglutide, metformin or their combination ameliorates DKD by rectifying renal function tests and protecting against fibrosis paralleled by restored mRNA levels of nephrin, DUOX1 and 2, and reduced ROS production. Treatment with liraglutide reduces TRPC6 expression, while metformin treatment shows no effect. Furthermore, TRPC6 was found to be directly interacting with nephrin, and indirectly interacting with DUOX1, DUOX2 and GLP1-R. Our findings suggest that treatment with liraglutide may prevent the progression of diabetic nephropathy by modulating the crosstalk between TRPC6 and NADPH oxidases.

Chromogranin A Deficiency Confers Protection from Autoimmune Diabetes Via Multiple Mechanisms

Recognition of beta-cell antigens by autoreactive T cells is a critical step in the initiation of autoimmune Type1 diabetes (T1D). A complete protection from diabetes development in non-obese diabetic (NOD) mice harboring a point mutation in the insulin B-chain 9-23 epitope points to a dominant role of insulin in diabetogenesis. Generation of NOD mice lacking the Chromogranin A protein (<a>NOD.ChgA^-/-</a>)completely nullified the autoreactivity of the BDC2.5 T cell and conferred protection from diabetes onset. These results raised the issue concerning the dominant antigen that drives the autoimmune process. Here we revisited the NOD.ChgA^-/-mice and found that their lack of diabetes development may not be solely explained by the absence of Chromogranin A reactivity. NOD.ChgA^-/-mice displayed reduced presentation of insulin peptides in the islets and periphery, which corresponded to impaired T cell priming. Diabetes development in these mice was restored by antibody treatment targeting regulatory T cells or inhibiting TGFb and PD-1 pathways. Therefore, the global deficiency of chromogranin A impairs recognition of the major diabetogenic antigen insulin, leading to broadly impaired autoimmune responses controlled by multiple regulatory mechanisms.

Chromogranin A Deficiency Confers Protection from Autoimmune Diabetes Via Multiple Mechanisms

Recognition of beta-cell antigens by autoreactive T cells is a critical step in the initiation of autoimmune Type1 diabetes (T1D). A complete protection from diabetes development in non-obese diabetic (NOD) mice harboring a point mutation in the insulin B-chain 9-23 epitope points to a dominant role of insulin in diabetogenesis. Generation of NOD mice lacking the Chromogranin A protein (<a>NOD.ChgA^-/-</a>)completely nullified the autoreactivity of the BDC2.5 T cell and conferred protection from diabetes onset. These results raised the issue concerning the dominant antigen that drives the autoimmune process. Here we revisited the NOD.ChgA^-/-mice and found that their lack of diabetes development may not be solely explained by the absence of Chromogranin A reactivity. NOD.ChgA^-/-mice displayed reduced presentation of insulin peptides in the islets and periphery, which corresponded to impaired T cell priming. Diabetes development in these mice was restored by antibody treatment targeting regulatory T cells or inhibiting TGFb and PD-1 pathways. Therefore, the global deficiency of chromogranin A impairs recognition of the major diabetogenic antigen insulin, leading to broadly impaired autoimmune responses controlled by multiple regulatory mechanisms.