Prevention of Type I Diabetes Mellitus: The Role of Immune Interventions

Ngugi, Mathew Piero

doi:10.4172/2155-9899.s2-005

Cited by 2 publications

(1 citation statement)

References 60 publications

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“…Likewise, another investigation showed that either with the use of drugs or by genetically knocking out of B cells is sufficient to dramatically suppress immune cell infiltration and inflammation in adipose tissue, finally enhancing sensitivity of insulin. 28 , 29 …”

Section: Diabetes Mellitus and Immunitymentioning

confidence: 99%

<p>Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications</p>

Yehualashet¹

2020

DMSO

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Diabetes mellitus (DM) is a chronic endocrine disease distinguished by hyperglycemia due to disturbance in carbohydrate or lipid metabolism or insulin function. To date, diabetes, and its complications, is established as a global cause of morbidity and mortality. The intended aim during the management of diabetes is to maintain blood glucose close to normal because the majority of patients have poor control of their elevated blood glucose and are highly prone to severe macrovascular and microvascular complications. To decrease the burden of the disease and its complications, scientists from various disciplines are working intensively to identify novel and promising drug targets for diabetes and its complications. Increased and ongoing investigations on mechanisms relating to diabetes and associated complications could potentially consider inflammatory cascades as a promising component of the strategy in the prevention and control of diabetes and its complications. The potential of targeting mediators of inflammation like toll-like receptors (TLRs) are part of current investigation by the scientific community. Hence, the aim of the present review is to discuss the role of TLRs as a potential drug target for diabetes and diabetes associated complications.

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Section: Diabetes Mellitus and Immunitymentioning

confidence: 99%

<p>Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications</p>

Yehualashet¹

2020

DMSO

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Apigenin Causes Biochemical Modulation, Glut4 and Cd38 Alterations to Improve Diabetes and to Protect Damages of Some Vital Organs in Experimental Diabetes

Hossain

Ghosh

Satapathy

et al. 2014

American Journal of Pharmacology and Toxicology

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Diabetes mellitus gradually leads to dysfunction and failure of some vital organs specially the eyes, kidneys, pancreas, brain, heart, liver and lungs. The study was aimed to evaluate the antidiabetic potential of apigenin and its mechanistic role in controlling damages of vital tissues in streptozotocin-induced diabetic rats. Streptozotocin-induced diabetic rats were treated with apigenin and glipizide. Various biochemical changes, GLUT4 and CD38 protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to compare the antidiabetic potentials of those two chemicals and to understand their capability to control the damages of the vital organs during diabetes. Effective control of blood glucose level along with the alteration of hepatic phase I and phase II drug metabolizing enzymes, antioxidant defense enzyme activities and lipid peroxidation level towards their normal values and enhanced GLUT4 translocation and downregulated CD38 expression by apigenin were observed. Apigenin was also found to prevent the deterioration of vital organs during diabetes. In conclusion, apigenin has predominant role in controlling blood glucose level along with the protection of vital organs eventually damaged during diabetes, by minimizing toxicities and associated diabetic complications in streptozotocin-induced diabetic rats and may explore as a potential antidiabetic agent in near future.

show abstract

Prevention of Type I Diabetes Mellitus: The Role of Immune Interventions

Cited by 2 publications

References 60 publications

<p>Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications</p>

<p>Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications</p>

Apigenin Causes Biochemical Modulation, Glut4 and Cd38 Alterations to Improve Diabetes and to Protect Damages of Some Vital Organs in Experimental Diabetes

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