Su1480 CONTROLLING GLYCEMIC HOMEOSTASIS ALLEVIATES ISLET β CELL DAMAGE AND REDUCES THE RISK OF DIABETES MELLITUS FOLLOWING ACUTE PANCREATITIS

2020 ◽  
Vol 158 (6) ◽  
pp. S-596-S-597
Author(s):  
Qiao Shi ◽  
Xiaoyi Zhang ◽  
Hanjun Li ◽  
Xingcheng Xiong ◽  
Weixing Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Acute Pancreatitis ◽  
Cell Damage ◽  
Β Cell

The protective ways of the body from cell damage at the diabetes mellitus

2016 ◽  
Vol 10 (1) ◽  
pp. 0-0
Author(s):  
Макишева ◽  
R. Makisheva
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Action ◽  
Cell Damage ◽  
Glycogen Synthesis ◽  
The Body ◽  
Diabetic Patients ◽  
Β Cell ◽  
Extracellular Medium ◽  
Compensation Mechanisms

Recognition hyperinsulinemia as the root cause of type 2 diabetes mellitus is becoming more supporters. The overload nutrition cell and insulin resistance is developing as a result of hyperinsulinemia. Insulin resistance is not the only one protection mechanism. Functional system to limited excessive insulin action includes other mechanisms. This review describes the reactions that develop in the tissues in diabetic patients and their relationship with excessive exposure to insulin. Negative feedback mechanism under excessive stimulation of insulin action includes action contrainsular hormones, no β-cell response on increasing the glucose in the extracellular medium, reduction of C-peptide, induction of β-cell apoptosis. The compensation mechanisms includes the restriction of consumption of substances and flow of information, the redirecting excess in the adi-pose tissue, the glycogen synthesis and the activation of kinase-3 synthase glycogen. The conditions GI insulin is able to bind and activate receptors IGF-type 1 to a greater extent than insulin receptors. At diabetes the repro-duction, the growth and the differentiation of cells are accelerated, leading to tumor growth, the accumulation of senescent cells. The depletion and reduction of telomerase activity in diabetes mellitus also have an adaptive value. Contact with receptors undifferentiated cells caused by their high sensitivity and low capacity for insulin resistance, operates referral mechanism power is the same as for obesity. Young cells of functionally active or-gans die, some cells accelerate differentiation and less active peripheral located in hypoxic conditions, may be-come cancerous. The author believes that the growth of tumors after intensive treatment of diabetes is associated with excess insulin action.

scholarly journals SARS-CoV-2 Infection and Pancreatic β Cell Failure

Biology ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 22
Author(s):  
Keiichiro Mine ◽  
Seiho Nagafuchi ◽  
Hitoe Mori ◽  
Hirokazu Takahashi ◽  
Keizo Anzai
Keyword(s):  
Diabetes Mellitus ◽  
Cell Damage ◽  
Study Groups ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Potential Association

SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in patients with COVID-19. According to the research reviewed in this paper, the pancreas and pancreatic β cells appear to be targets of SARS-CoV-2 and are damaged by direct or indirect effects of the infection. However, controversial results have been reported between study groups, mainly due to the limited number of cases with diabetes precipitated by COVID-19. In this review, we comprehensively discuss the published findings on the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic β-cell damage leading to diabetes onset. These findings will further contribute to our understanding of the pathogenesis of diabetes mellitus.

scholarly journals Is there a link between cytomegalovirus infection and new-onset posttransplantation diabetes mellitus? Potential mechanisms of virus induced β-cell damage

2005 ◽  
Vol 20 (11) ◽  
pp. 2311-2315 ◽  
Author(s):  
Jøran Hjelmesæth ◽  
Fredrik Müller ◽  
Trond Jenssen ◽  
Halvor Rollag ◽  
Solbjørg Sagedal ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cytomegalovirus Infection ◽  
Cell Damage ◽  
Β Cell ◽  
New Onset

scholarly journals The Landscape of microRNAs in βCell: Between Phenotype Maintenance and Protection

2021 ◽  
Vol 22 (2) ◽  
pp. 803
Author(s):  
Giuseppina Emanuela Grieco ◽  
Noemi Brusco ◽  
Giada Licata ◽  
Daniela Fignani ◽  
Caterina Formichi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Β Cell ◽  
Physiological Mechanisms ◽  
Effective Strategies ◽  
Chronic Hyperglycaemia ◽  
Shed Light

Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by chronic hyperglycaemia mainly due to pancreatic β cell death and/or dysfunction, caused by several types of stress such as glucotoxicity, lipotoxicity and inflammation. Different patho-physiological mechanisms driving β cell response to these stresses are tightly regulated by microRNAs (miRNAs), a class of negative regulators of gene expression, involved in pathogenic mechanisms occurring in diabetes and in its complications. In this review, we aim to shed light on the most important miRNAs regulating the maintenance and the robustness of β cell identity, as well as on those miRNAs involved in the pathogenesis of the two main forms of diabetes mellitus, i.e., type 1 and type 2 diabetes. Additionally, we acknowledge that the understanding of miRNAs-regulated molecular mechanisms is fundamental in order to develop specific and effective strategies based on miRNAs as therapeutic targets, employing innovative molecules.

scholarly journals Therapeutic opportunities for pancreatic β-cell ER stress in diabetes mellitus

2021 ◽  
Author(s):  
Jing Yong ◽  
James D. Johnson ◽  
Peter Arvan ◽  
Jaeseok Han ◽  
Randal J. Kaufman
Keyword(s):  
Diabetes Mellitus ◽  
Er Stress ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Diabetes and Thrombosis: A Central Role for Vascular Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 706
Author(s):  
Aishwarya R. Vaidya ◽  
Nina Wolska ◽  
Dina Vara ◽  
Reiner K. Mailer ◽  
Katrin Schröder ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Molecular Mechanisms ◽  
Vascular System ◽  
Cell Damage ◽  
National Health System ◽  
Vascular Damage ◽  
Circulating Cells ◽  
Environmental Causes ◽  
Vascular Oxidative Stress

Diabetes mellitus is the fifth most common cause of death worldwide. Due to its chronic nature, diabetes is a debilitating disease for the patient and a relevant cost for the national health system. Type 2 diabetes mellitus is the most common form of diabetes mellitus (90% of cases) and is characteristically multifactorial, with both genetic and environmental causes. Diabetes patients display a significant increase in the risk of developing cardiovascular disease compared to the rest of the population. This is associated with increased blood clotting, which results in circulatory complications and vascular damage. Platelets are circulating cells within the vascular system that contribute to hemostasis. Their increased tendency to activate and form thrombi has been observed in diabetes mellitus patients (i.e., platelet hyperactivity). The oxidative damage of platelets and the function of pro-oxidant enzymes such as the NADPH oxidases appear central to diabetes-dependent platelet hyperactivity. In addition to platelet hyperactivity, endothelial cell damage and alterations of the coagulation response also participate in the vascular damage associated with diabetes. Here, we present an updated interpretation of the molecular mechanisms underlying vascular damage in diabetes, including current therapeutic options for its control.

scholarly journals Post-Transplant Diabetes Mellitus and Prediabetes in Renal Transplant Recipients: An Update

Nephron ◽  
2021 ◽  
pp. 1-13
Author(s):  
Ana Elena Rodríguez-Rodríguez ◽  
Esteban Porrini ◽  
Mads Hornum ◽  
Javier Donate-Correa ◽  
Raúl Morales-Febles ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Renal Transplant ◽  
Cell Function ◽  
Cell Damage ◽  
Current Evidence ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Post Transplant ◽  
Β Cell Function

Post-transplant diabetes mellitus (PTDM) is a frequent and relevant complication after renal transplantation: it affects 20–30% of renal transplant recipients and increases the risk for cardiovascular and infectious events. Thus, understanding pathogenesis of PTDM would help limiting its consequences. In this review, we analyse novel aspects of PTDM, based on studies of the last decade, such as the clinical evolution of PTDM, early and late, the reversibility rate, diagnostic criteria, risk factors, including pre-transplant metabolic syndrome and insulin resistance (IR) and the interaction between these factors and immunosuppressive medications. Also, we discuss novel pathogenic factors, in particular the role of β-cell function in an environment of IR and common pathways between pre-existing cell damage and tacrolimus-induced toxicity. The relevant role of prediabetes in the pathogenesis of PTDM and cardiovascular disease is also addressed. Finally, current evidence on PTDM treatment is discussed.

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