scholarly journals Exosome microRNAs in Metabolic Syndrome as Tools for the Early Monitoring of Diabetes and Possible Therapeutic Options

2021 ◽  
Vol 14 (12) ◽  
pp. 1257
Author(s):  
Erika Cione ◽  
Roberto Cannataro ◽  
Luca Gallelli ◽  
Giovambattista De Sarro ◽  
Maria Cristina Caroleo
Keyword(s):  
Essential Role ◽  
Cell Injury ◽  
Cell Types ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Pathological Conditions ◽  
Novel Approach ◽  
Almost All

Exosomes are nano-sized extracellular vesicles produced and released by almost all cell types. They play an essential role in cell–cell communications by delivering cellular bioactive compounds such as functional proteins, metabolites, and nucleic acids, including microRNA, to recipient cells. Thus, they are involved in various physio-pathological conditions. Exosome-miRNAs are associated with numerous diseases, including type 2 diabetes, a complex multifactorial metabolic disorder linked to obesity. In addition, exosome-miRNAs are emerging as essential regulators in the progression of diabetes, principally for pancreatic β-cell injury and insulin resistance. Here, we have clustered the recent findings concerning exosome-miRNAs associated with β-cell dysfunction to provide a novel approach for the early diagnosis and therapy of diabetes.

scholarly journals An Immediate and Long-Term Complication of COVID-19 May Be Type 2 Diabetes Mellitus: The Central Role of β-Cell Dysfunction, Apoptosis and Exploration of Possible Mechanisms

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2475
Author(s):  
Melvin R. Hayden
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Injury ◽  
Light And Electron Microscopy ◽  
Β Cell ◽  
Cell Dysfunction

The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was declared a pandemic by the WHO on 19 March 2020. This pandemic is associated with markedly elevated blood glucose levels and a remarkable degree of insulin resistance, which suggests pancreatic islet β-cell dysfunction or apoptosis and insulin’s inability to dispose of glucose into cellular tissues. Diabetes is known to be one of the top pre-existing co-morbidities associated with the severity of COVID-19 along with hypertension, cardiocerebrovascular disease, advanced age, male gender, and recently obesity. This review focuses on how COVID-19 may be responsible for the accelerated development of type 2 diabetes mellitus (T2DM) as one of its acute and suspected long-term complications. These observations implicate an active role of metabolic syndrome, systemic and tissue islet renin–angiotensin–aldosterone system, redox stress, inflammation, islet fibrosis, amyloid deposition along with β-cell dysfunction and apoptosis in those who develop T2DM. Utilizing light and electron microscopy in preclinical rodent models and human islets may help to better understand how COVID-19 accelerates islet and β-cell injury and remodeling to result in the long-term complications of T2DM.

scholarly journals Diminished Sphingolipid Metabolism, a Hallmark of Future Type 2 Diabetes Pathogenesis, Is Linked to Pancreatic β Cell Dysfunction

iScience ◽  
2020 ◽  
Vol 23 (10) ◽  
pp. 101566
Author(s):  
Saifur R. Khan ◽  
Yousef Manialawy ◽  
Andreea Obersterescu ◽  
Brian J. Cox ◽  
Erica P. Gunderson ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Sphingolipid Metabolism ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

scholarly journals Inhibition of Forkhead Box O1 Protects Pancreatic β-Cells against Dexamethasone-Induced Dysfunction

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4065-4073 ◽  
Author(s):  
Xiongfei Zhang ◽  
Wei Yong ◽  
Jinghuan Lv ◽  
Yunxia Zhu ◽  
Jingjing Zhang ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Types ◽  
Pancreatic Β Cell ◽  
Rinm5f Cells ◽  
Β Cells ◽  
Β Cell ◽  
Rat Islets ◽  
Cell Dysfunction ◽  
Forkhead Box ◽  
Glucose Stimulated Insulin Secretion

Abstract Forkhead Box O1 (FoxO1) is a key transcription regulator of insulin/IGF-I signaling pathway, and its activity can be increased by dexamethasone (DEX) in several cell types. However, the role of FoxO1 in DEX-induced pancreatic β-cell dysfunction has not been fully understood. Therefore, in this study, we investigated whether FoxO1 could mediate DEX-induced β-cell dysfunction and the possible underlying mechanisms in pancreatic β-cell line RINm5F cells and primary rat islet. We found that DEX markedly increased FoxO1 mRNA and protein expression and decreased FoxO1 phosphorylation through the Akt pathway, which resulted in an increase in active FoxO1 in RINm5F cells and isolated rat islets. Activated FoxO1 subsequently inhibited pancreatic duodenal homeobox-1 expression and induced nuclear exclusion of pancreatic duodenal homeobox-1. Knockdown of FoxO1 by RNA interference restored the expression of pancreatic duodenal homeobox-1 and prevented DEX-induced dysfunction of glucose-stimulated insulin secretion in rat islets. Together, the results of present study demonstrate that FoxO1 is integrally involved in DEX-induced inhibition of pancreatic duodenal homeobox-1 and glucose-stimulated insulin secretion dysfunction in pancreatic islet β-cells. Inhibition of FoxO1 can effectively protect β-cells against DEX-induced dysfunction.

scholarly journals Altered pancreas remodeling following glucose intolerance in pregnancy in mice

2020 ◽  
Vol 245 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Sandra K Szlapinski ◽  
Anthony A Botros ◽  
Sarah Donegan ◽  
Renee T King ◽  
Gabrielle Retta ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Endocrine Pancreas ◽  
Late Gestation ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Low Protein ◽  
Glucose Tolerance Tests

Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of pro-inflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose-intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.

scholarly journals Plasma soluble leptin receptor levels are associated with pancreatic β-cell dysfunction in patients with type 2 diabetes

2017 ◽  
Vol 9 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Tomoaki Morioka ◽  
Masanori Emoto ◽  
Yuko Yamazaki ◽  
Masafumi Kurajoh ◽  
Koka Motoyama ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Leptin Receptor ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Soluble Leptin Receptor

scholarly journals Impact of Magnesium Deficiency on Pancreatic β-Cell Function in Type 2 Diabetic Nigerians

2020 ◽  
Author(s):  
Abdullahi Mohammed ◽  
Ibrahim M. Bello
Keyword(s):  
Cell Function ◽  
Magnesium Deficiency ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Mg Deficiency ◽  
Cell Dysfunction ◽  
North Eastern ◽  
Β Cell Function ◽  
Type 2 Diabetic

Objective: Pancreatic β-cell dysfunction is described to be present at the diagnosis of type 2 diabetes mellitus (T2DM) and progressively deteriorated with disease duration. However, its progression is variable and potentially influenced by several factors. The Magnesium (Mg) deficiency mediates insulin resistance but reports regarding its role in pancreatic β-cell dysfunction are scarce and conflicting. The aim of this study was to evaluate Mg deficiency effect on pancreatic β-cell function in T2DM patients at a specialist hospital in north eastern Nigeria. Materials and Methods: Study subjects were categorized in to two groups according to plasma Mg levels; 34 subjects with hypomagnesemia and 45 subjects with normal magnesium levels. Fasting blood samples were analyzed for Mg, glucose and insulin. Pancreatic β-cell function was estimated as HOMA-β. Results: Degree of pancreatic β-cell function, as measured by HOMA-β, was significantly lower among T2DM subjects with hypomagnesemia compared to the subjects with normal magnesium levels (38.1± 5.5 vs. 41.2± 6.2, Pvalue< 0.05). Lower plasma Mg was associated with decreased pancreatic β-cell function among the study subjects independent of age, BMI and duration of diabetes. Conclusion: We concluded that among subjects with T2DM in this study, Mg deficiency might be linked with worsening of pancreatic β-cell function.

scholarly journals Elevated Medium-Chain Acylcarnitines Are Associated With Gestational Diabetes Mellitus and Early Progression to Type 2 Diabetes and Induce Pancreatic β-Cell Dysfunction

Diabetes ◽  
2018 ◽  
Vol 67 (5) ◽  
pp. 885-897 ◽  
Author(s):  
Battsetseg Batchuluun ◽  
Dana Al Rijjal ◽  
Kacey J. Prentice ◽  
Judith A. Eversley ◽  
Elena Burdett ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Medium Chain ◽  
Cell Dysfunction ◽  
Early Progression
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