From Entero-Endocrine Cell Biology to Surgical Interventional Therapies for Type 2 Diabetes

2020 ◽  
pp. 273-297 ◽  
Author(s):  
Marta Guimarães ◽  
Sofia S. Pereira ◽  
Mariana P. Monteiro
Keyword(s):  
Type 2 Diabetes ◽  
Endocrine Cell ◽  
Cell Biology ◽  
Interventional Therapies

scholarly journals Expression Profiling of Genes Related to Endothelial Cells Biology in Patients with Type 2 Diabetes and Patients with Prediabetes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Sara Moradipoor ◽  
Patimah Ismail ◽  
Ali Etemad ◽  
Wan Aliaa Wan Sulaiman ◽  
Salma Ahmadloo
Keyword(s):  
Type 2 Diabetes ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Cell Biology ◽  
Control Group ◽  
Expression Levels ◽  
New Genes ◽  
Group 3 ◽  
Group 2

Endothelial dysfunction appears to be an early sign indicating vascular damage and predicts the progression of atherosclerosis and cardiovascular disorders. Extensive clinical and experimental evidence suggests that endothelial dysfunction occurs in Type 2 Diabetes Mellitus (T2DM) and prediabetes patients. This study was carried out with an aim to appraise the expression levels in the peripheral blood of 84 genes related to endothelial cells biology in patients with diagnosed T2DM or prediabetes, trying to identify new genes whose expression might be changed under these pathological conditions. The study covered a total of 45 participants. The participants were divided into three groups: group 1, patients with T2DM; group 2, patients with prediabetes; group 3, control group. The gene expression analysis was performed using the Endothelial Cell Biology RT2Profiler PCR Array. In the case of T2DM, 59 genes were found to be upregulated, and four genes were observed to be downregulated. In prediabetes patients, increased expression was observed for 49 genes, with two downregulated genes observed. Our results indicate that diabetic and prediabetic conditions change the expression levels of genes related to endothelial cells biology and, consequently, may increase the risk for occurrence of endothelial dysfunction.

scholarly journals m6A mRNA methylation regulates human β-cell biology in physiological states and in type 2 diabetes

2019 ◽  
Vol 1 (8) ◽  
pp. 765-774 ◽  
Author(s):  
Dario F. De Jesus ◽  
Zijie Zhang ◽  
Sevim Kahraman ◽  
Natalie K. Brown ◽  
Mengjie Chen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cell Biology ◽  
Β Cell ◽  
Mrna Methylation

Insights into �-Cell Biology and Type 2 Diabetes Pathogenesis from Studies of the Islet Transcriptome

2014 ◽  
pp. 111-121
Author(s):  
Martijn van de Bunt ◽  
Ignasi Morán ◽  
Jorge Ferrer ◽  
Mark I. McCarthy
Keyword(s):  
Type 2 Diabetes ◽  
Cell Biology

scholarly journals Minireview: Thioredoxin-Interacting Protein: Regulation and Function in the Pancreatic β-Cell

2014 ◽  
Vol 28 (8) ◽  
pp. 1211-1220 ◽  
Author(s):  
Anath Shalev
Keyword(s):  
Type 2 Diabetes ◽  
Cell Biology ◽  
Pancreatic Β Cell ◽  
Insulin Production ◽  
Β Cell ◽  
Interacting Protein ◽  
Thioredoxin Interacting Protein ◽  
And Function

Pancreatic β-cells are responsible for insulin production, and loss of functional β-cell mass is now recognized as a critical step in the pathogenesis of both type 1 and type 2 diabetes. However, the factors controlling the life and death of the pancreatic β-cell have only started to be elucidated. Discovered as the top glucose-induced gene in a human islet microarray study 12 years ago, thioredoxin-interacting protein (TXNIP) has now emerged as such a key player in pancreatic β-cell biology. Since then, β-cell expression of TXNIP has been found to be tightly regulated by multiple factors and to be dramatically increased in diabetic islets. Elevated TXNIP levels induce β-cell apoptosis, whereas TXNIP deficiency protects against type 1 and type 2 diabetes by promoting β-cell survival. TXNIP interacts with and inhibits thioredoxin and thereby controls the cellular redox state, but it also belongs to the α-arrestin family of proteins and regulates a variety of metabolic processes. Most recently, TXNIP has been discovered to control β-cell microRNA expression, β-cell function, and insulin production. In this review, the current state of knowledge regarding regulation and function of TXNIP in the pancreatic β-cell and the implications for drug development are discussed.

scholarly journals Cirurgia metabólica: cura para diabete tipo 2

2011 ◽  
Vol 24 (4) ◽  
pp. 312-317 ◽  
Author(s):  
Jorge Luiz de Mattos Zeve ◽  
Carlos Alberto Bezerra Tomaz
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
World Congress ◽  
Interventional Therapies ◽  
Diabete Tipo 2

INTRODUÇÃO: O diabete melito tipo 2 é doença metabólica caracterizada por hiperglicemia crônica que está associada com dano e insuficiência de vários órgãos. A evolução da doença é a causa mais comum de cegueira, amputações e insuficiência renal em adultos no ocidente, além de aumentar a incidência de infarto agudo do miocárdio e acidente vascular cerebral, com maior mortalidade dos pacientes. A associação dele com obesidade é relevante. Os pacientes obesos diabéticos quando submetidos ao tratamento cirúrgico da obesidade apresentam melhor controle da glicemia, mesmo antes de perderem peso. MÉTODO: Foi realizada revisão de literatura nos sites de pesquisa PubMed, Bireme e Scielo, com os descritores "Diabetes Mellitus", "Cirurgia Bariátrica" e "Obesidade". Selecionaram-se, principalmente, os estudos de aplicação de técnicas cirúrgicas nos tratamentos da obesidade e do diabete tipo 2. Adicionalmente foram revisados os trabalhos apresentados no 1st e 2nd World Congress of Interventional Therapies for Type 2 Diabetes. CONCLUSÃO: O tratamento cirúrgico de pacientes obesos e diabéticos tipo 2 tem mostrado bom resultado inicial, com controle clínico precoce da glicemia. Porém, os procedimentos e técnicas empregados devem ser melhor investigados em estudos randomizados e controlados, comparando os tratamentos cirúrgico e clinico, em animais de experimentação e em seres humanos.

scholarly journals β-Cell Deficit in Obese Type 2 Diabetes, a Minor Role of β-Cell Dedifferentiation and Degranulation

2016 ◽  
Vol 101 (2) ◽  
pp. 523-532 ◽  
Author(s):  
Alexandra E. Butler ◽  
Sangeeta Dhawan ◽  
Jonathan Hoang ◽  
Megan Cory ◽  
Kylie Zeng ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Endocrine Cell ◽  
Endocrine Cells ◽  
Cell Types ◽  
Minor Role ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dedifferentiation ◽  
The Impact

Abstract Context: Type 2 diabetes is characterized by a β-cell deficit and a progressive defect in β-cell function. It has been proposed that the deficit in β-cells may be due to β-cell degranulation and transdifferentiation to other endocrine cell types. Objective: The objective of the study was to establish the potential impact of β-cell dedifferentiation and transdifferentiation on β-cell deficit in type 2 diabetes and to consider the alternative that cells with an incomplete identity may be newly forming rather than dedifferentiated. Design, Setting, and Participants: Pancreata obtained at autopsy were evaluated from 14 nondiabetic and 13 type 2 diabetic individuals, from four fetal cases, and from 10 neonatal cases. Results: Whereas there was a slight increase in islet endocrine cells expressing no hormone in type 2 diabetes (0.11 ± 0.03 cells/islet vs 0.03 ± 0.01 cells/islet, P < .01), the impact on the β-cell deficit would be minimal. Furthermore, we established that the deficit in β-cells per islet cannot be accounted for by an increase in other endocrine cell types. The distribution of hormone negative endocrine cells in type 2 diabetes (most abundant in cells scattered in the exocrine pancreas) mirrors that in developing (embryo and neonatal) pancreas, implying that these may represent newly forming cells. Conclusions: Therefore, although we concur that in type 2 diabetes there are endocrine cells with altered cell identity, this process does not account for the deficit in β-cells in type 2 diabetes but may reflect, in part, attempted β-cell regeneration.

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