Institution
Indiana Biosciences Research Institute
Nonprofit•Indianapolis, Indiana, United States•
About: Indiana Biosciences Research Institute is a nonprofit organization based out in Indianapolis, Indiana, United States. It is known for research contribution in the topics: Beta cell & Diabetes mellitus. The organization has 52 authors who have published 91 publications receiving 1052 citations.
Papers
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TL;DR: New findings from studies performed on human β-cells or on samples obtained from patients with type 1 or type 2 diabetes mellitus are highlighted, focusing on studies performed at the β-cell level and the identification and characterization of the role of T1DM and T2DM candidate genes at theβ-celllevel.
Abstract: Loss of functional β-cell mass is the key mechanism leading to the two main forms of diabetes mellitus - type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). Understanding the mechanisms behind β-cell failure is critical to prevent or revert disease. Basic pathogenic differences exist in the two forms of diabetes mellitus; T1DM is immune mediated and T2DM is mediated by metabolic mechanisms. These mechanisms differentially affect early β-cell dysfunction and eventual fate. Over the past decade, major advances have been made in the field, mostly delivered by studies on β-cells in human disease. These advances include studies of islet morphology and human β-cell gene expression in T1DM and T2DM, the identification and characterization of the role of T1DM and T2DM candidate genes at the β-cell level and the endoplasmic reticulum stress signalling that contributes to β-cell failure in T1DM (mostly IRE1 driven) and T2DM (mostly PERK-eIF2α dependent). Here, we review these new findings, focusing on studies performed on human β-cells or on samples obtained from patients with diabetes mellitus.
331 citations
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TL;DR: In this paper, the authors highlight population-based studies that have linked cigarette smoking with an increased risk of type 2 diabetes and summarize clinical and preclinical studies offering insight into mechanisms through which cigarette smoking and nicotine exposure impact body composition, insulin sensitivity, and pancreatic β cell function.
153 citations
01 Jun 2017
TL;DR: Clinical and preclinical studies offering insight into mechanisms through which cigarette smoking and nicotine exposure impact body composition, insulin sensitivity, and pancreatic cell function are summarized and strategies for smoking cessation as a means to decrease diabetes risk are discussed.
Abstract: Despite accumulating evidence demonstrating strong epidemiologic and mechanistic associations between cigarette smoking, hyperglycemia, and the development of type 2 diabetes, tobacco abuse has not been uniformly recognized as a modifiable risk factor in diabetes prevention or screening strategies. In this review, we highlight population-based studies that have linked cigarette smoking with an increased risk of type 2 diabetes and summarize clinical and preclinical studies offering insight into mechanisms through which cigarette smoking and nicotine exposure impact body composition, insulin sensitivity, and pancreatic β cell function. Key questions for future studies are identified and strategies for smoking cessation as a means to decrease diabetes risk are discussed.
141 citations
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TL;DR: The data indicate a potential link between SARS-CoV-2 and diabetes through putative infection of pancreatic microvasculature and/or ductal cells and/ or through direct β-cell virus tropism.
Abstract: Increasing evidence demonstrated that the expression of Angiotensin I-Converting Enzyme type 2 (ACE2) is a necessary step for SARS-CoV-2 infection permissiveness. In light of the recent data highlighting an association between COVID-19 and diabetes, a detailed analysis aimed at evaluating ACE2 expression pattern distribution in human pancreas is still lacking. Here, we took advantage of INNODIA network EUnPOD biobank collection to thoroughly analyze ACE2, both at mRNA and protein level, in multiple human pancreatic tissues and using several methodologies. Using multiple reagents and antibodies, we showed that ACE2 is expressed in human pancreatic islets, where it is preferentially expressed in subsets of insulin producing β-cells. ACE2 is also highly expressed in pancreas microvasculature pericytes and moderately expressed in rare scattered ductal cells. By using different ACE2 antibodies we showed that a recently described short-ACE2 isoform is also prevalently expressed in human β-cells. Finally, using RT-qPCR, RNA-seq and High-Content imaging screening analysis, we demonstrated that pro-inflammatory cytokines, but not palmitate, increase ACE2 expression in the β-cell line EndoC-βH1 and in primary human pancreatic islets. Taken together, our data indicate a potential link between SARS-CoV-2 and diabetes through putative infection of pancreatic microvasculature and/or ductal cells and/or through direct β-cell virus tropism.
124 citations
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TL;DR: In this paper, Gpx4-deficient Treg cells elevate generation of mitochondrial superoxide and production of interleukin-1β (IL-1α) that facilitates T helper 17 (TH17) responses.
115 citations
Authors
Showing all 52 results
Name | H-index | Papers | Citations |
---|---|---|---|
Decio L. Eizirik | 89 | 406 | 28759 |
Rainer Fischer | 72 | 400 | 19108 |
Nitesh V. Chawla | 61 | 388 | 41365 |
Raghavendra G. Mirmira | 47 | 222 | 7327 |
Jonathan N. Flak | 23 | 34 | 1650 |
Teresa L. Mastracci | 20 | 40 | 1180 |
Daniel H. Robertson | 20 | 71 | 4481 |
Luiz Felipe Barella | 15 | 48 | 672 |
Emily Anderson-Baucum | 11 | 18 | 385 |
Jeffrey J. Sutherland | 11 | 18 | 756 |
Stéphane Demine | 9 | 13 | 349 |
Zane Baird | 8 | 27 | 308 |
Morgan A. Robertson | 6 | 8 | 198 |
Meeta Pradhan | 5 | 22 | 141 |
Bhupal Ban | 5 | 16 | 74 |