249-LB: Effects of Oxidative Phosphorylation Complex Defects on Beta-Cell Biology

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 249-LB
Author(s):  
ANNA L. LANG ◽  
ALEJANDRO CAICEDO
Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 104
Author(s):  
Elisa Fernández-Millán ◽  
Carlos Guillén

Type 2 diabetes (T2D) results from impaired beta-cell function and insufficient beta-cell mass compensation in the setting of insulin resistance. Current therapeutic strategies focus their efforts on promoting the maintenance of functional beta-cell mass to ensure appropriate glycemic control. Thus, understanding how beta-cells communicate with metabolic and non-metabolic tissues provides a novel area for investigation and implicates the importance of inter-organ communication in the pathology of metabolic diseases such as T2D. In this review, we provide an overview of secreted factors from diverse organs and tissues that have been shown to impact beta-cell biology. Specifically, we discuss experimental and clinical evidence in support for a role of gut to beta-cell crosstalk, paying particular attention to bacteria-derived factors including short-chain fatty acids, lipopolysaccharide, and factors contained within extracellular vesicles that influence the function and/or the survival of beta cells under normal or diabetogenic conditions.


2015 ◽  
Vol 42 ◽  
pp. 3-18 ◽  
Author(s):  
Ming Liu ◽  
Jinhong Sun ◽  
Jinqiu Cui ◽  
Wei Chen ◽  
Huan Guo ◽  
...  

2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Nayeem Quayum ◽  
Alecksandr Kutchma ◽  
Suparna A. Sarkar ◽  
Kirstine Juhl ◽  
Gerard Gradwohl ◽  
...  

Objective. We here describe the development of a freely available online database resource, GeneSpeed Beta Cell, which has been created for the pancreatic islet and pancreatic developmental biology investigator community.Research Design and Methods. We have developed GeneSpeed Beta Cell as a separate component of the GeneSpeed database, providing a genomics-type data repository of pancreas and islet-relevant datasets interlinked with the domain-oriented GeneSpeed database.Results. GeneSpeed Beta Cell allows the query of multiple published and unpublished select genomics datasets in a simultaneous fashion (multiexperiment viewing) and is capable of defining intersection results from precomputed analysis of such datasets (multidimensional querying). Combined with the protein-domain categorization/assembly toolbox provided by the GeneSpeed database, the user is able to define spatial expression constraints of select gene lists in a relatively rigid fashion within the pancreatic expression space. We provide several demonstration case studies of relevance to islet cell biology and development of the pancreas that provide novel insight into islet biology.Conclusions. The combination of an exhaustive domain-based compilation of the transcriptome with gene array data of interest to the islet biologist affords novel methods for multidimensional querying between individual datasets in a rapid fashion, presently not available elsewhere.


Endocrinology ◽  
2021 ◽  
Author(s):  
Nivedita Seshadri ◽  
Christine A Doucette

Abstract Beta cell dysfunction is central to the development of type 2 diabetes (T2D). In T2D, environmental and genetic influences can manifest beta cell dysfunction in many ways, including impaired glucose-sensing and secretion coupling mechanisms, insufficient adaptative responses to stress and aberrant beta cell loss through increased cell death and/or beta cell de-differentiation. In recent years, circadian disruption has emerged as an important environmental risk factor for T2D. In support of this, genetic disruption of the circadian timing system in rodents impairs insulin secretion and triggers diabetes development, lending important evidence that the circadian timing system is intimately connected to, and essential for the regulation of pancreatic beta cell function; however, the role of the circadian timing system in the regulation of beta cell biology is only beginning to be unravelled. Here, we review the recent literature that explores the importance of the pancreatic islet/beta cell circadian clock in the regulation of various aspects of beta cell biology, including transcriptional and functional control of daily cycles of insulin secretion capacity, regulation of postnatal beta cell maturation, and control of the adaptive responses of the beta cell to metabolic stress and acute injury.


2020 ◽  
Vol 103 ◽  
pp. 31-40 ◽  
Author(s):  
Nur Shabrina Amirruddin ◽  
Blaise Su Jun Low ◽  
Kok Onn Lee ◽  
E Shyong Tai ◽  
Adrian Kee Keong Teo

2010 ◽  
Vol 21 (12) ◽  
pp. 714-721 ◽  
Author(s):  
Douglas R. Cavener ◽  
Sounak Gupta ◽  
Barbara C. McGrath
Keyword(s):  

Islets ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 1-8
Author(s):  
Hyunwoo Chung ◽  
Sung Ji Hong ◽  
So Won Choi ◽  
Chung-Gyu Park

2014 ◽  
Vol 10 (2) ◽  
pp. 100
Author(s):  
Chantal Mathieu ◽  
Lut Overbergh ◽  
◽  

NAIMIT (acronym for Natural Immune Modulation for Intervention in Type 1 Diabetes) is a large-scale collaborative programme of the 7th framework from the European Commission. The aim of the consortium is to bring together a group of leading European researchers spanning the field from genetics, through pancreatic beta-cell, dendritic cells and T-cell biology, towards clinical interventions. The ultimate goal is to develop novel and personalised interventional therapies in recent-onset type 1 diabetic patients, with minimal immune system interference, leading to beta-cell protection and restoration, based on a solid understanding of the disease pathogenesis, enabling experimental findings to be adopted for clinical applications.


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