Unknown

Dataset Information

0

Shortened {beta}-cell lifespan leads to {beta}-cell deficit in a rodent model of type 2 diabetes.

ABSTRACT: Since the fundamental defect in both type 1 and type 2 diabetes is ?-cell failure, there is increasing interest in the capacity, if any, for ?-cell regeneration. Insights into typical ?-cell age and lifespan during normal development and how these are influenced in diabetes is desirable to realistically establish the prospects for ?-cell regeneration as means to reverse the deficit in ?-cell mass in diabetes. We assessed the mean ?-cell age and lifespan by the classical McKendrick-von Foester equation that describes the age-based heterogeneity of ?-cells in terms of the time-varying ?-cell formation and loss estimated by a ?-cell turnover model. This modeling approach was applied to evaluate ?-cell lifespan in a rodent model of type 2 diabetes in comparison with nondiabetic controls. When rats were 10 mo old, mean ?-cell lifespan was 1 mo vs. 6 mo in rats with type 2 diabetes vs. controls. A shortened ?-cell lifespan in a rat model of type 2 diabetes results in a decrease in mean ?-cell age and thus contributes to decreased ?-cell mass.

SUBMITTER: Manesso E 

PROVIDER: S-EPMC3279301 | biostudies-literature | 2011 May

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

Shortened {beta}-cell lifespan leads to {beta}-cell deficit in a rodent model of type 2 diabetes.

Manesso Erica E   Toffolo Gianna M GM   Butler Alexandra E AE   Butler Peter C PC   Cobelli Claudio C  

American journal of physiology. Endocrinology and metabolism 20110222 5

Since the fundamental defect in both type 1 and type 2 diabetes is β-cell failure, there is increasing interest in the capacity, if any, for β-cell regeneration. Insights into typical β-cell age and lifespan during normal development and how these are influenced in diabetes is desirable to realistically establish the prospects for β-cell regeneration as means to reverse the deficit in β-cell mass in diabetes. We assessed the mean β-cell age and lifespan by the classical McKendrick-von Foester eq  ...[more]

Similar Datasets

Unknown Single-cell gene expression analysis reveals β-cell dysfunction and deficit mechanisms in type 2 diabetes.
| S-EPMC6311914 | biostudies-literature
Unknown Yeast polyubiquitin gene UBI4 deficiency leads to early induction of apoptosis and shortened replicative lifespan.
| S-EPMC6045546 | biostudies-literature
Unknown Extinction learning deficit in a rodent model of attention-deficit hyperactivity disorder.
| S-EPMC3542014 | biostudies-literature
Unknown Fine Particulate Matter Leads to Unfolded Protein Response and Shortened Lifespan by Inducing Oxidative Stress in C. elegans.
| S-EPMC6925806 | biostudies-literature
Unknown Effects of Naringin on Cardiomyocytes From a Rodent Model of Type 2 Diabetes.
| S-EPMC8419284 | biostudies-literature
Unknown A Mouse Model of Beta-Cell Dysfunction as Seen in Human Type 2 Diabetes.
| S-EPMC5952555 | biostudies-literature
Unknown Characterisation of gut microbiota of obesity and type 2 diabetes in a rodent model.
| S-EPMC7817511 | biostudies-literature
Unknown Islet beta cell failure in type 2 diabetes.
| S-EPMC1483155 | biostudies-literature
Unknown CX3CR1 deficiency accelerates the development of retinopathy in a rodent model of type 1 diabetes.
| S-EPMC5071129 | biostudies-literature
Unknown Insights into pancreatic β cell energy metabolism using rodent β cell models.
| S-EPMC6854877 | biostudies-literature