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Scholar Results 1 - 10 of about 101 related to Tschen: Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell.... (0.13 sec) 

Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration …

- diabetesjournals.org
SI Tschen, S Dhawan, T Gurlo, A Bhushan - Diabetes, 2009 - Am Diabetes Assoc
2 Molecular Biology Institute, University of California, Los Angeles, Los
Angeles, California. ... Corresponding author: Anil Bhushan,
abhushan{at}mednet.ucla.edu. ... OBJECTIVE The aim of this study was to ...
Cited by 6 - Related articles - All 3 versions

Adaptive β-Cell Proliferation Is Severely Restricted With Advanced Age

- diabetesjournals.org
MM Rankin, JA Kushner - Diabetes, 2009 - Am Diabetes Assoc
OBJECTIVE Regeneration of the insulin-secreting β-cells is a fundamental
research goal that could benefit patients with either type 1 or type 2 diabetes.
β-Cell proliferation can be acutely stimulated by a variety of stimuli in ...
Cited by 6 - Related articles - All 3 versions

The long lifespan and low turnover of human islet beta cells estimated by mathematical …


M Cnop, SJ Hughes, M Igoillo-Esteve, MB … - Diabetologia - Springer
Abstract Aims/hypothesis Defects in pancreatic beta cell turnover are implicated
in the pathogenesis of type 2 diabetes by genetic markers for diabetes.
Decreased beta cell neogenesis could contribute to diabetes. The longevity ...
Related articles - All 2 versions

Connecting obesity, aging and diabetes


RS Ahima - Nature Medicine, 2009 - nature.com
Obesity accelerates the aging of adipose tissue, a process only now beginning to
come to light at the molecular level. Experiments in mice suggest that obesity
increases the formation of reactive oxygen species in fat cells, shortens ...
Related articles - All 3 versions

The roles of telomeres and telomerase in β-cell regeneration


CW Liew, A Holman, RN Kulkarni - Diabetes, Obesity and Metabolism, 2009 - interscience.wiley.com
Telomerase is a specialized reverse transcriptase that is responsible for
extending and preserving the end of the chromosomes (telomeres). Telomerase
plays a key role in regulating the lifespan of mammalian cells and is ...
Related articles

Dynamics of {beta}-cell turnover: evidence for {beta}-cell turnover and regeneration from …


E Manesso, GM Toffolo, Y Saisho, AE Butler, … - American Journal of Physiology- Endocrinology And …, 2009 - Am Physiological Soc
Type 2 diabetes is characterized by hyperglycemia, a deficit in β-cells,
increased β-cell apoptosis, and islet amyloid derived from islet amyloid
polypeptide (IAPP). These characteristics are recapitulated in the human ...
Related articles - All 3 versions

Involvement of PAS Kinase and ERK1/2 in Palmitate Inhibition of Insulin Gene Expression In …


G Fontés, M Semache, DK Hagman, C Tremblay … - Diabetes, 2009 - ncbi.nlm.nih.gov
Objective: Prolonged exposure of pancreatic beta cells to simultaneously
elevated levels of fatty acids and glucose (glucolipotoxicity) impairs insulin
gene transcription. However, the intracellular signalling pathways ...
Cited by 1 - Related articles - All 3 versions

Peroxisome Proliferator-Activated Receptor {gamma} Activation Restores Islet Function in …

- nih.gov
C Evans-Molina, RD Robbins, T Kono, SA … - Molecular and Cellular Biology, 2009 - Am Soc Microbiol
The nuclear receptor peroxisome proliferator-activated receptor (PPAR- ) is an
important target in diabetes therapy, but its direct role, if any, in the
restoration of islet function has remained controversial. To identify ...
Cited by 1 - Related articles - All 4 versions

Deletion of PKCε selectively enhances the amplifying pathways of glucose-stimulated insulin …


J Cantley, JG Burchfield, GL Pearson, C … - Diabetes, 2009 - Am Diabetes Assoc
Results: The enhanced GSIS could not be explained by increased expression of
another PKC isoform or by alterations in glucose stimulated Ca 2+ influx.
Instead an up-regulation of the amplifying pathways of GSIS in ...
Cited by 1 - Related articles - All 3 versions

Mitochondrial protein phosphorylation: instigator or target of lipotoxicity?


WF Graier, R Malli, GM Kostner - Trends in Endocrinology & Metabolism, 2009 - Elsevier
Lipotoxicity occurs as a consequence of chronic exposure of non-adipose tissue
and cells to elevated concentrations of fatty acids, triglycerides and/or
cholesterol. The contribution of mitochondria to lipotoxic cell ...
Cited by 1 - Related articles - All 3 versions


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