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Scholar Results 1 - 10 of about 15 citing Martinez: Inhibition of Foxo1 Protects Pancreatic Islet β-Cells Against Fatty Acid and Endoplasm.... (0.14 sec) 

Molecular mechanisms and therapeutic targets in steatosis and steatohepatitis

- aspetjournals.org
N Anderson, J Borlak - Pharmacological reviews, 2008 - ASPET
Cited by 14 - Related articles - All 4 versions

β-cell failure as a complication of diabetes


KJ Chang-Chen, R Mullur, E Bernal-Mizrachi - Reviews in Endocrine & …, 2008 - Springer
Abstract Type 2 diabetes mellitus is a complex disease characterized by b-cell failure in the setting
of insulin resistance. In early stages of the disease, pancreatic b-cells adapt to insulin resistance
by increasing mass and function. As nutrient excess persists, hyperglycemia and elevated ...
Cited by 12 - Related articles - All 2 versions

Cytokine-induced {beta}-cell death is independent of endoplasmic reticulum stress …

- diabetesjournals.org
MC Akerfeldt, J Howes, JY Chan, VA Stevens, N … - Diabetes, 2008 - Am Diabetes Assoc
RESULTS—Cytokines and palmitate triggered ER stress in β-cells as evidenced by increased
phosphorylation of PKR-like ER kinase (PERK), eukaryotic initiation factor (EIF)2α, and Jun NH
2 -terminal kinase (JNK) and increased expression of activating transcription factor ...
Cited by 9 - Related articles - All 3 versions

Glucolipotoxicity of the pancreatic beta cell


V Poitout, J Amyot, M Semache, B Zarrouki, D … - BBA-Molecular and Cell …, 2009 - Elsevier
The concept of glucolipotoxicity refers to the combined, deleterious effects of elevated
glucose, and fatty acid levels on pancreatic beta-cell function and survival. Significant progress
has been made in recent years towards a better understanding of the cellular and ...
Cited by 9 - Related articles - BL Direct - All 4 versions

Glucose amplifies fatty acid-induced endoplasmic reticulum stress in pancreatic β- …


E Bachar, Y Ariav, M Ketzinel-Gilad, E Cerasi, N … - PLoS One, 2009 - pubmedcentral.nih.gov
We found that glucose amplifies palmitate-induced ER stress by increasing IRE1α protein levels
and activating the JNK pathway, leading to increased β-cell apoptosis. Moreover, glucose increased
mTORC1 activity and its inhibition by rapamycin decreased β-cell apoptosis under ...
Cited by 6 - Related articles - All 5 versions

Opposite regulation of CD36 ubiquitination by fatty acids and insulin: effects on …

- jbc.org
J Smith, X Su, R El-Maghrabi, PD Stahl, NA … - Journal of Biological …, 2008 - ASBMB
FAT/CD36 is a membrane scavenger receptor that facilitates long chain fatty acid uptake by
muscle. Acute increases in membrane CD36 and fatty acid uptake have been reported in response
to insulin and contraction. In this study we have explored protein ubiquitination as one ...
Cited by 3 - Related articles - All 5 versions

MINIREVIEW: Meeting the demand for insulin: Molecular mechanisms of adaptive …


MM Sachdeva, DA Stoffers - Molecular Endocrinology, 2009 - Endocrine Soc
Type 2 diabetes results from pancreatic ß-cell failure in the setting of insulin resistance. This
model of disease progression has received recent support from the results of genome-wide association
studies that identify genes potentially regulating ß-cell growth and function as type 2 ...
Cited by 2 - Related articles - All 3 versions

Molecular mechanisms involved in NAFLD progression


M Malaguarnera, M Di Rosa, F Nicoletti, L … - Journal of Molecular …, 2009 - Springer
Abstract Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic-related disorder
characterized by fatty infiltration of the liver in the absence of alcohol consump- tion. NAFLD
ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which might ...
Cited by 2 - Related articles - All 2 versions

[PDF] Opposite Regulation of CD36 Ubiquitination by Fatty Acids and Insulin


EONFA UPTAKE - THE JOURNAL OF BIOLOGICAL CHEMISTRY, 2008 - ASBMB
FAT/CD36 is a membrane scavenger receptor that facilitates long chain fatty acid uptake by
muscle. Acute increases in mem- brane CD36 and fatty acid uptake have been reported in response
to insulin and contraction. In this study we have explored protein ubiquitination as one ...
Related articles

Inhibition of Forkhead Box O1 Protects Pancreatic {beta}-Cells against …


X Zhang, W Yong, J Lv, Y Zhu, J Zhang, F Chen, R … - Endocrinology, 2009 - Endocrine Soc
Forkhead Box O1 (FoxO1) is a key transcription regulator of insulin/IGF-I signaling pathway, and
its activity can be increased by dexamethasone (DEX) in several cell types. However, the role
of FoxO1 in DEX-induced pancreatic β-cell dysfunction has not been fully understood. ...
Related articles - All 3 versions


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