Glucose, dexamethasone, and the unfolded protein response regulate TRB3 mRNA expression in 3T3-L1 adipocytes and L6 myotubes
| Autor: | Sherif Z. Yacoub Wasef, Mary N. Berkaw, Maria G. Buse, Katherine A. Robinson |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Protein Folding
Snf3 medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism Blotting Western Muscle Fibers Skeletal Biological Transport Active Cell Cycle Proteins Biology Dexamethasone Mice Insulin resistance 3T3-L1 Cells Physiology (medical) Internal medicine Adipocytes medicine Animals RNA Messenger Phosphorylation Protein kinase B Reverse Transcriptase Polymerase Chain Reaction Kinase Glucose transporter 3T3-L1 medicine.disease Culture Media Insulin receptor Glucose Endocrinology Gene Expression Regulation Unfolded protein response biology.protein Proto-Oncogene Proteins c-akt Transcription Factor CHOP |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 291:E1274-E1280 |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.00117.2006 |
| Popis: | Tribbles 3 (TRB3) is a recently recognized atypical inactive kinase that negatively regulates Akt activity in hepatocytes, resulting in insulin resistance. Recent reports link TRB3 to nutrient sensing and regulation of cell survival under stressful conditions. We studied the regulation of TRB3 by glucose, insulin, dexamethasone (Dex), and the unfolded protein response (UPR) in 3T3-L1 adipocytes and in L6 myotubes. In 3T3-L1 adipocytes, incubation in high glucose with insulin did not increase TRB3 mRNA expression. Rather, TRB3 mRNA increased fourfold with glucose deprivation and two- to threefold after incubation with tunicamcyin (an inducer of the UPR). Incubation of cells in no glucose or in tunicamcyin stimulated the expression of CCAAT/enhancer-binding protein homologous protein. In L6 myotubes, absent or low glucose induced TRB3 mRNA expression by six- and twofold, respectively. The addition of Dex to 5 mM glucose increased TRB3 mRNA expression twofold in 3T3-L1 adipocytes but decreased it 16% in L6 cells. In conclusion, TRB3 is not the mediator of high glucose or glucocorticoid-induced insulin resistance in 3T3-L1 adipocytes or L6 myotubes. TRB3 is induced by glucose deprivation in both cell types as a part of the UPR, where it may be involved in regulation of cell survival in response to glucose depletion. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|