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Am J Physiol Endocrinol Metab (July 11, 2006). doi:10.1152/ajpendo.00117.2006
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Submitted on March 13, 2006
Accepted on July 2, 2006

Glucose, dexamethasone and the unfolded protein response regulate TRB3 mRNA expression in 3T3-L1 adipocytes and L6 myotubes

Sherif Z. Yacoub Wasef1, Katherine A. Robinson1, Mary N. Berkaw1, and Maria G. Buse1*

1 Div. of Endocrinology, Dept. of Medicine, Medical University of South Carolina, Charleston,, South Carolina, United States

* To whom correspondence should be addressed. E-mail: busemg{at}musc.edu.

Tribble3 (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 4-fold with glucose deprivation and 2-3 fold after incubation with tunicamcyin (an inducer of the UPR). Incubation of cells in no glucose or in tunicamcyin, stimulated the expression of CHOP (C/EBP-homologous protein). In L6 myotubes, absent or low glucose induced TRB3 mRNA expression by 6-fold and 2-fold, respectively. The addition of DEX to 5mM glucose increased TRB3 mRNA expression 2-fold 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.




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