Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

Romero, R; Casanova, Benito; Pulido, N.; Suarez, AI; Rodriguez, E; Rovira, Adela

doi:10.1677/joe.0.1640187

Cited by 49 publications

(31 citation statements)

References 29 publications

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“…It is also intriguing that Rev-erb␣ mRNA expression modulates the alternative splicing of the gene for TR␣, which governs the ratio of TR␣1 and TR␣2, two factors that facilitate or inhibit thyroid hormone action, respectively (19,25). An accumulation of Rev-erb␣ on May 9, 2018 by guest http://mcb.asm.org/ mRNA in mature adipocytes would therefore favor TR␣1 mRNA production and increase the cellular response to thyroid hormone, which is important for maintaining metabolic homeostasis (22,32,45). In summary, we have uncovered a mechanism by which the rise and fall of Rev-erb␣ protein may benefit adipocyte differentiation.…”

Section: Discussionmentioning

confidence: 83%

Bifunctional Role of Rev-erbα in Adipocyte Differentiation

Wang

Lazar

2008

Molecular and Cellular Biology

106

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The nuclear receptor Rev-erb␣ is a potent transcriptional repressor that regulates circadian rhythm and metabolism. Here we demonstrate a dissociation between Rev-erb␣ mRNA and protein levels that profoundly influences adipocyte differentiation. During adipogenesis, Rev-erb␣ gene expression initially declines and subsequently increases. Remarkably, Rev-erb␣ protein levels are nearly the opposite, increasing early in adipogenesis and then markedly decreasing in adipocytes. The Rev-erb␣ protein is necessary for the early mitotic events that are required for adipogenesis. The subsequent reduction in Rev-erb␣ protein, due to increased degradation via the 26S proteasome, is also required for adipocyte differentiation because Rev-erb␣ represses the expression of PPAR␥2, the master transcriptional regulator of adipogenesis. Thus, opposite to what might be predicted from Rev-erb␣ gene expression, Rev-erb␣ protein levels must rise and then fall for adipocyte differentiation to occur.The conversion of fibroblastic preadipocytes to mature adipocytes involves the temporal and hierarchical coordination of intracellular signaling molecules and transcription factors (11,34). Differentiation of the widely used 3T3-L1 preadipocyte cell line requires extracellular signals, including cell contact, glucocorticoids, and serum-derived factors, as well as intracellular accumulation of cyclic AMP (39). Together, these initiators lead confluent preadipocytes to undergo two rounds of cell division that are required for adipogenesis (41). They also induce early transcription factors, notably, CCAAT enhancerbinding proteins (C/EBP) ␤ and ␦, to instigate a cascade of transcriptional events that ultimately results in withdrawal from the cell cycle in the process of differentiation into mature postmitotic adipocytes (8,47,49). C/EBP␤, in particular, induces nuclear receptor peroxisome proliferator-activated receptor ␥ (PPAR␥) (17,35,36,47), the master transcriptional regulator of adipogenesis whose high-level expression in adipocytes is both necessary and sufficient for adipocyte-specific gene expression and the adipocyte phenotypes (6,42,43). PPAR␥ and C/EBP␣ induce one another to maintain the differentiated adipocyte phenotype (9, 33). Other transcription factors, such as ADD1/SREBP and KLF5, also play important roles in adipogenesis (23, 30).Rev-erb␣ is an orphan nuclear receptor that has also been implicated in adipocyte differentiation (5,12,24). It is highly expressed in adipose tissue, and its gene expression is specifically induced in differentiating adipocytes (5, 14). Rev-erb␣ mRNA is transcribed from the opposite strand of the thyroid hormone receptor (TR) ␣ gene and is antisense to the TR␣2 splice product which encodes a non-thyroid hormone-binding TR variant (26, 29). The Rev-erb␣ protein lacks the classical nuclear receptor C-terminal activation domain but binds to nuclear receptor corepressor (N-CoR) and hence functions as a potent transcriptional repressor (18). Recently, Rev-erb␣ has been shown to function as a core negative ...

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Section: Discussionmentioning

confidence: 83%

Bifunctional Role of Rev-erbα in Adipocyte Differentiation

Wang

Lazar

2008

Molecular and Cellular Biology

106

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“…Those factors responsible for the high-fat diet induced GLUT4 repression could be arachidonic acids (24,25) or other long chain fatty acids, such as stearic acids, oleic acids, etc (25). Thyroid hormone treatment of rats caused an increase in GLUT4 mRNA and protein level in muscle (26,27) and adipocytes (28).…”

Section: Metabolic and Hormonal Control Of Glut4 In Muscle And Adiposmentioning

confidence: 95%

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Kwon

Kim

et al. 2007

IUBMB Life

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SummaryThe gene expression of glucose transporter type 4 isoform (GLUT4) is known to be controlled by metabolic, nutritional, or hormonal status. Understanding the molecular mechanisms governing GLUT4 gene expression is critical, because glucose disposal in the body depends on the activities of GLUT4 in the muscle and adipocytes. The GLUT4 activities are regulated by a variety of mechanisms. One of them is transcriptional regulation. GLUT4 gene expression is regulated by a variety of transcriptional factors in muscle and adipose tissue. These data are accumulating regarding the transcriptional factors regulating GLUT4 gene expression. These include MyoD, MEF2A, GEF, TNF-a, TR-1a, KLF15, SREBP-1c, C/EBP-a, O/E-1, free fatty acids, PAPRg, LXRa, NF-1, etc. These factors are involved in the positive or negative regulation of GLUT4 gene expression. In addition, there is a complex interplay between these factors in transactivating GLUT4 promoter activity. Understanding the mechanisms controlling GLUT4 gene transcription in these tissues will greatly promote the potential therapeutic drug development for obesity and T2DM.

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“…Non-specific deoxyglucose uptake was measured in the presence of 20 μmol/L cytochalasin B (Sigma), and specific glucose uptake was detected from the subtracted total uptake. Three replicate wells were set up and each experiment was repeated three times [8] . Additionally, a Cell Counting Kit-8 (CCK-8) was employed for the monitoring of the number and viability of the cells [9] .…”

Section: Establishment Of Insulin-resistance Model and Groupingmentioning

confidence: 99%

Berberine reverses free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ

Lu²,

Xu³

et al. 2008

WJG

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AIM:To i n v e s t i g a t e t h e e f f e c t s a n d m o l e c u l a r mechanisms of berberine on improving insulin resistance induced by free fatty acids (FFAs) in 3T3-L1 adipocytes. METHODS:The model of insulin resistance in 3T3-L1 adipocytes was established by adding palmic acid ( 0 . 5 m m o l / L ) t o t h e c u l t u re m e d i u m . B e r b e r in e treatment was performed at the same time. Glucose uptake rate was determined by the 2-deoxy-[3 H]-Dglucose method. The levels of IkB kinase beta (IKKβ) Ser 181 phosphorylation, insulin receptor substrate-1(IRS-1) Ser 307 phosphorylation, expression of IKKβ, IRS-1, nuclear transcription factor kappaB p65 (NF-κB p65), phosphatidylinositol-3-kinase p85 (PI-3K p85) and glucose transporter 4 (GLUT4) proteins were detected by Western blotting. The distribution of NF-κB p65 proteins inside the adipocytes was observed through confocal laser scanning microscopy (CLSM). RESULTS:After the intervention of palmic acid for 24 h, the insulin-stimulated glucose transport in 3T3-L1 adipocytes was inhibited by 67%. Meanwhile, the e x p re s s i o n o f I R S -1 a n d P I-3 K p 8 5 p ro t e i n wa s reduced, while the levels of IKKβ Ser 181 and IRS-1 Ser 307 phosphorylation, and nuclear translocation of NF-κB p65 protein were increased. However, the above indexes, which indicated the existence of insulin resistance, were reversed by berberine although the expression of GLUT4, IKKβ and total NF-κB p65 protein were not changed during this study. CONCLUSION:Insulin resistance induced by FFAs in 3T3-L1 adipocytes can be improved by berberine. Berberine reversed free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ.

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Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

Cited by 49 publications

References 29 publications

Bifunctional Role of Rev-erbα in Adipocyte Differentiation

Bifunctional Role of Rev-erbα in Adipocyte Differentiation

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Berberine reverses free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ

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