Inhibition of Preadipocyte Differentiation by Myostatin Treatment in 3T3-L1 Cultures

Kim, Hyunsook; Liang, Li-Fang; Dean, Roger G.; Hausman, Dorothy B.; Hartzell, Diane L.; Baile, Clifton A.

doi:10.1006/bbrc.2001.4435

Cited by 110 publications

(71 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The results of several studies have indicated that myostatin inhibits adipogenesis and decreases lipid accumulation in mouse 3T3-L1 preadiopocytes and bovine preadiopocytes by suppressing Pparg and Cebpa expression (Kim et al 2001, Hirai et al 2007, Li et al 2011. Consistent with these results, the results of the present study also indicated that myostatin significantly decreased the intracellular lipid contents, as determined by Oil red O staining and intracellular TG contents assay in 3T3-L1 adipocytes.…”

Section: Discussionsupporting

confidence: 91%

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Zhu¹,

Pan²,

Zhang³

et al. 2015

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Myostatin is a critical negative regulator of skeletal muscle development, and has been reported to be involved in the progression of obesity and diabetes. In the present study, we explored the effects of myostatin on the proliferation and differentiation of 3T3-L1 preadipocytes by using 3-[4,5-dimethylthiazol-2-yl] 2,5-diphenyl tetrazolium bromide spectrophotometry, intracellular triglyceride (TG) assays, and real-time quantitative RT-PCR methods. The results indicated that recombinant myostatin significantly promoted the proliferation of 3T3-L1 preadipocytes and the expression of proliferation-related genes, including Cyclin B2, Cyclin D1, Cyclin E1, Pcna, and c-Myc, and IGF1 levels in the medium of 3T3-L1 were notably upregulated by 35.2, 30.5, 20.5, 33.4, 51.2, and 179% respectively (all P!0.01) in myostatin-treated 3T3-L1 cells. Meanwhile, the intracellular lipid content of myostatin-treated cells was notably reduced as compared with the non-treated cells. Additionally, the mRNA levels of Pparg, Cebpa, Gpdh, Dgat, Acs1, Atgl, and Hsl were significantly downregulated by 22-76% in fully differentiated myostatin-treated adipocytes. Finally, myostatin regulated the mRNA levels and secretion of adipokines, including Adiponectin, Resistin, Visfatin, and plasminogen activator inhibitor-1 (PAI-1) in 3T3-L1 adipocytes (all P!0.001). Above all, myostatin promoted 3T3-L1 proliferation by increasing the expression of cell-proliferation-related genes and by stimulating IGF1 secretion. Myostatin inhibited 3T3-L1 adipocyte differentiation by suppressing Pparg and Cebpa expression, which consequently deceased lipid accumulation in 3T3-L1 cells by inhibiting the expression of critical lipogenic enzymes and by promoting the expression of lipolytic enzymes. Finally, myostatin modulated the expression and secretion of adipokines in fully differentiated 3T3-L1 adipocytes.

show abstract

Section: Discussionsupporting

confidence: 91%

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Zhu¹,

Pan²,

Zhang³

et al. 2015

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…6 Several possible mechanisms have been proposed to explain these findings, including a direct effect of myostatin on adipocyte differentiation and maturation. In vitro studies have shown that myostatin can inhibit adipocyte differentiation in 3T3-L1 mouse preadipocytes, 7 and myostatin may also inhibit Reduced body fat gain in double-muscled Mice MW Hamrick et al BMP-7 mediated adipogenesis by binding to the same receptor as BMP-7, the activin IIB receptor. 8 These data suggest that loss of myostatin function should increase adipogenesis, but the in vivo data obviously do not support this prediction.…”

Section: Discussionmentioning

confidence: 99%

Resistance to body fat gain in ‘double-muscled’ mice fed a high-fat diet

et al. 2006

View full text Add to dashboard Cite

Objective: To determine if myostatin deficiency attenuates body fat gain with increased dietary fat intake. Methods: Normal and myostatin-deficient mice were fed control (8-10 kcal %fat) and high-fat (HF) (45 kcal %fat) diets for a period of 8 weeks, starting at 2 months of age. Body composition, including percent body fat, lean mass, and fat mass, were measured using DXA. Serum adipokines were measured using a Beadlyte assay. Results: Two-factor ANOVA revealed significant treatment Â genotype interactions for body fat (g), percent body fat, and serum leptin. The HF diet significantly increased body fat, percent body fat, and serum leptin in normal mice but not in myostatindeficient mice. Conclusion: Loss of myostatin function not only increases muscle mass in animal models but also attenuates the body fat accumulation that usually accompanies an HF diet.

show abstract

“…In addition to the induction of differentiation factors, inhibitors of adipogenesis, such as myostatin, 19 tumor necrosis factor-a, 20 retinoic acid 21 and rapamycin, 22 have also been described. Genistein, a class of flavonoid, has also been shown to inhibit 3T3-L1 proliferation and differentiation.…”

Section: Introductionmentioning

confidence: 99%

Grape-seed derived procyanidins interfere with adipogenesis of 3T3-L1 cells at the onset of differentiation

et al. 2005

View full text Add to dashboard Cite

OBJECTIVE: Our group's previous results on the effects of a grape seed procyanidin extract (GSPE) on adipose metabolism showed that peroxisome proliferator-activated receptor-g (PPARg) plays a central role in the lipolytic effects of GSPE on adipocytes. Since PPARg2 is a main regulator of the differentiation process of adipocytes, we investigated whether GSPE affects the adipogenesis of 3T3-L1 cells. DESIGN: We performed a time point screening by treating 3T3-L1 cells with GSPE during the differentiation process for 24 h. MEASUREMENTS: Differentiation markers and differential gene expression due to GSPE treatment (using the microarray technique). RESULTS: Twenty four hour-GSPE treatment at the onset of differentiation reduces adipose-specific markers and maintains the expression of preadipocyte marker preadipocyte factor-1 (Pref-1) significantly elevated. These effects were not found in other time points. Microarray analysis of gene expression after GSPE treatment at the early stage of differentiation showed a modified gene expression profile in which cell cycle and growth-related genes were downregulated by GSPE. CONCLUSION: These results suggest that GSPE affects adipogenesis, mainly at the induction of differentiation, and that procyanidins may have a new role in which they impede the formation of adipose cells.

show abstract

Inhibition of Preadipocyte Differentiation by Myostatin Treatment in 3T3-L1 Cultures

Cited by 110 publications

References 27 publications

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Resistance to body fat gain in ‘double-muscled’ mice fed a high-fat diet

Grape-seed derived procyanidins interfere with adipogenesis of 3T3-L1 cells at the onset of differentiation

Contact Info

Product

Resources

About