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Twist 1 regulates the expression of PPARγ during hormone-induced 3T3-L1 preadipocyte differentiation: a possible role in obesity and associated diseases.

Ma W, Lu S, Sun T, Wang X, Ma Y, Zhang X, Zhao R, Wang Y - Lipids Health Dis (2014)

Bottom Line: Twist 1 mRNA and protein levels were reduced in diet-induced obese mice and rats and in obese humans.Retroviral interference of Twist 1 expression did not significantly impair lipid formation; however, retroviral interference induced PPARγ mRNA and protein expression on day 4 of differentiation induction.Adipokine array analyses revealed increased secretion of CXCR4 (19.55-fold), VEGFR1 (92.13-fold), L-21 R (63.55-fold), and IL-12 R beta 1 (59.66-fold) and decreased secretion of VEGFR3 (0.01-fold), TSLP R (0.071-fold), MIP-1 gamma (0.069-fold), TNF RI/TNFRSF1A (0.09-fold), and MFG-E8 (0.06-fold).

View Article: PubMed Central - PubMed

Affiliation: Medical Research & Laboratory Diagnostic Center, Jinan Center Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P,R, China. mwsqianyi@163.com.

ABSTRACT

Background: Twist 1 is highly expressed in adipose tissue and has been associated with obesity and related disorders. However, the molecular function of Twist 1 in adipose tissue is unclear. Twist 1 has been implicated in cell lineage determination and differentiation. Therefore, we investigated both the role of Twist 1 in adipocyte precursor mobilization and the relationship of Twist 1 with other molecular determinants of adipocyte differentiation.

Methods: We examined Twist 1 mRNA and protein expression in subcutaneous adipose tissues from diet-induced obese C57/BL6 mice and Wistar rats and in obese patients undergoing liposuction or adipose transplant surgeries. Twist 1 expression was measured on days 0, 2, 4, 8, and 12 of 3T3-L1 differentiation in vitro. The role of Twist 1 in adipogenesis was explored using retroviral interference of Twist 1 expression. Adipokine secretion was evaluated using a RayBio® Biotin Label-based Adipokine Array.

Results: Twist 1 mRNA and protein levels were reduced in diet-induced obese mice and rats and in obese humans. Twist 1 was upregulated during 3T3-L1 preadipocyte differentiation in vitro, beginning from the fourth day of differentiation induction. Retroviral interference of Twist 1 expression did not significantly impair lipid formation; however, retroviral interference induced PPARγ mRNA and protein expression on day 4 of differentiation induction. Adipokine array analyses revealed increased secretion of CXCR4 (19.55-fold), VEGFR1 (92.13-fold), L-21 R (63.55-fold), and IL-12 R beta 1 (59.66-fold) and decreased secretion of VEGFR3 (0.01-fold), TSLP R (0.071-fold), MIP-1 gamma (0.069-fold), TNF RI/TNFRSF1A (0.09-fold), and MFG-E8 (0.06-fold).

Conclusions: Twist 1 is a regulator of adipocyte gene expression although it is not likely to regulate differentiation. We identified PPARγ as a potential target of Twist 1 and found variation in the secretion of multiple adipokines, which might indicate a prospective mechanism linking Twist 1 expression with obesity or associated diseases.

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Development and verification of diet-induced obesity models in C57/BL6 mice and Wistar rats. (A) Change in the body weight of C57/BL6 mice during the development of the obesity model. (B) Serum CHOL, TG, and GLU levels of C57/BL6 mice were assayed. CHOL and GLU were obviously increased in obese mice compared to the control group (The data are presented as the mean ± SE. *P < 0.05, control vs. high-fat diet group). (C) Change in the body weight of Wistar rats during the development of the obesity model. (D) Serum CHOL, TG, and GLU levels of Wistar rats were assayed. CHOL and GLU were obviously increased in obese mice compared to the control (*P < 0.05, control vs. high-fat diet group).
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Fig1: Development and verification of diet-induced obesity models in C57/BL6 mice and Wistar rats. (A) Change in the body weight of C57/BL6 mice during the development of the obesity model. (B) Serum CHOL, TG, and GLU levels of C57/BL6 mice were assayed. CHOL and GLU were obviously increased in obese mice compared to the control group (The data are presented as the mean ± SE. *P < 0.05, control vs. high-fat diet group). (C) Change in the body weight of Wistar rats during the development of the obesity model. (D) Serum CHOL, TG, and GLU levels of Wistar rats were assayed. CHOL and GLU were obviously increased in obese mice compared to the control (*P < 0.05, control vs. high-fat diet group).

Mentions: During breeding, four C57/BL6 mice and two Wistar rats in the HFD-treated group died for unknown reasons, while all animals in the control group remained alive. Thus, there were 12 experimental animals in both of the control groups, eight C57/BL6 mice in the HFD-treated group, and ten Wistar rats in the HFD-treated group. During breeding, the body weights of C57/BL6 mice and Wistar rats increased gradually (Figure 1A/C). At the end of the experiments, the body weight of obese C57/BL6 mice was 34.86 ± 2.98 g, which was significantly higher than that of the control mice (26.15 ± 2.95 g; P < 0.05). The body weight of obese Wistar rats was 438.61 ± 37.65 g, while that of the control rats was 342.66 ± 31.46 g (P < 0.05). Serum CHOL and GLU levels were both obviously increased in obese mice and rats compared with the control (Figure 1B/D) (P < 0.05). However, no significant difference in TG levels was observed (P > 0.05).Figure 1


Twist 1 regulates the expression of PPARγ during hormone-induced 3T3-L1 preadipocyte differentiation: a possible role in obesity and associated diseases.

Ma W, Lu S, Sun T, Wang X, Ma Y, Zhang X, Zhao R, Wang Y - Lipids Health Dis (2014)

Development and verification of diet-induced obesity models in C57/BL6 mice and Wistar rats. (A) Change in the body weight of C57/BL6 mice during the development of the obesity model. (B) Serum CHOL, TG, and GLU levels of C57/BL6 mice were assayed. CHOL and GLU were obviously increased in obese mice compared to the control group (The data are presented as the mean ± SE. *P < 0.05, control vs. high-fat diet group). (C) Change in the body weight of Wistar rats during the development of the obesity model. (D) Serum CHOL, TG, and GLU levels of Wistar rats were assayed. CHOL and GLU were obviously increased in obese mice compared to the control (*P < 0.05, control vs. high-fat diet group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4150960&req=5

Fig1: Development and verification of diet-induced obesity models in C57/BL6 mice and Wistar rats. (A) Change in the body weight of C57/BL6 mice during the development of the obesity model. (B) Serum CHOL, TG, and GLU levels of C57/BL6 mice were assayed. CHOL and GLU were obviously increased in obese mice compared to the control group (The data are presented as the mean ± SE. *P < 0.05, control vs. high-fat diet group). (C) Change in the body weight of Wistar rats during the development of the obesity model. (D) Serum CHOL, TG, and GLU levels of Wistar rats were assayed. CHOL and GLU were obviously increased in obese mice compared to the control (*P < 0.05, control vs. high-fat diet group).
Mentions: During breeding, four C57/BL6 mice and two Wistar rats in the HFD-treated group died for unknown reasons, while all animals in the control group remained alive. Thus, there were 12 experimental animals in both of the control groups, eight C57/BL6 mice in the HFD-treated group, and ten Wistar rats in the HFD-treated group. During breeding, the body weights of C57/BL6 mice and Wistar rats increased gradually (Figure 1A/C). At the end of the experiments, the body weight of obese C57/BL6 mice was 34.86 ± 2.98 g, which was significantly higher than that of the control mice (26.15 ± 2.95 g; P < 0.05). The body weight of obese Wistar rats was 438.61 ± 37.65 g, while that of the control rats was 342.66 ± 31.46 g (P < 0.05). Serum CHOL and GLU levels were both obviously increased in obese mice and rats compared with the control (Figure 1B/D) (P < 0.05). However, no significant difference in TG levels was observed (P > 0.05).Figure 1

Bottom Line: Twist 1 mRNA and protein levels were reduced in diet-induced obese mice and rats and in obese humans.Retroviral interference of Twist 1 expression did not significantly impair lipid formation; however, retroviral interference induced PPARγ mRNA and protein expression on day 4 of differentiation induction.Adipokine array analyses revealed increased secretion of CXCR4 (19.55-fold), VEGFR1 (92.13-fold), L-21 R (63.55-fold), and IL-12 R beta 1 (59.66-fold) and decreased secretion of VEGFR3 (0.01-fold), TSLP R (0.071-fold), MIP-1 gamma (0.069-fold), TNF RI/TNFRSF1A (0.09-fold), and MFG-E8 (0.06-fold).

View Article: PubMed Central - PubMed

Affiliation: Medical Research & Laboratory Diagnostic Center, Jinan Center Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P,R, China. mwsqianyi@163.com.

ABSTRACT

Background: Twist 1 is highly expressed in adipose tissue and has been associated with obesity and related disorders. However, the molecular function of Twist 1 in adipose tissue is unclear. Twist 1 has been implicated in cell lineage determination and differentiation. Therefore, we investigated both the role of Twist 1 in adipocyte precursor mobilization and the relationship of Twist 1 with other molecular determinants of adipocyte differentiation.

Methods: We examined Twist 1 mRNA and protein expression in subcutaneous adipose tissues from diet-induced obese C57/BL6 mice and Wistar rats and in obese patients undergoing liposuction or adipose transplant surgeries. Twist 1 expression was measured on days 0, 2, 4, 8, and 12 of 3T3-L1 differentiation in vitro. The role of Twist 1 in adipogenesis was explored using retroviral interference of Twist 1 expression. Adipokine secretion was evaluated using a RayBio® Biotin Label-based Adipokine Array.

Results: Twist 1 mRNA and protein levels were reduced in diet-induced obese mice and rats and in obese humans. Twist 1 was upregulated during 3T3-L1 preadipocyte differentiation in vitro, beginning from the fourth day of differentiation induction. Retroviral interference of Twist 1 expression did not significantly impair lipid formation; however, retroviral interference induced PPARγ mRNA and protein expression on day 4 of differentiation induction. Adipokine array analyses revealed increased secretion of CXCR4 (19.55-fold), VEGFR1 (92.13-fold), L-21 R (63.55-fold), and IL-12 R beta 1 (59.66-fold) and decreased secretion of VEGFR3 (0.01-fold), TSLP R (0.071-fold), MIP-1 gamma (0.069-fold), TNF RI/TNFRSF1A (0.09-fold), and MFG-E8 (0.06-fold).

Conclusions: Twist 1 is a regulator of adipocyte gene expression although it is not likely to regulate differentiation. We identified PPARγ as a potential target of Twist 1 and found variation in the secretion of multiple adipokines, which might indicate a prospective mechanism linking Twist 1 expression with obesity or associated diseases.

Show MeSH
Related in: MedlinePlus