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Role of protease inhibitors and acylation stimulating protein in the adipogenesis in 3T3-L1 cells.

Soliman MM, El-Senosi YA, Salem MM, Abdel Hamid OM, Kazuhiro K - J. Vet. Sci. (2009)

Bottom Line: Addition of PI during adipocytes differentiation dose dependently and significantly (p < 0.5) inhibited the degree of triglycerides (TG) accumulation.Finally, when ASP in different doses (Low, 16.7; Medium, 45 and High, 450 ng/mL) incubated with a dose of x150 PI, ASP partially inhibited the PI-inhibited adipogenesis and TG accumulation.The results in this study show that PI inhibit lipids accumulation and confirm role of ASP in TG biosynthesis and adipogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Veterinary Medicine, Benha University, 020-013, Egypt. mohamedsoliman8896@yahoo.com

ABSTRACT
Treatment of AIDS (HIV) and hepatitis C virus needs protease inhibitors (PI) to prevent viral replication. Uses of PI in therapy are usually associated with a decrease in body weight and dyslipidemia. Acylation stimulating protein (ASP) is a protein synthesized in adipocytes to increase triglycerides biosynthesis, for that the relation of PI and ASP to adipogenesis is tested in this work. ASP expression was increased during 3T3-L1 differentiation and reached a peak at day 8 with cell maturation. Addition of PI during adipocytes differentiation dose dependently and significantly (p < 0.5) inhibited the degree of triglycerides (TG) accumulation. Moreover, presence of ASP (450 ng/mL) in media significantly (p < 0.5) stimulated the degree of TG accumulation and there was additive stimulation for ASP when added with insulin (10 microg/mL). Finally, when ASP in different doses (Low, 16.7; Medium, 45 and High, 450 ng/mL) incubated with a dose of x150 PI, ASP partially inhibited the PI-inhibited adipogenesis and TG accumulation. The results in this study show that PI inhibit lipids accumulation and confirm role of ASP in TG biosynthesis and adipogenesis.

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Related in: MedlinePlus

Effect of PI on adipogenesis in 3T3-L1 cells. Cells were incubated with insulin for 4 days and then with PI in different dose to observe lipids accumulation. (A) Control; Showing fibroblast like cells without lipids accumulation. (B) Insulin alone (10 µg/mL); Cells became round and a marked increase in lipids was recorded. (C-F) C; Insulin plus PI (×300), D; Insulin plus PI (×200), E; Insulin plus PI (×150) and F; Insulin plus PI (×100). Oil red O stain, ×400.
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Figure 2: Effect of PI on adipogenesis in 3T3-L1 cells. Cells were incubated with insulin for 4 days and then with PI in different dose to observe lipids accumulation. (A) Control; Showing fibroblast like cells without lipids accumulation. (B) Insulin alone (10 µg/mL); Cells became round and a marked increase in lipids was recorded. (C-F) C; Insulin plus PI (×300), D; Insulin plus PI (×200), E; Insulin plus PI (×150) and F; Insulin plus PI (×100). Oil red O stain, ×400.

Mentions: As seen in Fig. 1, the ASP expression was examined up to 12 days as seen it was time dependently increased using RT-PCR analysis. This increase in ASP expression was recorded in day 4 and reached the plateau at 8 days, and continued high up to 12 days. Next, the degree of lipids accumulation was examined microscopically in presence or absence of PI. The presence of insulin alone (10 µg/mL) increased the lipids accumulation. Addition of PI dose dependently inhibited adipogenesis and lipids accumulation (Fig. 2). When the degree of lipids accumulation measured specrophotometrically, the effect was clear and significantly (p < 0.05) increased with insulin (2 fold increase) and inhibited when co-treated with different doses of PI in comparing with insulin and control (Fig. 3).


Role of protease inhibitors and acylation stimulating protein in the adipogenesis in 3T3-L1 cells.

Soliman MM, El-Senosi YA, Salem MM, Abdel Hamid OM, Kazuhiro K - J. Vet. Sci. (2009)

Effect of PI on adipogenesis in 3T3-L1 cells. Cells were incubated with insulin for 4 days and then with PI in different dose to observe lipids accumulation. (A) Control; Showing fibroblast like cells without lipids accumulation. (B) Insulin alone (10 µg/mL); Cells became round and a marked increase in lipids was recorded. (C-F) C; Insulin plus PI (×300), D; Insulin plus PI (×200), E; Insulin plus PI (×150) and F; Insulin plus PI (×100). Oil red O stain, ×400.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2801122&req=5

Figure 2: Effect of PI on adipogenesis in 3T3-L1 cells. Cells were incubated with insulin for 4 days and then with PI in different dose to observe lipids accumulation. (A) Control; Showing fibroblast like cells without lipids accumulation. (B) Insulin alone (10 µg/mL); Cells became round and a marked increase in lipids was recorded. (C-F) C; Insulin plus PI (×300), D; Insulin plus PI (×200), E; Insulin plus PI (×150) and F; Insulin plus PI (×100). Oil red O stain, ×400.
Mentions: As seen in Fig. 1, the ASP expression was examined up to 12 days as seen it was time dependently increased using RT-PCR analysis. This increase in ASP expression was recorded in day 4 and reached the plateau at 8 days, and continued high up to 12 days. Next, the degree of lipids accumulation was examined microscopically in presence or absence of PI. The presence of insulin alone (10 µg/mL) increased the lipids accumulation. Addition of PI dose dependently inhibited adipogenesis and lipids accumulation (Fig. 2). When the degree of lipids accumulation measured specrophotometrically, the effect was clear and significantly (p < 0.05) increased with insulin (2 fold increase) and inhibited when co-treated with different doses of PI in comparing with insulin and control (Fig. 3).

Bottom Line: Addition of PI during adipocytes differentiation dose dependently and significantly (p < 0.5) inhibited the degree of triglycerides (TG) accumulation.Finally, when ASP in different doses (Low, 16.7; Medium, 45 and High, 450 ng/mL) incubated with a dose of x150 PI, ASP partially inhibited the PI-inhibited adipogenesis and TG accumulation.The results in this study show that PI inhibit lipids accumulation and confirm role of ASP in TG biosynthesis and adipogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Veterinary Medicine, Benha University, 020-013, Egypt. mohamedsoliman8896@yahoo.com

ABSTRACT
Treatment of AIDS (HIV) and hepatitis C virus needs protease inhibitors (PI) to prevent viral replication. Uses of PI in therapy are usually associated with a decrease in body weight and dyslipidemia. Acylation stimulating protein (ASP) is a protein synthesized in adipocytes to increase triglycerides biosynthesis, for that the relation of PI and ASP to adipogenesis is tested in this work. ASP expression was increased during 3T3-L1 differentiation and reached a peak at day 8 with cell maturation. Addition of PI during adipocytes differentiation dose dependently and significantly (p < 0.5) inhibited the degree of triglycerides (TG) accumulation. Moreover, presence of ASP (450 ng/mL) in media significantly (p < 0.5) stimulated the degree of TG accumulation and there was additive stimulation for ASP when added with insulin (10 microg/mL). Finally, when ASP in different doses (Low, 16.7; Medium, 45 and High, 450 ng/mL) incubated with a dose of x150 PI, ASP partially inhibited the PI-inhibited adipogenesis and TG accumulation. The results in this study show that PI inhibit lipids accumulation and confirm role of ASP in TG biosynthesis and adipogenesis.

Show MeSH
Related in: MedlinePlus