Display Settings:

Items per page

Results: 8

1.
Fig. 4.

Fig. 4. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Platensimycin inhibits fatty acid oxidation in primary rat hepatocytes. n = 3 wells. Data are expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 versus vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
2.
Fig. 5.

Fig. 5. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Platensimycin reduces fatty acid oxidation (A) and increases whole-body glucose oxidation (B) in vivo. db/db mice of 14.5 wk of age were used (n = 7 mice per group). *P < 0.05, **P < 0.01 versus vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
3.
Fig. 1.

Fig. 1. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Effect of platensimycin (A), two widely used FAS inhibitors (cerulenin and C75, B and C), and the ACC inhibitor TOFA (D) on fatty acid and sterol synthesis in rat primary hepatocytes.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
4.
Fig. 3.

Fig. 3. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Platensimycin levels in liver are positively correlated with DNL inhibition in db/db mice. (A) rate of hepatic lipogenesis as a function of time and PTM dosages; (BD) correlation of liver PTM levels and lipogenesis inhibition at 2, 4, and 8 h. Veh, vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
5.
Fig. 6.

Fig. 6. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Platensimycin increases malonyl-CoA but not acetyl-CoA or CoA levels in the livers of db/db mice at 1 h postdosing. Mice received an oral dose of platensimycin as indicated at 9:00 AM and food was removed. Livers were collected and quickly frozen at 1, 4, and 8 h postdose. n = 5 per group. *P < 0.05, **P < 0.01 versus vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
6.
Fig. 7.

Fig. 7. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Chronic platensimycin treatment leads to a reduction of liver triglyceride levels (A) and increased insulin sensitivity as determined by an insulin tolerance test (B). Dosed animals were db/+ mice fed a high-fructose diet (n = 8 mice per group). *P < 0.05, ***P < 0.001 versus vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
7.
Fig. 2.

Fig. 2. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Platensimycin preferentially distributes to the liver following oral dosing (n = 3) (A) and inhibits fatty acid synthesis in the liver, but not in adipose tissue (WAT) (n = 5) (B). db/db mice were used. For A, PTM was dosed orally at 100 mpk; for B, PTM was administered via i.p. injection at the doses indicated. Lower limits of detection were 0.0045, 0.045, and 0.009 μM for plasma, brain, and liver. For fatty acid synthesis measurements, the [3H]H20 incorporation method was used.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.
8.
Fig. 8.

Fig. 8. From: Antidiabetic and antisteatotic effects of the selective fatty acid synthase (FAS) inhibitor platensimycin in mouse models of diabetes.

Chronic treatment of db/db mice with platensimycin lowers plasma glucose and plasma ketone bodies, and leads to a trend toward liver TG reduction. (A) Time course of plasma glucose changes. (B) Change in glucose as a percentage of vehicle as a function of treatment duration. Vehicle glucose was set as 100%, and glucose levels in the treated groups were normalized to the respective vehicle groups. (C) Terminal liver TG levels. (D) Terminal plasma β-HBA level (n = 7–8 mice per group). *P < 0.05, **P < 0.01, ***P < 0.001 versus vehicle.

Margaret Wu, et al. Proc Natl Acad Sci U S A. 2011 March 29;108(13):5378-5383.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk