Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistance
J. Clin. Invest. Li Liu, et al. 117:1679 doi:10.1172/JCI30565 [Go to this article.]

Figure 3
Myocellular DGAT1 overexpression reproduces the athlete’s paradox and protects against FA-induced insulin resistance. (A and B) Muscle TG (A) and DAG and ceramide (B) contents in soleus muscles isolated from WT and transgenic mice on NC diet. (C and D) Muscle TG (C) and DAG and ceramide (D) contents in soleus muscles isolated from WT and transgenic mice after 8 weeks of HFD treatment. (E) Representative cross-sections of soleus muscles from HFD-fed WT and MCK-Dgat1 transgenic mice, stained for neutral lipids (primarily TG) with oil red O. (F–H) GTT in age- and diet-matched male WT (n = 9) and transgenic (n = 5) mice on NC diet (F), HFD for 5 weeks (G), or HFD for 8 weeks (H). (I) ITT in age-matched male WT and transgenic mice on NC diet or HFD for 8 weeks. ^#P < 0.05 compared with HFD-fed WT mice. (J) Quantification of total and percentage of membrane-bound GLUT4 in soleus muscles isolated from WT mice on NC diet, WT mice on HFD, and transgenic mice on HFD. The quantification is based on Western blot analysis of the myocellular membrane-bound (Mb) and cytosol (Cyt) fractions of GLUT4 (n = 4 in each group); a typical Western blot is presented as an inset. (K) Quantification of total and percentage of membrane-bound GLUT1 from the muscle specimens described in J. *P < 0.05; **P < 0.01.