Fig. 4.
Hyperandrogenism facilitated BMAL1-mediated insulin resistance through the NAMPT/NAD+/SIRT1 pathway in mature adipocytes. a The mature adipose cells were differentiated from 3 T3-L1 preadipocytes after oil red O staining. b Glucose uptake after NC siRNA, testosterone (10− 6 M for 24 h), Bmal1 siRNA, or Nampt siRNA treatment in mature adipocytes. Glucose uptake was measured after insulin stimulation (100 nM for 20 min). cBmal1, Sirt1, Nampt, Glut4, and Pparg mRNA expressions after knocking down Bmal1 in mature adipocytes. d Cellular NAD+ level after knocking down Bmal1 in mature adipocytes. eBmal1, Sirt1, Nampt, Glut4, and Pparg mRNA expressions after knocking down Sirt1 in mature adipocytes. fBmal1, Sirt1, Nampt, Glut4, and Pparg mRNA expressions after knocking down Nampt in mature adipocytes. gBmal1, Clock, Per1, Per2, Sirt1, and Nampt mRNA expressions after treatment with different doses of testosterone for 24 h in mature adipocytes. hBmal1, Nampt, Sirt1, Glut4, and Pparg mRNA expressions after Bmal1 overexpression and further incubation with testosterone (10− 6 M for 24 h) in mature adipocytes. * P < 0.05, ** P < 0.01, *** P < 0.001 against NC siRNA cells or against T0 0 M cells or against Control-vec cells; # P < 0.05, ## P < 0.01, ### P < 0.001 against BMAL1-vec cells