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. 2019 Oct 7;17(10):e3000444. doi: 10.1371/journal.pbio.3000444

Fig 5. OVX accelerates HFD-induced body weight gain, defect on glucose disposal, and hepatic lipogenic gene expression.

Fig 5

(A) Illustration of the experimental timeline. OVX or sham surgery was performed on mice at the age of 5 weeks. After 1-week recovery, mice were fed with LFD or HFD for 6 weeks, with IPITT and IPGTT performed on indicated time. (B) Weekly body weight recording. (C–D) IPITT and IPGTT performed at fifth week and sixth week, respectively. “*” indicates LFD/Sham versus HFD/Sham; “&” indicates LFD/OVX versus HFD/OVX; “§” indicates LFD/Sham versus LFD/OVX; “#” indicates HFD/Sham versus HFD/OVX. (E) Western blotting shows the detection of p-ACC (Ser79), SREBP-1c, and ChREBP in the indicated group of mice. GAPDH is the house keep protein. (F) Densitometrical analysis of panel E. (G–J) Western blotting show the detection of PKB S473 phosphorylation in the liver (G–H) and fat (I–J) in response to insulin i.p. injection in indicated group of mice. Mice were injected with PBS or insulin 10 minutes before their euthanization. N = 3–5 for panels B–D. Values represent mean ± SD. For panels E–J, N = 3. Underlying numerical values can be found in S1 Data. AUC, area under the curve; ChREBP, carbohydrate-responsive element-binding protein; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; HFD, high-fat diet; i.p., intraperitoneal; IPGTT, intraperitoneal glucose tolerance test; IPITT, intraperitoneal insulin tolerance test; LFD, low-fat diet; OVX, ovariectomy; p-ACC, phosphorylated acetyl-coA carboxylase; PKB, protein kinase B; SREBP-1c, sterol regulatory element-binding protein 1-c.