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. 2004 Oct 1;114(7):917–927. doi: 10.1172/JCI21484

Figure 2.

Figure 2

βHT-IRS2 mice showed leptin resistance. (A) Body weights of control and βHT-IRS2 mice. Values are means ± SE of data obtained from the analysis of control (filled squares, n = 10) and βHT-IRS2 mice (open circles, n = 11). (B) WAT mass of epididymal fat pads of control and βHT-IRS2 mice at 12 weeks. Values are means ± SE of data obtained from the analysis of control (black bar, n = 5) and βHT-IRS2 mice (white bar, n = 9). (C) Fasting serum leptin levels of control and βHT-IRS2 mice at 8 weeks. Values are means ± SE of data obtained from the analysis of control (black bar, n = 10) and βHT-IRS2 mice (white bar, n = 11). (D) Leptin-mediated suppression of food intake (left) and body weight (right) at 8 weeks. Baseline food intake was measured during PBS injection. Values are means ± SE of data obtained from the analysis of control (black bar, n = 9) and βHT-IRS2 mice (white bar, n = 7). (E) In situ hybridization of the leptin receptor and Irs2 in hypothalami from control and βHT-IRS2 mice. Scale bar represents 1 mm. (F) Insulin-stimulated phosphorylation of Akt (top) and leptin-stimulated phosphorylation of Stat3 (bottom). Upper panels: lysates from untreated and insulin-treated mice were immunoblotted for anti_phospho-Akt (pAkt) and anti-Akt. Lower panels: lysates from untreated and leptin-treated mice were immunoblotted for anti_phospho-Stat3 (pStat3) and anti-Stat3. In graphs, white bars represent insulin- (left) or leptin- (right) stimulated phosphorylation. Data (means ± SE) are representative of at least 3 independent experiments. *P < 0.05; **P < 0.01.