Results: 5

1.
Figure 1

Figure 1. From: Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts.

Plasma levels of Ang II in treated and untreated mice. Ang II was measured by RIA in four groups of mice: wt control (wt, n = 6), wt captopril treated (wt+CP, n = 4), ob/ob (ob, n = 6), and ob/ob captopril treated (ob+CP, n = 5) after 4 wk of treatment with captopril (4 mg/kg·d). #, P = 0.02 vs. wt.

Imene Tabbi-Anneni, et al. Endocrinology. 2008 August;149(8):4043-4050.
2.
Figure 4

Figure 4. From: Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts.

MVO2 and cardiac power in isolated working hearts. A, The hearts used for MVO2 calculations were the same as those used for palmitate metabolism measurements in Fig. 3 (n = 3–5/group). B, For each perfusion condition, cardiac power data from glycolysis and palmitate oxidation experiments were combined (n = 6–10/group. *, P < 0.05 vs. wt no insulin; **, P < 0.05 vs. equivalently treated wt; ¶, P = 0.06 vs. ob/ob captopril (ob+C basal); §, P < 0.05 vs. ob+C basal.

Imene Tabbi-Anneni, et al. Endocrinology. 2008 August;149(8):4043-4050.
3.
Figure 2

Figure 2. From: Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts.

Glucose and insulin concentrations in treated and untreated mice. A, GTTs were performed in wt (n = 9), wt captopril (wt+C, n = 10), ob/ob (ob, n = 10), and ob+C (n = 10) mice after 4 wk of treatment with or without captopril (4 mg/kg·d). *, P < 0.05 vs. wt at the same time point. B, Insulin concentrations were determined at both the fasting (fast) and peak feeding (fed) state in wt and ob/ob mice treated or not for 4 wk with captopril (n = 3 per group). *, P < 0.05 vs. wt fast; **, P < 0.05 vs. ob fast; §, P < 0.05 vs. wt+C fast; ¶, P < 0.05 vs. ob+C fast.

Imene Tabbi-Anneni, et al. Endocrinology. 2008 August;149(8):4043-4050.
4.
Figure 3

Figure 3. From: Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts.

Substrate metabolism in isolated working hearts. Rates of glycolysis (A) and palmitate oxidation (B) were measured in hearts from wt and ob/ob mice treated or not for 4 wk with captopril (n = 3–5/group). Perfusions were performed at 0.4 mm palmitate and 5 mm glucose in the absence or presence of 1 nm insulin. *, P < 0.05 vs. wt (no insulin); **, P < 0.05 vs. equivalently treated wt; §, P < 0.05 vs. ob/ob captopril treated (ob+C basal). g dwt, gram dry heart weight.

Imene Tabbi-Anneni, et al. Endocrinology. 2008 August;149(8):4043-4050.
5.
Figure 5

Figure 5. From: Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts.

Akt and AMPK phosphorylation in isolated perfused hearts. Hearts from wt and ob/ob mice (ob) treated or not for 4 wk with captopril (CP) were perfused in the Langendorff mode in the absence or presence of 1 nm insulin (Ins; n = 3–7/group). A, Phospho-Akt (Thr308) normalized to total Akt (Tot-Akt). B, Total IR normalized to total proteins at 96 kDa. C, p-Tyr (PY20) immunoblot; arrows denote the band corresponding to the IR (96 kDa) and IRS1 (180 kDa) proteins, respectively. Upper panel, Coomassie blue staining (CB) was used to normalize for protein loading. D, Phospho-AMPK (Thr172) normalized to total AMPK were determined in heart homogenates by Western blot. Experiments were repeated twice for each protein, and similar results were obtained. Because no significant changes were observed in phospho-AMPK (Thr172)/total AMPK between basal and insulin stimulated hearts for each respective group of mice, data were pooled. A representative Western blot and a histogram showing densitometry (mean ± se) are shown. *, P < 0.05 vs. wt no insulin; §, P < 0.05 vs. ob+C basal; ***, P < 0.01 vs. ob; $, P < 0.01 vs. ob basal; ##, P < 0.05 vs. ob+ins.

Imene Tabbi-Anneni, et al. Endocrinology. 2008 August;149(8):4043-4050.

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