Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression

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Presentation transcript:

Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression Paulo A. Amorim, MD, T. Dung Nguyen, BS, Yasushige Shingu, MD, Michael Schwarzer, PhD, Friedrich W. Mohr, MD, PhD, Andrea Schrepper, MS, Torsten Doenst, MD, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 140, Issue 5, Pages 1160-1167 (November 2010) DOI: 10.1016/j.jtcvs.2010.08.003 Copyright © 2010 Terms and Conditions

Figure 1 Substrate oxidation rates of isolated working rat hearts from rats that underwent left coronary artery ligation or a sham procedure and their response to insulin. A, Rates of basal and insulin-stimulated glucose oxidation. Insulin-stimulated increase in glucose oxidation as B, absolute values and C, percentage of basal rates. D, Rates of basal and insulin-stimulated fatty acid oxidation. Insulin-stimulated decrease in fatty acid oxidation as E, absolute values and F, percentage of baseline. Open bars indicate sham control group; solid bars, infarct group. Values presented as mean ± standard error of mean; n = 5 to 7 per group. ∗P < .05 compared with control, #P < .05 compared with basal values of same group. The Journal of Thoracic and Cardiovascular Surgery 2010 140, 1160-1167DOI: (10.1016/j.jtcvs.2010.08.003) Copyright © 2010 Terms and Conditions

Figure 2 Basal and insulin-stimulated phosphorylation of Akt in infarcted and sham control hearts. A, Total protein expression of Akt. Level of phosphorylated Akt at B, Ser473 and C, Thr308 with (hatched bars) and without (solid bars) insulin stimulation in control and infarcted hearts. White solid bars indicate control group without insulin; light-hatched bars, control group with insulin; black solid bars, infarct group without insulin; and dark-hatched bars, infarct group with insulin. Representative Western blots shown. Values presented as mean ± standard error of mean; n = 4 per group. #P < .05 compared with levels without insulin from same group. The Journal of Thoracic and Cardiovascular Surgery 2010 140, 1160-1167DOI: (10.1016/j.jtcvs.2010.08.003) Copyright © 2010 Terms and Conditions

Figure 3 mRNA expression of genes involved in substrate use and mitochondrial biogenesis in infarcted and sham-control hearts. mRNA expression of A, glucose transporter type 4 (GLUT4); B, carnitine palmitoyltransferase 1 (CPT-1); C, long-chain-acyl-coenzyme A dehydrogenase (LCAD); D, peroxisome proliferator-activated receptor-α (PPARα); E, mitochondrial transcription factor A (Tfam); and F, peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α). Values are presented as mean ± standard error of mean, n = 8 to 10 per group. ∗P < .05 compared with control group. The Journal of Thoracic and Cardiovascular Surgery 2010 140, 1160-1167DOI: (10.1016/j.jtcvs.2010.08.003) Copyright © 2010 Terms and Conditions

Figure 4 Protein expression of p38 mitogen-activated protein kinase (MAPK) in sham-operated control and infarcted hearts. Representative Western blots shown. Values presented as mean ± standard error of mean, n = 4 per group. ∗P < .05 compared with control group. The Journal of Thoracic and Cardiovascular Surgery 2010 140, 1160-1167DOI: (10.1016/j.jtcvs.2010.08.003) Copyright © 2010 Terms and Conditions