31Jan 2017

THE EFFECT OF DIABETES ON ACETOACETATE METABOLISM IN HEART.

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Background Aims: In this study, the effects of perfusion pressure, insulin, L-carnitine, propionate and 2,4-dinitrophenol on the utilization and oxidation of acetoacetate were investigated in the isolated non-working perfused heart from normal and diabetic rats. Materials and Method: Hearts from Male Wistar albino rats were used. In the diabetic subgroup, Diabetes was induced by an intravenous injection of alloxan. The hearts were perfused at a perfusion pressure of 40 or 80 mmHg for 1 h with Krebs-Henseleit Medium, with the concentrations of calcium and magnesium halved, and oxygenated by equilibration with 5% carbon dioxide and 95% oxygen. Determination of acetoacetate and D-3-hydroxybutyrate levels were made by the method of Mellanby and Williamson and Williamson and Mellanby respectively, and comparison between groups was done using the two-tailed Student’s t-test for independent samples. Results • Increasing Perfusion Pressure: No effect in both normal or diabetic hearts. • Insulin: No effect on acetoacetate utilization. • Diabetes: A decrease in the utilization and oxidation of acetoacetate and the production of D-3-hydroxybutyrate. • L- carnitine: o Normal hearts: no effect on acetoacetate utilization. o Diabetic hearts: acetoacetate utilization was enhanced • Propionate: o Normal hearts: Inhibited utilization of acetoacetate without affecting the rate of oxidation. The rate of D-3-hydroxybutyrate production was inhibited. o Diabetic hearts: Enhanced the utilization and oxidation of acetoacetate while reducing the production of D-3-Hydroxybutyrate • Dinitrophenol: o Normal hearts: Enhanced the utilization and oxidation of acetoacetate and decreased the production of D-3- hydroxybutyrate o Diabetic hearts: utilization and oxidation of acetoacetate were enhanced without effect on production of D-3- hydroxybutyrate. Conclusion: Diabetes inhibits and insulin has no significant effect on myocardial acetoacetate utilization and oxidation. Insulin, L-carnitine, or propionate are not suitable to ameliorate the utilization of acetoacetate in hearts from normal or diabetic animals, whereas Dinitrophenol enhances the catabolism of acetoacetate.

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[Abdurazzaq M. N. Sultan, Daniya M. Alturkistani, Camellia A. Sultan, Nada A. Sagr, Heba A. Bargawi, Khulud K. Natto, Rabeea F. Farhan, Sultan A. Sultan, Abdulrahman A. Alghamdi, Qusai A. Sultan, Moayad. Filimban and Bayan H. Alghamdi. (2017); THE EFFECT OF DIABETES ON ACETOACETATE METABOLISM IN HEART. Int. J. of Adv. Res. 5 (Jan). 2877-2882] (ISSN 2320-5407). www.journalijar.com

Abdurazzaq M. N. Sultan
(Professor) Department of Biochemistry, Faculty of Medicine, Umm Al-Qura University.

DOI:

Article DOI: 10.21474/IJAR01/3086      
DOI URL: http://dx.doi.org/10.21474/IJAR01/3086

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