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The metabolic mechanisms involved in the heart protection from myocardial infarction induced by diabetes
Author(s) -
Malfitano Christiane,
Carbonaro M,
Souza AL,
Alba-Loureiro TC,
Souza LE,
Figueroa D,
Silva K,
Curi R,
Irigoyen MC
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1136.11
Subject(s) - medicine , myocardial infarction , ventricle , endocrinology , glycogen , phosphofructokinase , diabetes mellitus , chemistry , hexokinase , insulin , glycolysis , cardiology , metabolism
Metabolic mechanisms involved in heart protection of myocardial infarction (control = C, diabetic = D, myocardial infracted = MI and diabetic myocardial infarcted = DI) rats were investigated. After 30 days of diabetes and 15 days of MI, the left ventricle (LV) function and energy substrate levels were evaluated by echocardiogram and biochemistry methods. The infarcted area in DI was 36% lower than in MI and the ejection (DI: 82 3 vs 55 3% in MI) and shortening (DI: 48 2 vs MI: 25 2%) fractions were improved. Plasma levels (mg/dl) of free fatty acids (21 ± 3) and triglycerides (252 ± 44) were increased in D vs DI (12 ± 0.9; 110 ± 19), respectively. In the LV, the contents of free fatty acids (mg/g of tissue) and glycogen (mg of glucosyl unit/mg of tissue) were reduced in D (0.45 ± 0.09 and 91± 12) vs DI (1.1 ± 0.2 and 31 ± 2), respectively. LV activities (umol/min/mg protein) of citrate synthase in the MI were reduced (3.6 ± 0.2) and in D were similar (D: 5 ± 0.9; DI: 4.3 ± 0.6) to C (6.2 ± 0.3); CPT 1 content in DI was 46% lower than in the D; hexokinase activity was 50% reduced in D vs C. The phosphofructokinase and glucose‐6‐phosphate dehydrogenase activities were not changed. The content of coenzyme A (μmol/ g tissue) was increased in DI (4.2 ± 2.9) vs MI (3.6 ± 0.1). These findings suggest an increase in the heart capacity for ATP generation maintaining the cardiac function in infarction. Support: CAPES, CNPq, FAPESP, UNEMAT