Mitochondrial creatine phosphokinase deficiency in diabetic rat heart.
The role of the mitochondrial end of the phosphocreatine energy shuttle was studied in the streptozotocin diabetic rat heart. Diabetic rats had 45 +/- 5% lower body weight and yielded 46 +/- 6% less mitochondria gm of protein than normals. Diabetic heart mitochondria had 32 +/- 7% lower creatine phosphokinase (CPK) activity and 59 +/- 10% lower oxygen consumption rate than normal heart mitochondria. Creatine (25 mM) did not stimulate oxygen uptake by diabetic heart although control (normal) heart mitochondria were stimulated. Inadequate mitochondrial energy production in the form of phosphocreatine could result in lower energy delivery to the myofibrillar contraction sites and might be an important factor in diabetic cardiomyopathy and weight loss.
Savabi
F
F
Department of Pharmacology and Nutrition, University of Southern California, School of Medicine, Los Angeles 90033.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D003401:Creatine / Q000378:metabolism; D003402:Creatine Kinase / Q000172:deficiency* / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology* / Q000378:metabolism; D007700:Kinetics; D008297:Male; D008929:Mitochondria, Heart / Q000201:enzymology* / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values
D000227:Adenine Nucleotides; D003402:Creatine Kinase; D003401:Creatine