Cardiac Metabolism in Health and Disease by L. M. King, L. H. Opie (auth.), Salah Abdel-Aleem, James E.

By L. M. King, L. H. Opie (auth.), Salah Abdel-Aleem, James E. Lowe (eds.)

This detailed factor of Molecular and mobile Biochemistry includes unique study papers in addition to invited experiences concentrated within the box of cardiac metabolism and its legislation less than general and ailment stipulations. those papers conceal many parts less than in depth and speedy improvement corresponding to the law of fatty acid oxidation within the center, the function of cardiac glycogen in the course of ischemia, the position of CPT I isoenzymes, the pathophysiology of diabetic cardiomyopathy, cardiac safeguard via rules of power creation, the function of fatty acid binding protein less than basic and pathological stipulations, and a number of other vital subject matters during this sector of analysis. we are hoping that this targeted factor of Molecular and CellularBiochemistry presents an up to date resource of data for scientists and clinicians attracted to the mechanism through which cardiac metabolism is regulated in overall healthiness and sickness and the mechanistic dating among disturbances in cardiac metabolism and the genesis of cardiovascular diseases.

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Extra resources for Cardiac Metabolism in Health and Disease

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These observations suggest that developmental expression of CPT-I is regulated by changes in the glucagon/insulin ratio that occur at birth and by the abundance of long-chain fatty acids. Using the nuclear run on assay, it was found that the rate of transcription ofthe L-CPT-I gene was elevated in the livers of rats on high fat diets and decreased in the livers of rats on high carbohydrate diets [36]. Insulin inhibits transcription of the L-CPT-I gene in isolated hepatocytes, and cAMP stimulates transcription [36].

First, through the enzyme camitine palmityl transferase (CPT-I), camitine reacts with long chain fatty acids to make long chain acyl carnitine esters. The second role ofcamitine is to shuttle free carnitine and long chain acyl carnitine across the inner mitochondrial membrane. Inside the mitochondrial matrix, long chain acyl camitine is converted back to free camitine and long chain fatty acids via CPT-II. Since, the normal heart obtains approximately 60% of its total energy production from fatty acid oxidation [2], this function of carnitine is thought to be of major importance.

Deficiencies of carnitine have been induced in rats by dietary depletion, intraperitoneal injection of Dcarnitine [64], uremia, and administration of oral sodium pivalate [65, 66]. Only a few of these studies have addressed the cardiovascular consequences of camitine deficiency in these models. In experimental animals, it has been shown that carnitine levels are depressed in the diabetic [55], pressure and volume overloaded [67] and Syrian hamster cardiomyopathic [68] heart. Cardiac contractile function is depressed in all of these hearts, however, the role of the carnitine deficiency in this cardiac depression is uncertain.

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