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Titolo:
Myocardial energy metabolism and diabetes
Autore:
Grynberg, A;
Indirizzi:
Fac Pharm, NASA, INRA, Paris, France Fac Pharm Paris FranceFac Pharm, NASA, INRA, Paris, France
Titolo Testata:
DIABETES & METABOLISM
fascicolo: 5, volume: 27, anno: 2001,
parte:, 2
pagine: S12 - S19
SICI:
1262-3636(200111)27:5<S12:MEMAD>2.0.ZU;2-0
Fonte:
ISI
Lingua:
FRE
Soggetto:
FATTY-ACID OXIDATION; ACETYL-COA CARBOXYLASE; LIPID-METABOLISM; RAT-HEART; ARACHIDONIC-ACID; TRIMETAZIDINE; CARDIOMYOCYTES; PHOSPHOLIPIDS; TRANSPORT; MYOCYTES;
Keywords:
diabetes; heart; fatty acids; metabolism;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Grynberg, A Fac Pharm, NASA, INRA, 4 Av Observ, Paris, France Fac Pharm 4 Av Observ Paris France Av Observ, Paris, France
Citazione:
A. Grynberg, "Myocardial energy metabolism and diabetes", DIABETE MET, 27(5), 2001, pp. S12-S19

Abstract

The capacity of cardiac myocyte to regulate ATP production to face any change in energy demand is a major determinant of cardiac function. Because FAis the main heart fuel (although the most expensive one in oxygen, and prompt to induce deleterious effects), this process is based on a balanced fatty acid (FA) metabolism. Several pathological situations are associated with an accumulation of FA or derivatives, or with an excessive b-oxidation. The diabetic cardiomyocyte is characterised by an over consumption of FA. The control of the FA/glucose balance clearly appears as a new strategy for cytoprotection, particularly in diabetes and requires a reduced FA contribution to ATP production. Cardiac myocytes can control FA mitochondrial entry,but display weak ability to control FA uptake, thus the fate of non P-oxidized FA appear as a new impairment for the cell. Both the trigger and the regulation of cardiac contraction result from membrane activity, and the other major FA function in the myocardium is their role in membrane homeostasis, through the phospholipid synthesis and remodeling pathways. Sudden death, hypercatecholaminemia, diabetes and heart failure have been associated with an altered PUFA content in cardiac membranes. Experimental data suggest that the 2 metabolic pathways involved in membrane homeostasis may represent therapeutic targets for cytoprotection. The drugs that increase cardiac phospholipid turnover (trimetazidine, ranolazine,...) display anti-ischemic non hemodynamic effect. This effect is based on a redirection of FA utilization towards phospholipid synthesis, which decrease their availability for energy production. A nutritional approach gave also promising results, Besides its anti-arrhythmic effect, the dietary docosahexaenoic acid is able toreduce FA energy consumption and hence oxygen demand. The cardiac metabolic pathways involving FA should be considered as a whole, precariously balanced. The diabetic heart being characterised by a different metabolic "status" with similarities to that of myocardium in coronary disease. Diabetes and other chronic cardiac diseases share common FA metabolism disorders leading to an altered energy balance, a decrease in long chain polyunsaturated Fas, and altered FA profiles in cardiac membranes. These disturbances, however, do not represent independent therapeutic targets, and should be considered as a whole.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:40:46