Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the (n-3) family, play pivotal roles as "fuel partitioners" in that they direct fatty acids away from triglyceride storage and toward oxidation, and that they enhance glucose flux to glycogen. In doing this, PUFA may protect against the adverse symptoms of the metabolic syndrome and reduce the risk of heart disease. PUFA exert their beneficial effects by up-regulating the expression of genes encoding proteins involved in fatty acid oxidation while simultaneously down-regulating genes encoding proteins of lipid synthesis. PUFA govern oxidative gene expression by activating the transcription factor peroxisome proliferator-activated receptor alpha. PUFA suppress lipogenic gene expression by reducing the nuclear abundance and DNA-binding affinity of transcription factors responsible for imparting insulin and carbohydrate control to lipogenic and glycolytic genes. In particular, PUFA suppress the nuclear abundance and expression of sterol regulatory element binding protein-1 and reduce the DNA-binding activities of nuclear factor Y, Sp1 and possibly hepatic nuclear factor-4. Collectively, the studies discussed suggest that the fuel "repartitioning" and gene expression actions of PUFA should be considered among criteria used in defining the dietary needs of (n-6) and (n-3) and in establishing the dietary ratio of (n-6) to (n-3) needed for optimum health benefit.
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PMID:Polyunsaturated fatty acid regulation of gene transcription: a molecular mechanism to improve the metabolic syndrome. 1128 13

Obesity is an epidemic condition strongly associated with cardiovascular morbidity and mortality. Heart disease secondary to obesity is associated with myocardial steatosis, leading to ceramide synthesis and cell dysfunction in a process known as lipotoxicity. Soy protein has been demonstrated to reduce lipotoxicity in the liver and pancreas in different rodent models of obesity. Thus, our purpose in the present work was to assess the effect of dietary soy protein on cardiac lipid accumulation and ceramide formation during obesity and to evaluate its effect in the following 2 rodent models of obesity: 1) a diet-induced obesity model in Sprague-Dawley rats was produced by feeding rats a control or a high-fat casein or soy protein diet for 180 d; and 2) wild-type and ob/ob mice were fed a casein or soy protein diet for 90 d. Soy protein intake led to lower cholesterol and triglyceride concentrations in the hearts of rats and ob/ob mice in association with a greater PPARalpha mRNA concentration and a lower level of sterol regulatory element binding protein-1 mRNA than those fed casein. The ceramide concentration was also lower in hearts of rats and ob/ob mice that were fed soy protein in association with lower serine palmitoyl transferase (SPT)-1 and tumor necrosis factor-alpha mRNA concentrations. These results indicate that dietary soy protein can reduce the heart ceramide concentration by reducing the expression of SPT-1, a key enzyme in the formation of this sphingolipid in the heart of obese rodents, and by reducing lipid accumulation. Thus, soy protein consumption may be considered as a dietary therapeutic approach for lipotoxic cardiomyopathy prevention.
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PMID:Dietary soy protein reduces cardiac lipid accumulation and the ceramide concentration in high-fat diet-fed rats and ob/ob mice. 1982 84