Which of the following growth media would you expect to result in synthesis of high levels of mRNA for the enzymes of the E.
The level of mRNA synthesis from the lac operon is also regulated by the intracellular concentration of glucose via a mechanism called catabolite repression. Antianginal drugs that exert their anti-ischaemic effects primarily by altering myocardial metabolism have recently attracted attention. Considerable progress has been made over the last 25 years in expanding the therapeutic options available in ischaemic heart disease, including both pharmacological and interventional measures that improve symptoms and prognosis.
The modes of action of most prophylactic antianginal agents involve haemodynamic changes, such as reduction in systemic vascular resistance, coronary vasodilatation, or negative inotropism, thus improving the imbalance in myocardial oxygen supply and demand. Under aerobic conditions the predominant substrate used by the normal adult human heart are free fatty acids (FFA), accounting for 60–90% of the energy generated1 (Fig. Carbohydrate metabolism, on the other hand, contributes only about 10–40% of energy generated by the healthy adult human heart.2 Glucose taken up by the myocardial cell is either stored as glycogen or converted into pyruvate by glycolysis. In contrast to the adult heart, the fetal heart (which operates under hypoxic conditions) uses glucose as its predominant fuel. However, a theoretical downside exists to metabolic modulation by inhibiting FFA metabolism. They have the potential to relieve symptoms in patients with refractory angina who are already on “optimal” medical therapy and have disease that is not amenable to revascularisation, making these drugs an attractive addition to therapy, particularly for the elderly population. However, many patients continue to experience intractable symptoms despite being on “optimal” medical therapy.

Recently, it has become apparent that certain antianginal treatments exert a primarily metabolic action and have little or no effect on coronary haemodynamics. Pyruvate is then oxidised within the mitochondria by pyruvate dehydrogenase into acetyl CoA. The switch to free fatty acids as the predominant substrate occurs in the early postnatal period.3 All metabolic adaptive mechanisms during ischaemia, whether physiologic or pharmaceutical, effectively recapitulate fetal energy metabolism by shifting substrate use towards glucose metabolism.
Furthermore, accumulation of LCFA intermediates during ?-oxidation has previously been shown to reduce the ventricular arrhythmia threshold12 and induce diastolic dysfunction13 during ischaemia. In addition, an increasing number of patients, particularly elderly patients, are deemed to be unsuitable for coronary revascularisation.
These drugs have considerable potential as adjunctive therapy for angina, particularly in patients refractory to standard therapies, and may be a primary therapeutic option in certain circumstances. The energetic advantages of incremental glucose utilisation arise from the fact that though fatty acid oxidation yields more ATP than glycolysis in aerobic conditions (in terms of ATP per gram of substrate), this is at the expense of greater oxygen consumption. These drugs increase glucose metabolism at the expense of free-fatty-acid metabolism, enhancing oxygen efficiency during myocardial ischaemia. A novel medical treatment would be particularly beneficial in relieving the significant morbidity that exists in this group.
They generally do not adversely affect blood pressure, pulse rate, or left ventricular systolic function, offering a significant advantage in patients in whom conventional agents may induce symptomatic hypotension, inappropriate bradycardia, or worsening heart failure. Whilst they have been demonstrated to reduce ischaemia in several clinical trials, their use remains limited.

The purpose of this review is to draw attention to some of these “metabolic” agents, while at the same time surveying the current level of evidence supporting their clinical use and mode of action. Following cellular uptake, LCFA entry into the mitochondria is facilitated by the enzymes carnitine-palmitoyl-transferase (CPT) I and II (Fig. This review aims to draw attention to these “metabolic” antianginal drugs while surveying the evidence supporting their use and mode of action. Two commonly used treatments for ischaemic heart disease that also exert metabolic effects have been included (?-blockers and glucose–insulin–potassium). Four metabolic antianginal drugs are reviewed: perhexiline, trimetazidine, ranolazine, and etomoxir.
We also discuss the metabolic actions of glucose–insulin–potassium and ?-blockers and describe myocardial metabolism during normal and ischaemic conditions. The potential of these metabolic agents may extend beyond the treatment of ischaemia secondary to coronary artery disease. They offer significant promise for the treatment of symptoms occurring due to inoperable aortic stenosis, hypertrophic cardiomyopathy, and chronic heart failure.

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