Abstract

OUR recent hypothesis1 that “anorectic agents” such as fenfluramine and mazindol owe at least part of their anti-obesity properties to a peripheral action on glucose metabolism by causing an increase in glucose uptake into skeletal muscle and a subsequent “wasting of calories” has been criticised2 on the grounds that there is no information on the fate of the glucose so taken up, nor convincing evidence for an increase in metabolic rate with these drugs. We have now studied the effect of fenfluramine on lactate production in isolated human skeletal muscle, our previous work having shown no increase in glycogen levels3 nor in carbon dioxide production4. An increase in lactate production would indicate metabolism of the glucose entering the cell under the influence of fenfluramine.

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