The absorption of monosodium glutamate triggers mechanisms for assimilating proteins.
WHY DO WE STOP EATING even though only a small quantity of metabolites has entered the bloodstream? The sensation of a full stomach does not signal satiety: A rat whose belly has been pumped full of air does not cease to eat. Through a series of reflexes, however, the organism is able to anticipate the metabolism of foods. For example, a bit of sugar placed on the tongue triggers the almost immediate release of glucose by the liver.
Around 1960, Stylianos Nicolaïdis and his colleagues at the Collège de France observed that the stimulation of the taste receptors by saccharine caused two hormones to be released by the pancreas: glucagon, which is responsible for the release of glucose, and insulin, which is responsible for the metabolism of glucose. Moreover, stimulation of receptors for the sweet taste produces an anticipated reaction that enables the body to metabolize glucides.
More recently, Nicolaïdis and a team of researchers including Claire Viarouge, Patrick Even, and Roland Caulliez examined reflexes that are triggered by detection of the taste of proteins and prepare the organism to metabolize them. One aspect of their investigation involved the ingestion of monosodium glutamate, which earlier studies had suggested is perceived by the organism as a signal to begin absorbing proteins. Previously limited to the seasoning of oriental soups, monosodium glutamate is now very commonly used in the food industry as a flavor enhancer. In addition to a salty taste, for some people it possesses a particular taste called umami that is distinct from the four classically recognized tastes (salt, sweet, sour, and bitter); mind you, the classic theory is wrong, as all good neurophysiologists know. Two questions presented themselves. First, does monosodium glutamate increase metabolic intensity in the same way that the absorption of proteins does? Second, does it trigger the same reflexive release of hormones (glucagon and insulin) as the one normally induced by the appearance of amino acids in the bloodstream?
To study these questions the team at the Collège de France constructed a device capable of isolating the various components of the metabolism and separately recording the metabolic demands associated with locomotion and thermogenesis, or heat production, in relation to food intake. Thermogenesis measures metabolic intensity without regard for an animal’s locomotive behavior. Experiments performed in 1991 to determine levels of thermogenesis during periods of activity and in the resting animal showed that stimulation of rats by intravenous administration of monosodium glutamate in the mouth and stomach produced only a weak hormonal reaction. Although it induced an anticipatory reflex, the monosodium glutamate seemed to be effective only when it was associated with other signals characteristic of food intake.
To test this hypothesis, the physiologists placed cannulas in the mouths of rats in order to be able to directly inject solutions of monosodium glutamate or distilled water using a catheter connected to the top of their cage. The rats were free to move around, and their metabolism was continuously monitored.
Immediately after implantation of the cannulas, the rats were trained to receive water or monosodium glutamate solutions through these tubes. One group of rats was injected with various concentrations of monosodium glutamate while they were eating. The other group, used as a control, received only distilled water during this time.
The physiologists were able to verify that the taste of sodium, when it accompanies a complete meal, causes notable metabolic changes. The thermogenesis induced by food intake increased much more, and much more rapidly, in the rats injected with monosodium glutamate than in the control group, suggesting that monosodium glutamate acts as a sort of protein “saccharine” capable of misleading the organism by its taste. Although it consisted mostly of carbohydrates, the meal was perceived as primarily protein.
How long the organism allows itself to be fooled when this gustatory information is not confirmed during the course of metabolism and whether the anticipatory reflexes contribute to satiation are questions that remain to be answered.