https://www.slan.org.ve/publicaciones/pdf/Nonnutritive%20sweetener%20consumption%20in%20humans%20-%20effects%20on%20appetite%20and%20food%20intake%20and%20their%20putative%20mechanisms.pdf

Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms

The ventromedial hypothalamic syndrome, satiety, and a cephalic phase hypothesis.

Food-associated drinking in the rat.

In 3 experiments with a total of 72 male albino Wistar or Sprague-Dawley rats, liquid or solid diets differing in carbohydrate or triglyceride content were presented 1 at a time to each S once or twice a day. For a given S, each caloric density consistently had a particular odor and/or taste. Results show the size of the feeding bout on the dilute nutrient became larger than that on the more concentrated nutrient after several pairs of presentations. This differentiation was at least partly controlled by the oral cues which had been paired with nutrient differences. Results were attributable to acquired differences in the development of feeding inhibition during the meal, and not to original or acquired differences in initial rate of feeding or in the preference for 1 diet over the other in 2 stimulus tests.

Conditioned satiety in the rat.

In this paper we would like to discuss the role of sensory and metabolic signals in the control of food intake. The problem can be defined by perusing FIGURE 1, which presents a simplified version of a previously published schema outlining the control of intake in flow chart form (Jacobs, 1962). The initial conditions assume an animal already eating food. We shall not be concerned with the particular causes initiating the meal. Starting with the top of the FIGURE 1, then, we may ask classical question of physiologists analyzing intake regulation: What does the diet contain that can act as a signal to monitor subsequent intake? This signal can increase intake in a short-term positive feedback loop, as seen in the lower right side of the Figure, or decrease it in a negative feedback loop. The latter case we have called satiety. The two classes of physicochemical stimuli which interest us are labeled calories and taste. Both sets of signals are initiated in specialized receptor systems and relayed to the central nervous system (CNS) by nervous and/or humoral paths. It should be pointed out that our choice of the terms, taste and calories, is an oversimplification of the actual situation, which is at least hinted at in FIGURE 2. This diagram shows the same system, with the physicochemical stimuli expanded. What we have called calories are in fact only one of a large number of potential metabolic signals, and taste, only one of a number of potential seniory signals. The metabolic class includes all of the classical factors that physiologists have implicated in food intake. When a single factor is singled out and perhaps overemphasized, we have a “theory” of intake, as in the classical glucostatic and thermostatic hypotheses. Some would also consider a lipostatic or perhaps an “aminostatic” theory as well. Most people working in this area now accept Edward Adolph’s dictum that food intake is under multiple factor control, and that some combination of all of the metabolic signals is involved. The sensory category summarizes the classes of stimuli contained in food which have been of interest to the sensory psychologist, but which, for the most part, have been ignored by the regulatory physiologist. FIGURE 2 suggests many interesting problems, e.g. which receptor system responds to which classes of stimuli? Where are the latter located? Are they independent? For the purpose of this discussion, we can ignore these complexities. Returning to the simpler case (FIGURE 1 ) , we can now point out that the terms,

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Papers

Regulation of food intake in normal rats and in rats with hypothalamic hyperphagia.