This study was performed on healthy non-obese subjects to verify the effect of a 300 ml non-caloric, commercial carbonated or de-gassed beverage, on satiety compared to water. The main methodological interest of this article is the contemporary evaluation of satiety, gastric volume by means of a non-invasive method, and some gastrointestinal hormones involved in food intake control. Mainly, we found a clear increase in gastric volume immediately after the consumption of a carbonated beverage without any influence whatsoever on food intake. Therefore, in a normal subject, carbon dioxide at its maximum concentration (3.7 volume) contained in a 300 ml beverage consumed 3 min prior to the meal did not seems to influence satiety or food intake compared to the consumption of still water or the same beverage without carbon dioxide. This study also showed that a carbonated beverage does not modify the quantity of solid or liquid food consumed. In short, the intake of a solid meal remains unaltered if the subject, prior to consuming such food, drinks the same quantity of water, carbonated or de-gassed beverage. The same occurs with a liquid meal. However, some slight differences were found in hormone kinetics, likely related to both meal consistency and beverage carbonation.
The increased gastric volume following carbonated beverage consumption found in our study was a predictable result, yet the lack of any influence on food intake following the consumption of a carbonated beverage is intriguing. The process that limits meal size derives from a coordinated series of neural and humoral signals that originate from the gut in response to the mechanical and chemical properties of the food ingested . Among these factors, a mechanical distension has been described as a relevant aspect [25, 26]. In our study, the increase in gastric volume following the consumption of a carbonated beverage appeared to be related to the gas content of the beverage. However, we observed a similar increase in gastric volume after carbonated beverage consumption and at maximum satiety with respects to the basal value (~500 ml). These data suggest a different hypothesis to explain the lack of satiety following the consumption of the carbonated beverage. Firstly, the duration of gastric distension due to carbon dioxide can be very short due to either the absorption of gas by the gastric wall or its rapid elimination by eructation. Moreover, the absence of nutrients in the non-caloric beverage could explain the lack of other factors (i.e. hormone release) involved in satiety .
The level of beverage carbonation was shown to affect food intake only with consumptions exceeding 300 ml. Moorhead et al compared the effects of identical sugar-sweetened beverages (400 ml; 639 kJ), with three levels of carbonation, consumed 10 min before an ad libitum lunch. These results showed that the beverages with higher carbonation led to higher satiety until lunch and lower energy intakes at lunch . These authors concluded that the level of carbonation affects satiety and subsequent intakes in the short term, and speculated that this may be due to effects on gastric distension. In our study we used a 300 ml non-caloric pre-meal beverage with 3.7 volume of carbon dioxide and did not find any interference with the intake of a meal consumed at a constant rate.
We also found earlier satiety during consumption of a liquid meal compared to a solid meal, regardless of the beverage administered. The two meals (solid and liquid) were isocaloric but the liquid meal had a slightly increased fat content while the solid one had a higher protein content usually considered to be more satiating than fat [27, 28]. Therefore it is likely that the satiating effect observed may be mainly due to meal consistency or meal volume rather to its nutrient content. Our results showed that gastric volumes at maximum satiety were similar for both the solid and the liquid meals. Therefore, the consistency of the meal and particularly its viscosity can be a relevant cause that triggered satiety .
The gastric regional meal distribution showed that the relevant effect on gastric distension seemed to affect the proximal gastric region. However, distal volume at maximum satiety decreased during the liquid meal compared to the solid one. This finding can explain some differences in food intake between solid and liquid meals, and supports the hypothesis of a different physical gastric distribution or an increased gastric emptying rate of a liquid compared to a solid meal, without any influence related to beverage type.
The analysis of hormone kinetics showed a decrease in ghrelin expressed as area under the curve during the liquid meal compared to the solid one after all beverage consumption. Our results support the hypothesis that, apart from a more rapid gastric emptying, also an increased interaction of nutrients with the taste receptors of ghrelin cells is able to limit liquid food intake . Moreover, by analyzing the effect of the beverages, we observed that water and non-caloric carbonated beverage pre-load administered before a solid meal determined a significant decrease in ghrelin compared to a de-gassed beverage. Therefore, a sweetened non-caloric and de-gassed beverage determined a significantly lower meal-induced ghrelin decrease compared to water. The carbonation of the non-caloric beverage was able to amplify ghrelin decrease until the level determined by the water pre-load was reached. A similar, yet non significant effect was observed during the consumption of the liquid meal.
Ghrelin levels increase with fasting and decrease after meals . In addition to fasting, ghrelin expression can be stimulated in rats by means of insulin-induced hypoglycemia , and some observations indicate a direct inhibitory effect of glucose on ghrelin-containing cells in the oxyntic mucosa . On the basis of these concepts and considering that, in our experiments, glucose levels (data not shown) were similar in all beverages and meals, we can speculate that the sweeteners (aspartame and acesulfame K) were able to decrease the effect of nutrients on the cells containing ghrelin, by means of a receptor-competition mechanism [33–35]. Carbonated beverages seem to determine a more significant negative feedback relating to ghrelin secretion. This effect appeared more evident during the solid meal compared to the liquid one. Also, we can speculate that the presence of carbon dioxide in the beverage, with a consequently increased acidity [15, 36], was able to improve the interaction between glucose or sweeteners and ghrelin cell. Moreover, the sour sensing taste receptors present in the stomach could possibly mediate the effect on ghrelin release. Both carbonated drinks and acids can interact via carbonic anhydrase with a member of the transient receptor potential (TRP) ion channel family PKD2L1 (poly kidney disease-2-like 1) [15, 36]. However, despite the difference found in our results, no effect on amount of food intake was observed. Perhaps, other conditions, such as increased beverage volume or meal quality, could modify food intake by means of carbonated and de-gassed non-caloric beverages, by amplifying the effect on ghrelin secretion.