The present study demonstrates that experimental animals exposed to caloric soft drinks and/or ultra-processed food consumption (cafeteria diet) developed hyperphagia and significant changes in normal feeding patterns. These affirmations are made based on the results showing that exposure to caloric soft drinks decreases chow intake by 30%. This decrease in the consumption of standard chow was even more drastic when a caloric soft drink was offered in association with the cafeteria diet, leading to a drastic reduction (90%) in the consumption of standard feed. The caloric soft drink consumption was greater than the non-caloric soft drink intake regardless of its exposure alone (68% increase) or in conjunction with a cafeteria diet (38% increase). The chow intake of animals exposed to non-caloric soft drinks did not decrease compared to the control group, reflecting lower total energy consumption in non-caloric soft drinks compared to caloric soft drinks. However, the cafeteria diet was responsible for an increase in energy intake from solid foods. It was 32% more in CD than in CON, 24% more in CD + CS than in CS, and 34% more in CD + NCS than in NCS. These results demonstrated that the animals replaced the standard chow with caloric soft drinks and/or ultra-processed foods. Over the past few years, this concern has grown and motivated other studies that have shown similar results [26–29].
The higher caloric soft drink intake of the CS group resulted in an increase of 33% in carbohydrate consumption in the CON group, while the lipid and protein consumption was lower than that in the CON and NCS groups. However, the intake of non-caloric soda did not significantly alter the total solid foods and energy consumption, body weight gain, and liposomal index when compared to the CON group. Owing to the greater consumption of soft drinks, the animals in the CS and NCS groups, which received only standard feed as solid food, consumed less water than CON. Water was replaced by caloric soda as it has a high content of sucrose (a simple carbohydrate) and is highly palatable. This is considered one of the main contributors to the increase in the number of overweight and obese people [3, 29, 30] and abdominal adiposity . Similar results were found in another study by our group, which analyzed the effects of caloric and non-caloric soft drink consumption during 17 weeks of treatment in rats . A study on the food consumption in the Brazilian population, through a telephone survey, identified an increase in caloric soft drink consumption from 60% in 2007 to 67% in 2009 .
The dopaminergic system (reward system) may be involved in the increase in soda consumption, which in turn induces gastric distension and decreases the standard feed intake. The reward system is complex and comprises several phases. In the anticipatory phase, expectations are created regarding food/sucrose, followed by the acquisition phase with decision-making assessing the benefit-risk, followed by consumption. In this phase, positive feedback is generated through sensory analysis in the first contact with food, thus increasing motivation and appetite. Finally, the post-consumption phase runs until the beginning of the next cycle . When palatable foods such as those rich in sucrose are consumed, there is an increase in dopamine release in the nucleus accumbens, which stimulates food preference and increases sucrose intake, playing these roles in the preparatory and food consumption phases . It is important to note that the reward mechanism involved in the intake of palatable food (such as sucrose) is not only related to the nucleus accumbens, but other structures such as the dorsal striatum and the orbitofrontal cortex are also strongly involved . Taste receptors found in the oral cavity can also be expressed in epithelial cells of the intestine and hypothalamus. The feeling of satisfaction when eating palatable food, instead of generating acute pleasure, lasts for some time, which most likely contributes to the desire to eat again . Another factor that seems to contribute to reward generation during and after a meal is the action of nutrient sensors in the gastrointestinal tract [9, 35].
A previous clinical study showed that the consumption of ultra-processed foods led to an increase in carbohydrate and fat intake and a reduction in protein consumption, resulting in an increase in the weight of the participants . A Brazilian study identified that the prevalence of obesity in 2019 exceeded twice the values registered in 2002-2003, among both men (from 9.6% to 22.8%) and women (from 14.5% to 30.2%). Obese people represent more than a third of the total overweight men and almost half of the overweight women .
The caloric soda intake and the consequent decrease in solid food consumption can be explained by the high palatability and satiety provided by caloric soda. Postprandial hyperglycemia activates satiety nuclei in the ventromedial hypothalamus, which inhibits the nucleus related to the feeding of the lateral hypothalamus and induces food intake suppression, which is known as the hunger glycostatic theory . The caloric soda consumption amount in the CS group was higher than that in CD + CS group because the latter, in addition to receiving caloric soda, received solid palatable food in the cafeteria diet.
The total solid food intake was similar for the groups that received the cafeteria diet, but higher than the CON, CS, and NCS groups in detriment of the standard feed consumption, demonstrating the high intake of the cafeteria diet. This resulted in high lipid and low protein consumption, leading to a 450% increase in the lipid consumption and a 50% reduction in the protein intake. The high palatability of the cafeteria diet contributes to increased energy consumption, triggering an increase in body fat, and consequent obesity in animal models [19, 27, 39–41] and in humans . Our study showed a significant increase in the weight of animals receiving a cafeteria diet. These animals showed a 60% increase in body weight compared to animals in the control group, increased body fat, triglyceride, and leptin levels. Likewise, it was observed by another study carried out with Wistar rats fed a high-fat diet . Thus, this diet increased the metabolic risk, as was observed, demonstrating HOMA changes. It should be noted that soft drink consumption can decrease adherence to healthy diets by decreasing the intake of nutrients such as fibers and micronutrients (e.g., folic acid and calcium) among children and young people [26, 44, 45].
The carbohydrate and nitrogen balance is facilitated by the body's ability to adjust the glucose and amino acid oxidation rates, respectively, in relation to food consumption. In the case of fats, however, the increase in consumption is not oxidized to the same extent. Approximately 96% of the lipids ingested in the diet induce a positive lipid balance and are stored as body fat [46, 47]. Another important result of our study is related to the increase in sodium levels among animals consuming the cafeteria diet. This result was expected because processed foods are rich in sodium content.
The use of drinks sweetened with ingredients that do not provide calories is controversial according to some authors. This study found that despite having solid food consumption and total energy like those in the CD and CD + CS groups, the CD + NCS group had a significantly lower LI, demonstrating less visceral fat deposition. The results of this study were different from those obtained by some other studies which identified that artificial sweeteners caused an increase in body weight in the group that received sucrose, but the total energy consumption was not significantly different [48, 49]. However, a study carried out in Denmark observed an increase in weight and body fat in individuals who received drinks and foods sweetened with sucrose, and there was a reduction in body weight and body fat in individuals who received drinks and foods sweetened with artificial sweeteners . Similarly, another research found less weight gain in rats that received cola drinks and a high-fat diet as compared to controls who received the same diet but drank water for 28 weeks. The lower weight gain was attributed to the possible increase in muscle thermogenesis induced by caffeine in cola soft drinks . Other studies have also shown beneficial effects of caffeine on the adiposity of animals fed high-fat diets, demonstrating a reduction in body fat mass and percentage of body fat, possibly due to increased lipolysis via catecholamines [52, 53]. The lower LI in the CD + NCS group may be related to the lower insulinogenic effect of the non-caloric soda due to the greater presence of caffeine in the drink and the 17% reduction in carbohydrates compared to the CD + CS group. Caffeine generates a lipolytic effect by stimulating the release of adrenaline by the adrenal glands, thereby reducing lipogenesis [54, 55]. Another study demonstrated beneficial effects of caffeine consumption on health and a negative association with the incidence of DM2, as well as in helping control body weight .
This result suggests that the consumption of caffeine present in non-caloric cola-type soda may help prevent obesity, which is related to the absence of sucrose and caffeine content. However, further studies are needed on the effects of consuming caloric and non-caloric soda with a cafeteria diet on metabolism. It is also necessary to compare the effect of sugary drink intake with that of artificially sweetened, caffeine-free drinks associated with a cafeteria diet.
Strength and Limits
The strengths of this study are the significant changes in normal feeding patterns due to the consumption of caloric soft drink and ultra-processed foods (cafeteria diet). Due to its high palatability, the cafeteria diet caused hyperphagia, increased lipid consumption (450%), decreased protein intake (50%), resulting in a 60% increase in body weight. On the other hand, the non-caloric soft drink reduced the visceral fat, suggesting its use in obesity prevention. As a limitation of the study, we cannot affirm for sure that the non-caloric soda caffeine was responsible for the visceral fat reduction in animals. Therefore, specific studies are necessary to compare the sugary caffeine-free soft drink intake effect with that artificially sweetened caffeine-free soda, associated with a cafeteria diet.
What is already known on this subject?
Previous clinical and animal studies showed that ultra-processed food consumption led to an increase in carbohydrate and fat intake and a reduction in protein consumption, increasing the bodyweight of the individuals. But the effect of the association of caloric and non-caloric soft drink intake with ultra-processed and highly palatable food on the eating behavior and metabolic parameters was still to be assessed.
What your study adds?
The study demonstrated a great increase in caloric soft drink consumption concerning the non-caloric soft drink, showed that the caloric soda intake had a negative influence on the standard food (healthy food) consumption, while the non-caloric soda intake did not interfere. It was not yet known that the non-caloric soft drink intake doesn't have the same effect on visceral fat deposition compared to the caloric soft drink consumption in rats fed a cafeteria diet.