The study explores the complex relationship between gustation, specifically sweet taste, and its influence on food intake, satiety, and energy balance. While sweet taste is a powerful driver of food choice, its precise mechanistic role remains unclear. Existing research presents conflicting findings on the correlation between sweet taste sensitivity and preference, with some studies indicating a negative correlation and others a positive one. Despite these inconsistencies, a strong association between sweet liking and weight gain is often assumed. The global rise in obesity, paralleled by increased sugar consumption, particularly in sugar-sweetened beverages, has highlighted the need for a better understanding of how sugar and its perception contribute to energy imbalance. The use of high-intensity sweeteners as a strategy to reduce caloric intake while maintaining sweetness has also introduced controversies. There is ongoing debate about their metabolic effects and the potential role of both caloric and non-caloric sweeteners in modulating cephalic phase insulin release (CIPR). The discovery of extraoral sweet taste receptors in the gastrointestinal tract has further complicated the picture, leading to discussions about the receptor's involvement in nutrient sensing and the body's physiological responses to sweeteners. Previous studies from the authors’ group and others highlight the complex interplay between carbohydrate type, perceived sweetness, and metabolic responses. While the role of sweet taste receptor activation in metabolic regulation is increasingly studied, the impact of individual sweet taste perception and sensitivity remains under-investigated. The study aims to clarify the influence of varying sweetness levels of isocaloric sucrose solutions on glucose regulation and energy intake, taking into account individual sweet taste sensitivity thresholds.

The literature review summarizes existing research on the connection between sweet taste, food intake, and metabolic health. Studies have shown conflicting results regarding the correlation between sweet taste sensitivity and preference. While some studies suggest that higher sensitivity leads to decreased preference for sweet tastes, others find a positive association. The global increase in sugar consumption and obesity rates highlights the importance of understanding the impact of sugars on weight gain, though meta-analyses show inconsistent evidence of simple sugars' specific role in this. Sugar-sweetened beverages, however, are linked to poor satiety and energy compensation. High-intensity sweeteners are presented as a potential alternative, but their metabolic effects remain controversial, with some studies indicating potential negative effects on metabolic health despite their reduced caloric content. The presence of sweet taste receptors outside the oral cavity raises questions about the role of these receptors in nutrient sensing. Research involving sweet taste receptor activation and the regulation of satiety hormones like serotonin, GLP-1, and PYY adds complexity to this interplay. Studies on the impact of sweet taste thresholds on blood glucose levels and potential associations with diabetes have also yielded conflicting results. Ultimately, the literature indicates a need for further investigation into the role of individual sweet taste perception and its interaction with metabolic processes.

This study employed a single-blinded, randomized, crossover design. 29 healthy young men participated, undergoing four treatments on separate days, each at least 7 days apart. Participants underwent a medical screening including an oral glucose tolerance test (oGTT) and assessment of anthropometric data such as body composition using a Bod Pod. A SCOFF questionnaire screened for eating disorders. Four isocaloric 10% sucrose solutions were prepared: a control (sucrose only), a high-sweetness solution (sucrose + RebM), an equi-sweetness solution (sucrose + RebM + lactisole), and a low-sweetness solution (sucrose + lactisole). Before each treatment, participants rated their hunger on a VAS scale. They consumed 300ml of the assigned solution and provided blood samples at intervals (0, 15, 30, 60, 90, and 120 min). Postprandial glucose, insulin, glucagon, GLP-1, GIP, and serotonin levels were measured. Participants also rated the sweetness of the solution on a VAS scale. Two hours after the solution, a standardized breakfast was provided, and remaining food was weighed to assess energy intake. Sucrose detection thresholds were established for each participant before the study. A food frequency questionnaire (FFQ) and a liking questionnaire assessed dietary habits and preferences toward sweet foods. Statistical analyses employed robust two-way ANOVA for medians and post-hoc comparisons. Incremental area under the curve (AUC) was used for analysis of time-dependent hormone regulation data.

The study's key findings demonstrate that manipulating the sweetness intensity of isocaloric sucrose solutions did not significantly alter hunger, energy intake, or blood glucose and related hormone responses (glucose, insulin, glucagon, GLP-1, GIP, serotonin) in healthy males. Participants' subjective feelings of hunger did not correlate with sweetness perceptions across treatments. While total energy intake did not vary significantly across treatments, individuals with higher sucrose detection thresholds (those less sensitive to sweetness) consumed significantly more energy (402 ± 78.8 kcal, 39 ± 21%) compared to participants with lower thresholds. The high threshold group exhibited a higher glucose/insulin ratio, suggesting improved post-prandial glucose response. This group also had a trend towards higher fat-free mass, potentially contributing to the observed difference in energy intake. Although there was no overall treatment difference in incretin hormones (GLP-1, GIP), the low-threshold group had higher GIP levels. No significant difference in leptin levels was observed between threshold groups. Participants with higher sucrose thresholds demonstrated a poorer discrimination of sweetness levels in sensory evaluations. The high-threshold group reported a significantly higher liking for sweet-tasting foods despite not showing differences in consumption patterns compared to the low-threshold group.

The study's findings challenge the initial hypothesis that sweetness intensity directly impacts energy intake and glucose regulation. While no significant effect of sweetness modulation was found, the results suggest that individual sucrose detection threshold may be a more critical factor influencing energy intake and metabolic response. The higher energy intake observed in the high-threshold group, coupled with their improved glucose/insulin ratio, indicates a potential link between sucrose detection threshold, metabolic efficiency, and food intake. The observed difference in fat-free mass between groups may confound the interpretation of these results, as higher fat-free mass is associated with higher resting metabolic rate and energy intake. The higher liking for sweet foods among participants with higher sucrose detection thresholds provides further context to the findings, hinting at a possible interplay between taste sensitivity, preference, and dietary behavior. The lack of significant differences in satiety hormones like GLP-1 and glucagon across treatments may imply a minor role for sweetness perception in their regulation compared to the amount of ingested carbohydrate. The study highlights the complex relationship between individual taste perception, metabolic responses, and body composition.

The study demonstrated that manipulating the sweetness of isocaloric sucrose solutions had no significant effect on postprandial energy intake or blood glucose regulation. However, individuals with higher sucrose detection thresholds consumed more energy and had a more favorable glucose response. This suggests that individual taste sensitivity might play a greater role than perceived sweetness intensity. The study's limitations should be considered in future studies to establish causality and to investigate the influence of other factors such as physical activity on sweet taste sensitivity and preference.

The study’s limitations include the exclusion of female participants due to potential hormonal fluctuations, the lack of detailed physical activity data, and the focus on healthy volunteers, limiting generalizability to individuals with impaired glucose tolerance. The relatively small sample size may also influence the statistical power to detect certain effects. Future studies should address these limitations to enhance understanding of the complex interplay between sweet taste perception, body composition, and metabolic health.