Obesity and its metabolic sequelae still comprise a challenge when it comes to understanding mechanisms, which drive these pandemic diseases. The human microbiome as a potential key player has attracted the attention of broader research for the past decade. Most of it focused on the gut microbiome while the oral microbiome has received less attention. As the second largest niche, the oral microbiome is associated with a multitude of mechanisms, which are potentially involved in the complex etiology of obesity and associated metabolic diseases. These mechanisms include local effects of oral bacteria on taste perception and subsequent food preference as well as systemic effects on adipose tissue function, the gut microbiome and systemic inflammation. This review summarizes a growing body of research, pointing towards a more prominent role of the oral microbiome in obesity and associated metabolic diseases than expected. Ultimately, our knowledge on the oral microbiome may support the development of new patient oriented therapeutic approaches inevitable to relieve the health burden of metabolic diseases and to reach long-term benefits in patients´ lives.

Fibroblast growth factor 21 (FGF21) is a regulator of addictive behavior. Increasing evidence suggests an impact of FGF21 on eating behavior, food and drug cravings and on other adipokines like insulin-like growth factor 1 (IGF-1) or adiponectin. We investigated the association of serum FGF21 and genetic variants with aspects of food and drug craving and obesity related metabolic parameters including serum adipokine levels. Standardized questionnaires, blood samples and anthropometric data of the Sorbs cohort (n = 1046) were analyzed using SPSS. For genetic analyses, the FGF21-locus ±10 kb was genotyped and analyzed using PLINK. Validation was conducted in a second independent cohort (n = 704). FGF21 was significantly associated with alcohol and coffee consumption, smoking and eating behavior (disinhibition). We confirmed correlations of FGF21 serum levels with IGF-1, adiponectin, pro-enkephalin, adipocyte fatty-acid-binding protein, chemerin and progranulin. FGF21 genetic variants were associated with anthropometric and metabolic parameters, adipokines, food and drug craving while strongest evidence was seen with low-density lipoprotein cholesterol (LDL-C). We highlight the potential role of FGF21 in food and drug cravings and provide new insights regarding the link of FGF21 with other adipokines as well as with metabolic traits, in particular those related to lipid metabolism (LDL-C).

Sweet and salty tastes are highly palatable and drive food consumption and potentially uncontrolled eating, but it remains unresolved whether the ability to recognize sweet and salty affects food reward and uncontrolled eating. We investigate the association of sweet and salty taste recognition with liking and wanting and uncontrolled eating. Thirty-eight, mainly female (68%) participants of the Obese Taste Bud study, between 22 and 67 years old, with a median BMI of 25.74 kg/m² (interquartile range: 9.78 kg/m²) completed a taste test, the Leeds Food Preference Questionnaire to assess food reward, the Power of Food Scale (PFS) and the Three-Factor Eating Questionnaire to assess different aspects of uncontrolled eating. Better salty taste recognition predicted greater implicit wanting for high-fat savory foods (β = 0.428, p = 0.008) and higher PFS total (β = 0.315; p = 0.004) and PFS present subscale scores (β = 0.494, p = 0.002). While neither sweet nor salty taste recognition differed between lean individuals and individuals with obesity, those with greater trait uncontrolled eating showed significantly better salty taste recognition (U = 249.0; p = 0.009). Sweet taste recognition did not associate with food reward or uncontrolled eating. Better salty but not sweet taste recognition associates with a greater motivation for, but not liking of, particularly savory high-fat foods and further relates to greater loss of control over eating. Salty taste perception, with taste recognition in particular, may comprise a target to modulate food reward and uncontrolled eating.

Background and aims: Saliva is essential for the proper dilution and distribution of taste molecules on the tongue. It harbors extracellular vesicles (EVs), which mediate cell–cell communication. Changes in the composition of salivary EVs may arise under obese conditions and may potentially be involved in taste sensation and dysregulated eating behavior. Therefore, this study addresses the relationship between the size and concentration of salivary EVs and metabolic shifts in obesity or factors of taste sensation. Materials and methods: A total of 119 participants in the Obese Taste Bud (OTB) Study were included, who performed a standardized taste test, underwent taste bud density assessment, and were phenotypically characterized for anthropometrics, blood- and saliva adipokine levels, and various metabolic factors. Utilizing size exclusion chromatography followed by ultrafiltration, EVs were extracted from 2 mL of actively secreted saliva. EVs were characterized using nanoparticle tracking analyses, Western blot, and scanning transmission electron microscopy. Finally, group comparisons and bivariate correlation analyses were conducted. Results: Among the total cohort, the median size of salivary EVs was 190.05 nm, and the overall concentration ranged from 1.4 × 10⁷ to 1.76 × 10⁹ per mL of saliva. The size range and concentration of EVs per mL are negatively correlated (p = 0.0002, r = −0.264). Comparing lean participants (mean rank of 45.98) with those presenting obesity (mean rank of 34.46), a significant difference in the salivary EV content was observed (p = 0.029). Body weight, BMI, arm and calf circumferences, as well as the percentage of body fat were all negatively related to the concentration of EVs in all study participants (all p < 0.05, r > −0.2). No associations were found between the EV parameters and taste perception but serum alkaline phosphatase levels were negatively correlated (p = 0.007, r = −0.284) and adiponectin serum levels were positively correlated to the EV concentration (p = 0.036, r = 0.208). Conclusion: The current study provides evidence for the relation between salivary EVs and anthropometric as well as metabolic parameters of obesity. This can provide the basis for further research on the cargo of salivary EVs and how they may influence taste sensation, and may elucidate their potential connection to altered eating habits in obesity.

Extracellular vesicles (EVs), conveyors of microRNAs, have recently been linked to obesity. As taste is a potent driver of eating behaviour and food intake, it's connection to EVs is of increasing interest. This study aimed at deciphering the salivary EV-microRNA profile in relation to taste perception and metabolic pathways of obesity. Small RNA sequencing was performed on isolated salivary EVs of 90 participants from the Obese-Taste-Bud study. Pathway enrichment and association analyses were conducted to link identified microRNAs to taste recognition, eating behaviour, food intake and various anthropometric-, metabolic- and oral health parameter. The 626 identified microRNAs clustered into pathways related to energy regulation, obesity and diabetes, cell signaling and taste perception. The top three enriched microRNAs are miR-1246, miR-1290 and miR-148a-3p which showed significant associations with fasting blood glucose and cholesterol level, anthropometrics and blood pressure (p < 0.05). Additionally, these microRNAs associate with trait eating behaviour (p < 0.05). Several other microRNAs were linked to differences in taste recognition scores and are further related to parameters of glucose metabolism and periodontal health, salivary insulin level or food intake (p < 0.05). This study, one of the largest on salivary EVs, supports an interrelation of EV's microRNA load with metabolism, eating behaviour and taste recognition offering potential targets for obesity intervention.