Abstract
Aims
This cross‐sectional study examined associations between self‐reported taste perception changes and appetite‐related outcomes in individuals with obesity treated with glucagon‐like peptide‐1 receptor agonist (GLP‐1 RAS) or dual glucose‐dependent insulinotropic polypeptide (GIP)/GLP‐1 RAS in real‐world conditions.
Materials and Methods
Four hundred and eleven adults on Wegovy® (n = 217), Ozempic® (n = 148) and Mounjaro® (n = 46) completed an online survey assessing sociodemographic, anthropometric and sensory changes and appetite‐related outcomes. Multivariable logistic regression was used to assess associations between taste changes and satiety, appetite and craving.
Results
Participants (69.6% female; median age 39 [interquartile range, IQR 33–47]) had baseline body mass index (BMI) of 35.6 (Wegovy®), 34.7 (Ozempic®) and 36.2 kg/m2 (Mounjaro®). Adjusted models for baseline BMI, treatment duration, dose, age and sex showed significant reductions in BMI of 17.6% (95% CI: 15.7–19.5) for Wegovy®, 17.4% (15.0–19.8) for Ozempic® and 15.5% (8.8–22.2) for Mounjaro®. Reduced appetite was reported by 58.4% of participants (Wegovy®: 54.4%, Ozempic®: 62.1%, Mounjaro®: 56.5%) and increased satiety by 63.5% (Wegovy®: 66.8%, Ozempic®: 58.8%, Mounjaro®: 63.1%). Additionally, 21.3% reported increased sweet taste perception and 22.6% reported increased salty taste perception. Independent of the type of therapy, increased sweet taste perception was significantly associated with increased satiety (adjusted odds ratios [AOR] = 2.02; 95% CI: 1.15–4.57), decreased appetite (AOR = 1.67; 95% CI: 1.04–3.25) and decreased craving (AOR = 1.85; 95% CI: 1.05–3.29). Increased salty taste perception was associated with increased satiety (AOR = 2.17; 95% CI: 1.16–5.17; all p < 0.05).
Conclusions
Self‐reported changes in taste perception during GLP‐1 or dual GIP/GLP‐1 RAS therapy were associated with favourable appetite‐related outcomes, suggesting a potential mechanism contributing to treatment response.
Keywords: appetite regulation, incretin‐based therapy, obesity treatment, observational study, weight management
1. INTRODUCTION
Globally, obesity is a growing health burden that exerts considerable strain on healthcare systems. Current estimates suggest that 2.1 billion adults are affected by overweight or obesity worldwide. 1 Obesity is a complex, multifactorial disease with genetic, behavioural, socioeconomic and environmental origins, leading to increased risk of both morbidity and mortality. 2 Pharmacological interventions have emerged as promising strategies to support weight management in individuals with obesity, particularly through appetite regulation. 3 Semaglutide, a glucagon‐like peptide‐1 (GLP‐1) receptor agonist (GLP‐1 RAS), has been shown to reduce body weight by approximately 15% compared to placebo over a treatment period of 68 weeks. 4 It also improves appetite control, reduces cravings for salty foods and improves overall craving regulation. 5 Beyond GLP‐1 RAS, dual‐acting therapies have gained attention for their potential to further improve weight loss outcomes. Tirzepatide, a dual glucose‐dependent insulinotropic polypeptide (GIP) and GLP‐1 receptor agonist, has been shown to result in greater weight loss than GLP‐1 receptor agonists such as semaglutide and liraglutide, particularly at higher doses. 6 , 7
GLP‐1 exerts pleiotropic effects and functions beyond its role as an incretin hormone; GLP‐1 receptors have been identified in several organ systems outside the gastrointestinal tract, including the heart, kidney and central nervous system, suggesting a broader physiological impact. 8 The effectiveness of pharmacological interventions can be explained by their action on brain regions associated with appetite and food perception. 9 GLP‐1 RAS influence food intake by targeting receptors located in multiple brain areas involved in taste perception, olfaction and reward processing. These include the ventromedial and dorsomedial hypothalamus, amygdala, insula, putamen, caudate nucleus and orbitofrontal cortex. 10 Neural signals from the gustatory cortex are processed in the limbic system, where their hedonic value is evaluated, suggesting that GLP‐1 RAS play a crucial role in reward‐based food preferences. 11 GLP‐1 is endogenously produced by distinct neuronal populations within the nucleus of the solitary tract the primary brainstem relay centre for taste signal processing. In addition, GLP‐1 is expressed in specialized taste bud cells on the tongue, where it may modulate taste signalling through interactions with adjacent sensory nerve fibres. 12 Studies investigating the effects of GLP‐1 RAS on taste perception have yielded contrasting results. A recent randomized, placebo‐controlled trial in woman with obesity showed improved taste sensitivity, significant changes in the tongue‐specific transcriptome and increased neural activation in the angular gyrus in response to sweet stimuli. 13 In contrast, another study using a comprehensive psychophysical battery (WETT®) found an objective reduction in taste function in GLP‐1 RAS users. 14 Notwithstanding, these findings suggest that GLP‐1 RAS influence eating behaviour through both central satiety pathways and peripheral modulation of taste signals. Building on these findings and the diverse, at times conflicting, results in the literature, our study pursued two main objectives: (1) to examine whether and to what extent self‐reported changes in taste perception are associated with appetite‐related parameters satiety, appetite and food craving in adults with obesity or overweight and weight‐related comorbidities; and (2) to assess group differences in subjective taste perception, appetite regulation and BMI reduction across three commonly prescribed incretin‐based therapies. By investigating the role of taste modulation within this context, our study may provide novel insights into the mechanisms underlying the efficacy of GLP‐1 and dual GIP/GLP‐1 receptor agonists, thereby supporting the development of more personalized therapeutic strategies in obesity care.
2. METHODS
2.1. Study design and setting
This study is based on a cross‐sectional survey design. A questionnaire was developed and distributed between 13 January and 28 February 2025 via various social media platforms such as Facebook®, Instagram®, X® and WhatsApp®. Specifically, we targeted online communities and support groups dedicated to GLP‐1 or dual GIP/GLP‐1 RAS users. The administrators of these groups were contacted in advance to request permission to share the survey. Upon approval, the survey link was promoted directly on the respective group pages or channels, allowing members to participate voluntarily. In total, these GLP‐1 and GIP/GLP‐1 RAS‐focused online communities comprise more than 400 000 members; however, it should be noted that some individuals may have been members of multiple groups, and not all members may have been actively using these medications.
Ethical approval was obtained from the Ethics Committee of the Medical University of Vienna (approval number 2506/2024). Participation required explicit consent, which was provided by selecting the ‘Agree’ option, confirming both understanding of the participant information sheet and fulfilment of inclusion criteria. Participants were informed that they could withdraw at any time during completion of the questionnaire and that their data would be used exclusively for research purposes.
2.2. Eligibility criteria
The inclusion and exclusion criteria were clearly communicated in all recruitment materials (e.g., online support group postings). These criteria were explicitly confirmed by participants at the beginning of the questionnaire. The survey employed filter logic that automatically excluded respondents who did not meet the eligibility requirements. Incomplete responses were also excluded from the final analyses.
Our study included adults aged 18 years or older with obesity, defined as an initial body mass index (BMI) of ≥30 kg/m2 or BMI ≥27 kg/m2 to <30 kg/m2 with at least one weight‐related comorbidity. These comorbidities included dysglycaemia (prediabetes or type 2 diabetes mellitus), hypertension, dyslipidaemia, obstructive sleep apnoea or cardiovascular disease. All participants were required to be actively receiving treatment with a GLP‐1 or dual GIP/GLP‐1 receptor agonist at the time of survey participation, and to have been on therapy for at least three consecutive months. Furthermore, participants needed to be able to understand and complete the online questionnaire in English and have the capacity to provide informed consent.
2.3. Questionnaire content and structure
The publicly accessible online questionnaire was designed using ‘SoSci Survey’ (https://www.soscisurvey.de) in accordance with the Checklist for Reporting Results of Internet E‐Surveys (CHERRIES) guidelines. 15
To assess treatment‐related changes, we developed structured single items with Likert‐type response formats, each explicitly referring to subjective changes since the initiation of incretin therapy (e.g., ‘Since starting incretin therapy, how has your sense of taste changed?’). This approach was chosen because, to our knowledge, no validated self‐report instruments are currently available that specifically assess perceived within‐person changes in appetite, craving, satiety or taste perception in the context of pharmacological interventions, especially within a cross‐sectional design. Therefore, a comprehensive questionnaire was developed to collect a wide range of variables to examine the effects of GLP‐1 and dual GIP/GLP‐1 RAS therapy in a differentiated and patient‐centred manner.
Sociodemographic and lifestyle factors: Age, sex, education level, marital status, occupation and income, as well as lifestyle‐related variables such as frequency of alcohol and cigarette consumption, dietary habits and changes in physical activity (measured as moderate‐to‐vigorous physical activity per week since initiation of GIP/GLP‐1 therapy).
Anthropometric measurements and clinical parameters: We collected self‐reported data on height and weight before and during treatment. We used these values to calculate body mass index (BMI) for both time points. Participants were also asked to report the number of concomitant medications they were taking.
Medical history: Participants were asked to report existing medical conditions using a structured list of common obesity‐related comorbidities. These included type 2 diabetes, hypertension, sleep apnoea, dyslipidaemia, non‐alcoholic fatty liver disease, knee osteoarthritis, stroke and cardiovascular disease. Additionally, participants had the option to enter other diagnoses in a free‐text field.
Therapy‐specific information: Details of the incretin medication used, dosage, duration of treatment and the occurrence and type of side effects (e.g., nausea, vomiting, diarrhoea, headache). In addition, we asked participants whether they had noticed any change in their nicotine consumption (e.g., cigarettes, e‐cigarettes, nicotine replacement therapy) since starting the GLP‐1 and dual GIP/GLP‐1 RAS therapy.
Additionally, data on behavioural and sensory variables were collected, covering the following aspects:
Eating behaviour and appetite: Changes in appetite between meals, the intensity of hunger and the extent of food craving.
Satiety: Changes in the perception of satiety, specifically whether and how the feeling of fullness related to meals has changed.
Sensory perception: Alterations in the sense of smell and taste differentiated by the modalities of sweet, salty, bitter and sour.
2.4. Sample size
We used convenience sampling through social media recruitment, with the aim of including as many eligible participants as possible during the study period. This study followed an exploratory design; therefore, no formal sample size calculation was performed.
2.5. Statistics
The normal distribution of continuous variables was assessed using histograms and the Shapiro–Wilk test. Based on these results, appropriate descriptive statistics were selected: means and standard deviations (SDs) were reported for normally distributed variables and medians and interquartile ranges (IQRs) for non‐normally distributed variables.
For group and sex comparisons, Kruskal–Wallis tests were used for non‐normally distributed continuous variables across the three groups, while one‐way analysis of variance (ANOVA) was applied to normally distributed variables. Categorical variables were presented as absolute and relative frequencies, and Chi‐squared tests were used to assess group differences. When the overall Chi‐squared test indicated statistical significance, Bonferroni‐adjusted post hoc tests were conducted to examine pairwise differences.
Multivariable linear regression analysis was performed with BMI at follow‐up as the dependent variable. Independent variables included baseline BMI, medication type, medication dose, duration of medication use (in weeks), age and sex. Interaction terms between medication type and both dose and duration of treatment were included, as these parameters varied significantly between medication groups. Due to statistically significant interactions (p < 0.001), subgroup analyses were performed separately for each medication. Consequently, three different regression models were estimated, each including the above independent variables.
In addition, multivariable logistic regression models were used to examine associations between self‐reported changes in taste perception (sweet and salty) and perceived changes in satiety, appetite, and food craving in individuals with obesity undergoing GLP‐1 or dual GIP/GLP‐1 receptor agonist therapy. Participants who reported increased appetite, hunger, or craving (approximately 1%–3% of the sample) were combined with those who reported no change to form the reference category. All outcomes referred to perceived changes since the start of treatment.
Three separate binary logistic regression models were conducted:
Model 1: Moderate or marked increase in satiety (reference: no change or decrease).
Model 2: Moderate or marked reduction in appetite (reference: no change or increase).
Model 3: Moderate or marked reduction in food craving (reference: no change or increase).
Categorical independent variables included changes in sweet and salty taste perception, each with three categories: ‘more intense taste’, ‘less intense taste’ and ‘no change’ (reference category). Two different levels of adjustment were used. Model 1 adjusted for age and sex. Model 2 further adjusted for pre/post BMI difference, medication use, GIP/GLP‐1 dosage and treatment duration, dietary habits, smoking status, alcohol consumption, physical activity and comorbidities.
In a further analysis, we explored whether changes in taste perception were associated with a reduction in BMI. For this purpose, we conducted an additional multivariable linear regression analysis, using Delta BMI (baseline BMI minus current BMI) as the dependent variable. Self‐reported changes in perception of sweet and salty tastes were included as categorical predictors, using the same structure as in the logistic regression models. The covariates included the same adjustment factors: age, sex, all medication use, GIP/GLP‐1 dose and duration, diet, smoking status, alcohol consumption, side effects, physical activity and comorbidities.
Due to the exploratory nature of the study, p‐values were not adjusted for multiple comparisons. Adjusted odds ratios (AOR) with 95% confidence intervals (95% CI) and corresponding p‐values were calculated for all predictors across both models. Statistical significance was set at two‐sided p < 0.05. There were no missing values in the dataset. All analyses were performed with SPSS version 27.0 (IBM Corp., Armonk, NY).
3. RESULTS
In total, 3717 individuals accessed the questionnaire. Of these, 676 started the survey but did not complete it. A total of 411 participants completed the survey in full and were included in the analysis, corresponding to a click‐to‐complete rate of 11.1%. The median age of participants was 39 years (IQR: 33–47); of these, 295 (71.8%) were women. An omnivorous diet was most commonly reported: 70.0% of participants in the Wegovy® group, 66.9% in the Ozempic® group and 65.2% in the Mounjaro® group. High‐protein/low‐carbohydrate dietary patterns were followed by 21.2% (Wegovy®), 22.3% (Ozempic®) and 28.3% (Mounjaro®). Regarding physical activity, 52.1% of participants in the Wegovy® group, 73.0% in the Ozempic® group and 67.4% in the Mounjaro® group reported no engagement in moderate‐to‐vigorous physical activity. The prevalence of comorbidities varied across groups: dyslipidaemia was reported by 38.7% (Wegovy®), 34.5% (Ozempic®) and 13.0% (Mounjaro®); hypertension by 39.2%, 39.9% and 34.8%, respectively; type 2 diabetes by 31.8%, 41.9% and 30.4%; knee osteoarthritis by 10.6%, 10.8% and 15.2%; and non‐alcoholic fatty liver disease by 8.8%, 5.4% and 13.0%. Medication usage was comparable across groups, with participants typically taking a median of two medications (IQR: 1–2). For further details, see Table 1.
TABLE 1.
Sociodemographic and clinical characteristics of participants.
| Characteristic | Wegovy® (n = 217) | Ozempic® (n = 148) | Mounjaro® (n = 46) |
|---|---|---|---|
| Sex | |||
| Female, n (%) | 117 (53.9) | 73 (49.3) | 27 (58.7) |
| Age, median (IQR) | 40 (35–47) | 38 (31–48) | 39 (30–48) |
| Weight before treatment (kg), median (IQR) | 106.0 (89.6–122.8) | 102.1 (94.2–116.5) | 109.0 (98.8–115.6) |
| BMI before treatment (kg/m2), median (IQR) | 35.6 (33.3–38.2) | 34.7 (33.5–36.5) | 36.2 (34.3–37.1) |
| Alcohol consumption frequency, n (%) | |||
| Daily | 18 (8.3) | 7 (4.7) | 5 (10.9) |
| 3–5 days per week | 23 (10.6) | 18 (12.2) | 5 (10.9) |
| 1–2 days per week | 32 (14.7) | 24 (16.2) | 6 (13.0) |
| 1–3 days per month | 35 (16.1) | 38 (25.7) | 8 (17.4) |
| Rarely/special occasions | 89 (41.0) | 39 (26.4) | 15 (32.6) |
| Never | 20 (9.2) | 22 (14.8) | 7 (15.2) |
| Cigarette smoking frequency, n (%) | |||
| Daily | 60 (27.6) | 31 (20.9) | 10 (21.7) |
| 3–5 days per week | 2 (0.9) | 0 (0.0) | 0 (0.0) |
| 1–2 days per week | 0 (0.0) | 0 (0.0) | 0 (0.0) |
| 1–3 days per month | 4 (1.8) | 0 (0.0) | 1 (2.2) |
| Rarely/special occasions | 5 (2.3) | 7 (4.7) | 1 (2.2) |
| Never | 146 (67.3) | 110 (74.3) | 34 (73.9) |
| Diet type | |||
| High protein/low carb (e.g., keto, atkins) | 46 (21.2) | 33 (22.3) | 13 (28.3) |
| Vegetarian | 5 (2.3) | 9 (6.1) | 3 (6.5) |
| Vegan | 4 (1.8) | 4 (2.7) | 0 (0.0) |
| Gluten free/lactose free | 10 (4.6) | 3 (2.0) | 0 (0.0) |
| Omnivore | 152 (70.0) | 99 (66.9) | 30 (65.2) |
| Moderate‐to‐vigorous physical activity per week since starting GIP/GLP‐1 treatment | |||
| Never | 113 (52.1) | 108 (73.0) | 31 (67.4) |
| 1–3 times per month | 27 (12.4) | 14 (9.5) | 2 (4.3) |
| 1–2 times per week | 35 (16.1) | 12 (8.1) | 7 (15.2) |
| 3–4 times per week | 22 (10.1) | 12 (8.1) | 5 (10.9) |
| 5+ times per week | 20 (9.2) | 2 (1.3) | 1 (2.2) |
| Comorbidities, n (%) | |||
| Diabetes mellitus type 2 | 69 (31.8) | 62 (41.9) | 14 (30.4) |
| Hypertension | 85 (39.2) | 59 (39.9) | 16 (34.8) |
| Sleep apnea | 15 (6.9) | 19 (12.8) | 5 (10.9) |
| Dyslipidemia | 84 (38.7) | 51 (34.5) | 6 (13.0) |
| Non‐alcoholic fatty liver disease | 19 (8.8) | 8 (5.4) | 6 (13.0) |
| Knee osteoarthritis | 23 (10.6) | 16 (10.8) | 7 (15.2) |
| Stroke | 10 (4.6) | 13 (8.8) | 4 (8.7) |
| Wegovy® dose, n (%) | |||
| 1.7 mg | 52 (24.0) | NA | NA |
| 2.4 mg | 165 (76.0) | NA | NA |
| Ozempic® dose, n (%) | |||
| 0.5 mg | NA | 26 (17.6) | NA |
| 1.0 mg | NA | 63 (42.6) | NA |
| 2.0 mg | NA | 59 (39.9) | NA |
| Mounjaro® dose, n (%) | |||
| 5 mg | NA | NA | 6 (13.0) |
| 10 mg | NA | NA | 22 (47.8) |
| 12.5 mg | NA | NA | 18 (39.1) |
Abbreviations: BMI, body mass index; GIP, glucose‐dependent insulinotropic polypeptide; GLP‐1, glucagon‐like peptide‐1; IQR, interquartile range; NA, not applicable.
In Table 2, median treatment duration did not differ significantly between groups (Wegovy®: 40 weeks [IQR: 27–56], Ozempic®: 43 weeks [IQR: 33–60], Mounjaro®: 47 weeks [IQR: 35–60]; p = 0.122). Similarly, there was no statistically significant difference in average monthly weight loss (Wegovy® and Ozempic®: 1.5 kg [IQR: 1.2–1.8], Mounjaro®: 1.7 kg [IQR: 1.5–1.9]; p = 0.142). The most common adverse reactions in all groups were nausea, diarrhoea, vomiting, constipation and eructation. Nasopharyngitis was reported in 34.8% of Mounjaro®, 19.6% of Ozempic® and 8.3% of Wegovy® users, with no statistically significant difference observed between groups (p = 0.087). See Table 2.
TABLE 2.
Clinical outcomes and side effects.
| Parameters | Wegovy® (n = 217) | Ozempic® (n = 148) | Mounjaro® (n = 46) | p‐Value |
|---|---|---|---|---|
| Treatment duration (weeks) median (IQR) | 40 (27–56) | 43 (33–60) | 47 (35–60) | 0.122 |
| Δ Anthropometric measures median (IQR) | ||||
| Average monthly weight loss (kg), median (IQR) | 1.5 (1.2–1.8) | 1.5 (1.3–1.8) | 1.7 (1.5–1.9) | 0.142 |
| Side effects since the start of GIP/GLP‐1 therapy? n (%) | ||||
| Nausea | 80 (36.9) | 53 (35.8) | 14 (30.4) | 0.717 |
| Vomiting | 58 (26.7) | 36 (24.3) | 13 (28.3) | 0.821 |
| Diarrhoea | 69 (31.8) | 28 (18.9) | 12 (26.1) | 0.124 |
| Constipation | 58 (26.7) | 39 (26.4) | 15 (32.6) | 0.685 |
| Headache | 31 (14.3) | 12 (8.1) | 2 (4.3) | <0.001 |
| Abdominal pain | 19 (8.8) | 22 (14.9) | 7 (15.2) | 0.149 |
| Fatigue | 33 (15.2) | 25 (16.9) | 6 (13.0) | 0.802 |
| Eructation | 41 (18.9) | 36 (24.3) | 12 (26.1) | 0.345 |
| Dizziness | 27 (12.4) | 15 (10.1) | 7 (15.2) | 0.612 |
| Depressed mood | 46 (21.2) | 26 (17.6) | 8 (17.4) | 0.643 |
| Muscle weakness | 20 (9.2) | 13 (8.8) | 6 (13.0) | 0.677 |
| Nasopharyngitis | 18 (8.3) | 29 (19.6) | 16 (34.8) | 0.087 |
| Injection‐site hematoma | 34 (15.7) | 12 (8.1) | 5 (10.9) | <0.001 |
| Nicotine use changed since starting GIP/GLP‐1 therapy? n (%) | ||||
| I quit entirely | 13 (6.0) | 4 (2.7) | 1 (2.2) | 0.252 |
| Significantly reduced | 10 (4.6) | 14 (9.5) | 6 (13.0) | |
| Slightly reduced | 16 (7.4) | 15 (10.1) | 2 (4.3) | |
| No Change | 173 (79.7) | 113 (76.4) | 36 (78.3) | |
| Slightly increased | 5 (2.3) | 2 (1.4) | 1 (2.2) | |
| Significantly increased | 0 | 0 | 0 | |
Note: Δ = Delta weight change was calculated as the difference between self‐reported pre‐treatment weight and current weight, reported as median and interquartile range (IQR). Statistical analyses were performed using the Kruskal–Wallis test for non‐normally distributed continuous variables and the Chi‐square test for categorical variables. When significant differences were observed, post hoc Bonferroni corrections were applied to adjust for multiple comparisons.
Abbreviations: GIP, glucose‐dependent insulinotropic polypeptide; GLP‐1, glucagon‐like peptide‐1.
The prevalence of depressed mood and dizziness was comparable across the three groups. In contrast, headaches were reported significantly more frequently among participants receiving Wegovy® (14.3%) than among those treated with Ozempic® (8.1%) or Mounjaro® (4.3%) (p < 0.001). Regarding nicotine use, most participants reported no change after initiating GIP/GLP‐1 therapy (Wegovy®: 79.7%, Ozempic®: 76.4%, Mounjaro®: 78.3%), while smaller proportions reported having quit entirely (Wegovy®: 6.0%, Ozempic®: 2.7%, Mounjaro®: 2.2%) or significantly reduced use (Wegovy®: 4.6%, Ozempic®: 9.5%, Mounjaro®: 13.0%). These differences were not statistically significant (p = 0.252).
In multivariable regression models adjusted for baseline BMI, age, sex, treatment duration and dosage, estimated relative BMI reductions were 17.6% for Wegovy® (95% CI: 15.7–19.5), 17.4% for Ozempic® (95% CI: 15.0–19.8) and 15.5% for Mounjaro® (95% CI: 8.8–22.2) (Table 3). These adjusted estimates reflect the net effect of each medication when accounting for key confounding variables that differed between groups.
TABLE 3.
Changes during GLP‐1 and glucose‐dependent insulinotropic polypeptide (GIP)/glucagon‐like peptide‐1 receptor agonist (GLP‐1 RAS) treatment in satiety, hunger and taste sensation.
| Parameters | Wegovy® (n = 217) | Ozempic® (n = 148) | Mounjaro® (n = 46) | p‐ Value |
|---|---|---|---|---|
| Changes in appetite between meals, n (%) | ||||
| Yes, I feel my appetite is much reduced | 54 (24.9) | 48 (32.4) | 11 (23.9) | 0.220 |
| Yes, I feel my appetite is slightly reduced | 64 (29.5) | 44 (29.7) | 15 (32.6) | |
| Yes, I feel my appetite is slightly increased | 11 (5.1) | 2 (1.4) | NA | |
| Yes, I feel my appetite is much increased | NA | NA | NA | |
| No change | 88 (40.6) | 54 (36.5) | 20 (43.5) | |
| Changes in food craving, n (%) | ||||
| Yes, I feel my food craving is much reduced | 74 (34.1) | 44 (29.7) | 19 (41.3) | 0.071 |
| Yes, I feel my food craving is slightly reduced | 71 (32.7) | 51 (34.5) | 10 (21.7) | |
| Yes, I feel my food craving is slightly increased | 4 (1.8) | 5 (3.4) | NA | |
| Yes, I feel my food craving is much increased | NA | NA | NA | |
| No change | 68 (31.3) | 48 (32.4) | 17 (37.0) | |
| Changes in feeling of satiety, n (%) | ||||
| Yes, I feel satiated much sooner | 38 (17.5) | 22 (14.9) | 12 (26.1) | 0.346 |
| Yes, I feel satiated a little sooner | 107 (49.3) | 65 (43.9) | 17 (37.0) | |
| Yes, I feel satiated more slowly | 4 (1.8) | 4 (2.7) | NA | |
| Yes, I feel satiated much more slowly | NA | NA | NA | |
| No change | 68 (31.3) | 57 (38.5) | 17 (37) | |
| Changes in sense of smell, n (%) | ||||
| Yes, I perceive smells much more intensely | 43 (19.8) | 20 (13.5) | 8 (17.4) | 0.685 |
| Yes, I perceive smells slightly more intensely | 15 (6.9) | 14 (9.5) | 2 (4.3) | |
| Yes, I perceive smells slightly less intensely | 7 (3.2) | 4 (2.7) | 1 (2.2) | |
| Yes, I perceive smells much less intensely | 5 (2.3) | 6 (4.1) | 3 (6.5) | |
| No change | 147 (67.7) | 104 (70.3) | 32 (69.6) | |
| Changes in sweet taste perception, n (%) | ||||
| More intense | 42 (19.4) | 32 (21.6) | 10 (21.7) | 0.489 |
| Less intense | 20 (9.2) | 9 (6.1) | 1 (2.2) | |
| No change | 155 (71.4) | 107 (72.3) | 35 (76.1) | |
| Changes in salty taste perception, n (%) | ||||
| More intense | 58 (26.7) | 24 (16.2) | 7 (15.2) | 0.119 |
| Less intense | 21 (9.7) | 17 (11.5) | 4 (8.7) | |
| No change | 138 (63.6) | 107 (72.3) | 35 (76.1) | |
| Changes in bitter taste perception, n (%) | ||||
| More intense | 48 (22.1) | 24 (16.2) | 7 (15.2) | 0.581 |
| Less intense | 21 (9.7) | 17 (11.5) | 4 (8.7) | |
| No change | 148 (68.2) | 107 (72.3) | 35 (76.1) | |
| Changes in sour taste perception, n (%) | ||||
| More intense | 47 (21.7) | 21 (14.2) | 7 (15.2) | 0.512 |
| Less intense | 21 (9.7) | 17 (11.5) | 4 (8.7) | |
| No change | 149 (68.7) | 110 (74.3) | 35 (76.1) | |
Note: Data are presented as the number (percentage) of participants who reported changes in appetite, food craving, satiety and taste/smell perception during GIP/GLP‐1 treatment. Statistical analyses were performed using Chi‐square test for categorical variables. When significant differences were observed, post hoc Bonferroni corrections were applied to adjust for multiple comparisons.
Abbreviation: NA, not applicable (no participants reported this outcome in this category).
Table 4 shows that participants reported a reduction in appetite, with approximately 55% to 62% across all groups indicating either a slight or a marked decrease. The greatest proportion of participants reporting a strong reduction in appetite was observed in the Ozempic® group (32.4%), although the overall group difference was not statistically significant (p = 0.220). Food cravings were also reduced in all groups, with 41.3% of Mounjaro® users reporting a strong reduction, compared to 34.1% with Wegovy® and 29.7% with Ozempic® (p = 0.071). Most participants reported increased satiety, with approximately two‐thirds in each group stating they felt satiated either much or a little sooner than before. A notably higher proportion of Mounjaro® users (26.1%) reported feeling ‘much satiated’ compared to Wegovy® (17.5%) and Ozempic® (14.9%), though this difference was not statistically significant (p = 0.346). The proportion of participants reporting increased salty taste intensity was highest in the Wegovy® group (26.7%), compared to Ozempic® (16.2%) and Mounjaro® (15.2%) (p = 0.119). Increased sweet taste intensity was reported at similar frequencies in all groups (Wegovy® 19.4%, Ozempic® 21.6%, Mounjaro® 21.7%; p = 0.489). Group differences for bitter (p = 0.581) and sour (p = 0.512) taste perception, as well as smell perception (p = 0.685), were likewise not statistically significant.
TABLE 4.
Analysis of relative body mass index (BMI) reduction with Mounjaro, Ozempic and Wegovy.
| Medication | β | 95% CI | p‐Value | Estimated BMI reduction, % (95% CI) |
|---|---|---|---|---|
| Mounjaro | 0.845 | 0.778–0.912 | <0.0001 | 15.5 (8.8–22.2) |
| Ozempic | 0.826 | 0.802–0.850 | <0.0001 | 17.4 (15.0–19.8) |
| Wegovy | 0.824 | 0.805–0.843 | <0.0001 | 17.6 (15.7–19.5) |
Note: Values are derived from separate multivariable linear regression models stratified by medication. Models were adjusted for treatment duration (weeks), dosage, age, sex and baseline BMI.
Abbreviation: BMI, Body mass index; B, Unstandardized regression coefficient representing the proportion of baseline BMI retained after treatment (e.g., β = 0.845 indicates 84.5% of baseline BMI remains, corresponding to 15.5% reduction); CI, confidence interval.
In Table 5, the univariate analyses showed that participants with higher sweet taste intensity had approximately 4.7‐fold (95% CI: 1.44–09.87) greater odds of increased satiety, 2.7‐fold (95% CI: 1.13–6.93) greater odds of decreased appetite and 3.2‐fold (95% CI: 1.35–6.30) greater odds of decreased food craving. Similarly, increased salty taste intensity was associated with 4.8‐fold (95% CI: 1.49–9.12) greater odds of increased satiety, 2.5‐fold (95% CI: 1.12–6.88) greater odds of decreased appetite and 3.3‐fold (95% CI: 1.41–7.68) greater odds of decreased food craving. After multivariable adjustment, increased sweet taste intensity remained significantly associated with approximately 2.0‐fold (95% CI: 1.15–4.57) greater odds of increased satiety, 1.7‐fold (95% CI: 1.04–3.25) greater odds of decreased appetite and 1.9‐fold (95% CI: 1.06–3.29) greater odds of decreased food craving. Increased salty taste intensity continued to show a significant 2.2‐fold (95% CI: 1.16–5.17) greater odds of increased satiety. Lower sweet and salty taste intensity was not significantly associated with changes in satiety, appetite or food craving in either analysis.
TABLE 5.
Association of changes in sweet/salty taste intensity with satiety, appetite and food craving in obese individuals treated with glucose‐dependent insulinotropic polypeptide (GIP)/glucagon‐like peptide‐1 (GLP‐1).
| Taste | Categories | Univariate model 1 | Multivariable Model 2 |
|---|---|---|---|
| AOR (95% CI) | AOR (95% CI) | ||
| Moderate/marked increase in feeling of satiety versus no change/decrease in satiety(Ref) | |||
| Sweet | No change (reference) | ||
| Sense of taste has increased | 4.67 (1.44–09.87)*** | 2.02 (1.14–4.57)* | |
| Sense of taste has decreased | 0.84 (0.61–3.14) | 0.63 (0.37–1.89) | |
| Salty | No change (reference) | ||
| Sense of taste has increased | 4.84 (1.49–09.12)*** | 2.17 (1.16–5.17)* | |
| Sense of taste has decreased | 0.72 (0.48–2.55) | 0.68 (0.44–1.91) | |
| Moderate/marked reduction in appetite versus no change/increase in appetite(Ref) | |||
| Sweet | No change (reference) | ||
| Sense of taste has increased | 2.68 (1.13–6.93)** | 1.67 (1.04–3.25)* | |
| Sense of taste has decreased | 1.14 (0.76–2.66) | 0.88 (0.52–1.89) | |
| Salty | No change (reference) | ||
| Sense of taste has increased | 2.49 (1.12–6.88)** | 1.62 (0.91–2.92) | |
| Sense of taste has decreased | 0.67 (0.49–2.89) | 0.66 (0.47–2.18) | |
| Moderate/marked reduction in food craving versus no change/increase in craving(Ref) | |||
| Sweet | No change (reference) | ||
| Sense of taste has increased | 3.18 (1.35–6.30)** | 1.85 (1.06–3.29)* | |
| Sense of taste has decreased | 0.93 (0.63–1.58) | 0.82 (0.52–1.69) | |
| Salty | No change (reference) | ||
| Sense of taste has increased | 3.25 (1.41–7.68)** | 1.68 (0.88–3.68) | |
| Sense of taste has decreased | 0.78 (0.38–2.31) | 0.57 (0.31–2.07) | |
Note: Binary logistic regression models were used, with dichotomous outcome variables indicating a moderate or marked improvement in satiety, appetite, or food craving. The reference category combined individuals reporting no change and those reporting a deterioration. The independent variables were self‐reported changes in the perceived intensity of sweet and salty tastes, with “no change” used as the reference category Model 1: Adjusted for age and sex. Model 2: Additionally for medication use, GIP/GLP 1 dose and duration, diet, smoking status, quit smoking during treatment (yes/no), alcohol consumption, side effects, physical activity, and comorbidities.
Abbreviations: AOR, adjusted odds ratios; CI, confidence interval; GIP, Glucose‐dependent insulinotropic polypeptide; GLP‐1, Glucagon‐like peptide‐1; Ref, Reference category.
p = <0.05;
p = <0.01;
p = <0.001.
In the linear regression model predicting BMI reduction (Delta BMI), self‐reported changes in sweet (B = 0.088, p = 0.626) and salty (B = 0.097, p = 0.557) taste perception were not significantly associated with the outcome.
4. DISCUSSION
This cross‐sectional study provides insights into the effects of GLP‐1 and dual GIP/GLP‐1 receptor agonist therapy in individuals with obesity or overweight with comorbidities, including type 2 diabetes, under real‐world conditions. The present study further explores the associations between self‐reported changes in taste perception and key aspects of nutritional regulation, namely satiety, appetite and food craving.
Although direct comparisons with randomized controlled trials are not feasible due to differences in study design, treatment duration and population characteristics, the unadjusted median monthly weight loss, calculated individually based on each participant's treatment duration, was 1.5 kg (IQR: 1.2–1.8) in both the Wegovy® and Ozempic® groups and 1.7 kg (IQR: 1.5–1.9) in the Mounjaro® group. The differences between the groups were not statistically significant. When evaluating relative reductions in BMI using multivariable regression models adjusted for treatment duration, dosage, baseline BMI, age and sex the estimated reductions were 17.6% for Wegovy® (95% CI: 15.7–19.5), 17.4% for Ozempic® (95% CI: 15.0–19.8) and 15.5% for Mounjaro® (95% CI: 8.8–22.2). These findings reflect treatment effects under real‐world conditions, considering relevant covariates. For example, in SURMOUNT‐1, participants treated with tirzepatide 15 mg achieved a mean weight loss of 23.6 kg over 72 weeks, 16 while in STEP 1, semaglutide 2.4 mg resulted in a mean weight loss of 15.3 kg over 68 weeks. 17 However, when controlling for baseline BMI, treatment duration, dose, age, and sex in multivariable regression models, the estimated relative reduction in BMI was lower for Mounjaro® (15.5% [95% CI: 8.8–22.2]) than for Ozempic® (17.4% [95% CI: 15.0–19.8]) and Wegovy® (17.6% [95% CI: 15.7–19.5]).
In addition to weight loss, our results suggest notable changes in appetite regulation and sensory perception. More than half of the participants reported reduced appetite, with approximately one‐third describing it as substantially diminished. Additionally, about two‐thirds experienced decreased food cravings and accelerated satiety after meals. These findings align with the STEP‐1 study, 17 which documented a 35% reduction in food cravings after 3 months of semaglutide treatment, with 68% of participants reporting markedly decreased hunger within the first 12 weeks. The SURMOUNT‐1 study 18 comparing tirzepatide and semaglutide found that 82% of tirzepatide patients reported ‘hardly any food cravings’ after 24 weeks, compared to 58% of semaglutide patients. Although our cross‐sectional design precludes direct temporal comparisons, the magnitude of appetite and craving reductions observed suggests these effects persist throughout the treatment duration.
Studies have elucidated the mechanistic explanations, showing that 20‐week treatment with oral semaglutide 50 mg significantly reduced energy intake, improved appetite regulation, and reduced food cravings without delaying gastric emptying. 19 Further, a different study 20 suggested that semaglutide not only reduces appetite but also affects dopamine‐mediated reward signalling in the brain, which may explain the reduced food craving in patients. In addition, the STEP‐5 study 21 showed that improvements in eating behaviour control and craving reduction are sustained over time. Against this background, the sensory changes documented in our study are of particular interest.
Approximately 20%–30% of participants reported increased taste perception in the sweet, salty, bitter and sour modalities, depending on the drug group. Interestingly, participants with increased intensity in the sweet and salty taste modalities compared to those with decreased or unchanged taste intensity reported more pronounced associations with favourable appetite‐related outcomes, such as reduced cravings or earlier satiety, although the majority reported no overall change in taste perception. These findings add to the complexity of previous studies, some of which have produced conflicting results regarding the effects of GLP‐1 analogues on taste function, some suggesting improved taste perception and neural activation in response to taste stimuli, 13 and others showing objective reductions in taste sensitivity using psychophysical assessments. 14 In light of the observed associations between taste perception and appetite‐related outcomes, we examined whether these sensory changes might lead to weight loss. To explore this further, we performed a linear regression analysis, which showed no significant association between changes in taste perception and BMI reduction, after adjusting for relevant covariates. This finding suggests a distinction between the short‐term, subjective effects, such as reduced appetite or enhanced satiety, and the long‐term, objective changes in weight. Although altered taste perception may influence eating behaviour in the short term, it does not appear to result in measurable weight loss within the observed timeframe. Possible explanations include compensatory behaviours, metabolic adaptation or unmeasured influences on energy balance. These results indicate that although subjective sensory changes may contribute to treatment adherence or perceived efficacy, they do not independently predict weight loss outcomes.
Although our cross‐sectional data do not permit causal conclusions, the observed associations suggest a possible link between increased sensory perception and satiety‐related processes. The precise nature of this relationship and any underlying mechanisms remain to be elucidated. These observations align with neurophysiological findings regarding the distribution of GLP‐1 receptors within the gustatory system, reported both peripherally in taste buds and centrally in brain regions involved in taste processing. 22 , 23 Our findings raise the question of whether individual differences in sensory responses to GLP‐1 and dual GIP/GLP‐1 receptor agonists might contribute to variations in eating behaviour or treatment adherence. It is also possible that incretin‐based therapies are associated not only with oral taste perception, but also with extraoral chemosensory receptors, such as those in the gastrointestinal tract. Intestinal taste receptors, particularly from the T1R and T2R families, have been implicated in the modulation of appetite‐related peptides including GLP‐1, peptide YY and cholecystokinin in preclinical studies. 12 , 24 , 25 Although these mechanisms were not directly assessed in our study, they may contribute to the observed associations and should be further explored in mechanistic and longitudinal research. Nevertheless, our findings underscore the need for future studies using objective psychophysical measures and longitudinal designs to clarify the potential sensory effects of incretin‐based therapies.
4.1. Limitations
Several limitations must be considered when interpreting the results of our study. Firstly, the cross‐sectional design does not allow for conclusions about causation regarding the relationship between changes in taste perception and appetite‐related outcomes. To better assess causality, future research should employ prospective study designs, ideally RCT, with a control group of individuals with obesity who are not receiving GIP/GLP‐1 RAS treatment. These studies should measure changes in specific taste modalities, such as sweet, salty, bitter and sour, before and after the commencement of GLP‐1 or dual GIP/GLP‐1 receptor agonist therapy. Using objective psychophysical measures (e.g., threshold testing) alongside neurobiological methods could help to distinguish between the peripheral and central mechanisms involved in appetite regulation.
Secondly, convenience sampling via social media may have introduced selection bias, as individuals with particularly positive or negative treatment experiences may have been more likely to participate. Additionally, our study included only individuals who were actively using GLP‐1 or GIP/GLP‐1‐based therapy at the time of the survey. This likely excluded former users who discontinued treatment due to adverse effects or insufficient efficacy, potentially skewing the sample towards more favourable responses. However, even in RCT, systematic follow‐up of individuals who discontinue treatment remains a common methodological challenge. Since participants were not informed in advance that the study focused specifically on changes in taste or appetite, the risk of self‐selection based on these outcomes was likely reduced. Nevertheless, some residual bias may have persisted, as individuals experiencing more noticeable effects regardless of whether they were positive or negative may have been more motivated to respond. This could have led to an overestimation of the prevalence of reported appetite reductions and sensory changes.
In addition, self‐reported data without objective validation of anthropometric outcomes and taste intensity may have introduced measurement error. Finally, the relatively small number of participants in the dual GIP/GLP‐1 receptor agonist group (n = 46) limits the statistical power to detect specific effects of GIP agonism beyond those of GLP‐1. Consequently, comparisons involving this subgroup should be interpreted with caution. Despite these limitations, our findings provide valuable preliminary insights that can inform more rigorous future investigations into the sensory mechanisms that may contribute to the efficacy of GLP‐1 and dual GIP/GLP‐1 receptor agonists in obesity management.
5. CONCLUSION
Our cross‐sectional real‐world study provides evidence suggesting that altered taste perception during GLP‐1 and dual GIP/GLP‐1 RAS therapy is associated with favourable appetite‐related outcomes, including enhanced satiety and reduced food craving in individuals with obesity. These sensory changes might serve as clinically relevant indicators for personalized obesity treatment. Future prospective studies using objective sensory testing and controlled designs are needed to confirm these preliminary associations and to assess whether taste sensitivity assessment could support personalized therapeutic approaches in obesity management.
AUTHOR CONTRIBUTIONS
AK designed the study, supervised data collection, analysed and interpreted the data and wrote the manuscript. OM and RF contributed to data interpretation and critically revised the manuscript. TW provided statistical expertise, performed data analysis and critically revised the manuscript. SH contributed to the study design, interpretation of results and critically revised the manuscript. All authors approved the final version of the manuscript.
CONFLICT OF INTEREST STATEMENT
OM reports the following conflict of interest: Clinical trial support: Sêr Cymru II COFUND Fellowship/European Union, Novo Nordisk A/S, Novo Nordisk AT, Abbott Diabetes Care, Sanofi, Dexcom, Team Novo Nordisk, SAIL, Maisels Brauerei, Medtronic AT, EFSD/EASD, Falke, BISp, perfood, Ypsomed, Sinocare. Presenters' honoraria: Medtronic AT, Medtronic Int., Eli Lilly, Novo Nordisk, Sanofi, TAD Pharma, ADA, Diatec, Berufsverband deutscher Internist*innen, Dexcom, Astra Zeneca, Ypsomed, Insulet, Diabetologen Hessen, Abbott. Conference travel support: Novo Nordisk A/S, Novo Nordisk AT, Novo Nordisk UK, Medtronic AT, Sanofi, EASD, OEDG, DDG. Advisory board: Sanofi, TAD Pharma, Dexcom, perfood, Medtronic. The remaining authors declare no conflicts of interest.
PEER REVIEW
The peer review history for this article is available at https://www.webofscience.com/api/gateway/wos/peer‐review/10.1111/dom.16548.
ETHICS STATEMENT
The study protocol was reviewed and approved by the Ethics Committee of the Medical University of Vienna (approval number 2506/2024). Informed consent was obtained from all participants.
ACKNOWLEDGEMENTS
We thank all participants who completed the survey. Open access funding provided by Medizinische Universitat Wien/KEMÖ.
Kapan A, Moser O, Felsinger R, Waldhoer T, Haider S. Real‐world insights into incretin‐based therapy: Associations between changes in taste perception and appetite regulation in individuals with obesity and overweight: A cross‐sectional study. Diabetes Obes Metab. 2025;27(9):5008‐5018. doi: 10.1111/dom.16548
Funding information This study received no specific grant from any funding agency in the public, commercial or not‐for‐profit sectors.
DATA AVAILABILITY STATEMENT
The datasets generated and analysed during this study are available from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets generated and analysed during this study are available from the corresponding author upon reasonable request.