Impaired Gustation in Liver Diseases: A Comprehensive Narrative Literature Review

Abstract

Objective

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is one of the fastest-growing liver disorders worldwide. It is driven by obesity and type 2 diabetes. Taste perception plays a key role in appetite regulation and nutrition, also influencing other liver diseases progression. This review summarizes past and current evidence on taste disorders in liver diseases and their clinical implications.

Materials and Methods

A narrative review of PubMed, Web of Science, Google Scholar, and Research Gate databases was conducted using selected MeSH terms.

Results

Taste disturbances have been reported in viral hepatitis, cirrhosis, Wilson’s disease, amebic liver abscesses, and NAFLD/MASLD, as well as in nutritional deficiencies (zinc, magnesium, vitamin A, branched-chain amino acids). Dysgeusia was linked to reduced appetite, sarcopenia, malnutrition, altered food preferences, and obesity risk in MASLD. Taste impairments worsen with liver dysfunction progression. Several drugs (e.g., interferon, metronidazole) contribute to dysgeusia. Zinc deficiency was the most consistent factor. Glucagon-like peptide-1 (GLP-1) receptor modulators, affecting appetite and sweet/umami perception, appear promising in MASLD therapy.

Conclusions

Taste disorders are prevalent and still under-recognized in populations with liver diseases. The cause of these disorders remains unclear. Most of available studies affecting nutrients deficiencies are outdated. More research targeting molecular pathways of taste modulation (e.g., GLP-1 receptors), as well as determining the prevalence and clinical consequences of dysgeusia in specific liver disease stages is needed to better understand how micronutrient deficiencies and medications affect taste disorders.

Introduction

Proper gustation is an important element of the eating meals process which conditions food intake habits and physiological digestion. In fact it also affects mental health (1). There are five basic types of taste including: sour, sweet, salty, bitter and umami (2). Taste disorders can manifest in various forms including dysgeusia, defined as a distortion or abnormal perception of taste (such as metallic, bitter, or otherwise altered sensations), and hypogeusia, understood as a partial reduction in taste sensitivity (3).

Dietary and oral hygiene patterns can influence oral health, induce structural changes in the oral mucosa, tongue, or brain, and consequently affect taste perception in different populations. A studies conducted at the University of Zagreb demonstrated that attitudes toward oral hygiene are an important factor shaping oral health, which may directly affect taste perception and potentially modulate the risk of taste disorders in various population groups (4–8).

Taste disturbances may impact health outcomes and lead to a deterioration in quality of life, changes in eating habits, which may result in malnutrition or even obesity, potentially leading to MASLD (9, 10). By 2050, it is estimated that in the majority of U.S. states, one-third of adolescents (aged 15–24) and approximately two-thirds of adults (aged 25 and older) will be suffering from obesity (11). Additionally 19% of Americans at age over 40 reported taste impairments, and 5% of them had dysgeusia. Prevalence increases with age up to 27% for people ≥ 80 (12). Many causes of taste disorders have been identified so far. Liver diseases are considered to be one of them (13). Currently, most publications focus on the nutritional status of patients and the nutrient deficiencies. Disturbed taste sensation has been demonstrated in both acute and chronic liver disease, including alcoholic/viral hepatitis, cirrhosis or metabolic associated steatotic liver disease (MASLD) (14, 15). Changes in taste perception in this group may result from nutritional deficiencies, disturbances in signal transmission through neuronal pathways, coexisting diseases or medication intake (13). Taste disorders may contribute to reduced appetite in patients with liver cirrhosis, which, in turn, is significantly associated with the occurrence of sarcopenia and weight loss in this population (13, 16). Moreover, taste disturbances in this group of patients may also result from coexisting oral diseases. It has been confirmed that oral lichen planus (OLP) occurs more frequently in individuals with viral hepatitis and may contribute to the presence of dysgeusia (17, 18). Furthermore, vitamin D deficiency, which commonly coexists in patients with liver disease, is known to exacerbate the course of the OLP (19, 20).

Impaired zinc metabolism is another possible mechanism. Zinc deficiency in patients with chronic liver disease seems to result from multiple factors such as impaired intake, absorption, transport, storage, and excretion of zinc (21). Recent studies emphasize malnutrition as one of the main causes of taste disorders related to micronutrients deficiency (15, 22).

Considering a wide range of factors contributing to taste disturbances, liver diseases represent a significant area of interest due to their demonstrated impact on gustatory function. Evidence shows altered taste perception across various liver conditions - from hepatitis to cirrhosis which is often co-existing with nutritional deficiencies. However, the prevalence of dysgeusia and its connection to nutritional status in a group of liver diseases patients has not been thoroughly investigated. Existing studies on taste disturbances in cirrhosis are outdated, primarily centered on viral causes, and newer evidence shows that they do not evaluate the possible nutritional consequences (23–28). Understanding the relationship between liver dysfunction, micronutrient imbalances, and taste impairment can provide valuable insights into improving patient care and quality of life.

We aimed to compare older studies with the current knowledge to obtain a more comprehensive and up-to-date information on taste disorders, thus highlighting potential causes, clinical implications and avenues for future research.

Material and Methods

This review study was conducted through an analysis of articles available in the PubMed, Web of Science, Google Scholar and Research Gate databases. The MeSH terms used for search included: liver diseases, taste, taste perception, taste disorders, taste buds, taste receptors type 2, taste receptors type 1, liver cirrhosis, dysgeusia, MASLD.

Consistency and terminological accuracy were maintained in accordance with the principles of medical language and characteristic collocations (29).

1. Inclusion criteria for this review were as follows:

• Human clinical studies: RCTs, cohort, observational, or cross-sectional studies on taste disorders in liver diseases.

• Experimental animal studies addressing mechanisms of taste disturbances in liver disease.

• Case reports and case series on taste disorders related to liver disease or pharmacological treatment.

• Interventional studies evaluating drugs or supplements on taste perception.

• Systematic reviews and meta-analyses providing synthesized evidence on prevalence, mechanisms, and interventions.

• Publications in English or Polish.

2. Exclusion criteria:

• Studies which are not related to liver disease or taste disorders,

• Papers which are not available in full text or of insufficient methodological quality (e.g., no description of study population, no clear assessment of taste evaluation methods),

• Studies involving drugs no longer used in current clinical practice for the treatment of liver disease,

• Publications in foreign languages other than those mentioned in inclusion criteria.

A total of 65 articles were included in the review: 3 case reports (including case series), 28 review articles (including 3 meta-analyses), 32 original studies, and 2 studies conducted on animal models.

The selected articles explain the connection between taste disorders and various liver diseases both on humans and animal models. These study review papers describe the effects of drugs administration or potential impact of nutrients including zinc, vitamin A, magnesium or branched-chain amino acids (BCAA) on taste disorders. Despite many variables that qualify articles for review, searched databases contain a small amount of up to date studies directly involving this issue.

Results

Alterations in Taste Perception in Liver Disease

Associations between oral health and liver diseases suggest that periodontitis may lead to progression of liver disease (30, 31). It is also known that taste impairments may be induced by periodontitis through mediation by halitosis (32). The available literature contains the results of the occurrence of taste disorders in both acute and chronic liver diseases. The analyzed studies often included groups with different stages of liver injury. Symptoms may be less severe in mild stages. However, in advanced stages including liver cirrhosis, severe taste impairments and oral pain are observed, co-existing with poorer oral hygiene (31, 33). Disturbances in feeling of salty and umami flavors are mostly observed in this group (34).

Evidence for the occurrence of taste impairments in the viral liver infection is the case of a patient with acute hepatitis- E virus (HEV)-associated Guillain-Barre syndrome (GBS). Despite the illness related symptoms, the patient also referred dysgeusia of sweet, salty, sour, and bitter and umami tastes. Intravenous immunoglobulin (IVIg) was administered to the patient in dose 400 mg/kg per day for five days with effect of full gustatory function recovery. The authors revealed its two potential mechanisms including: acute hepatitis and GBS (35). During the acute phase of hepatitis, urinary zinc excretion may increase, leading to a decrease in serum zinc concentration (36). The underlying mechanism likely involved damage to gustatory neural pathways-from taste buds and peripheral nerves to central structures such as the brainstem, thalamus, and cortex (37).

Smith et al. (38) investigated taste disturbances in a cohort of 22 patients with acute viral hepatitis and 16 patients with chronic liver disease, including 14 patients with cirrhosis. Compared with a healthy control population, the patients demonstrated both subjective complaints and objective impairments in gustatory function. Specifically, the mean detection thresholds for bitter, salty, sweet, and sour tastes, as well as the mean recognition thresholds for bitter, salty, and sour tastes, were significantly elevated in both the acute and chronic hepatitis groups. The alterations were reversible with hepatic function recovery. Although the exact mechanism of hypogeusia remained unclear, the current evidence suggests that nutritional disturbances associated with cirrhosis are the most likely a contributing factor.

Probably, the first published study examining the relationship between the perception of all five tastes and patients with liver disease was the research conducted by Musialik et al. Forty patients with chronic viral C hepatitis (CHC) were examined (39). Patients were stratified according to the degree of liver fibrosis, with one subgroup representing an early-stage fibrosis and the other representing advanced fibrosis. The results showed that recognition of sour, bitter, and sweet tastes was similar between CHC patients and the healthy controls. However, the recognition threshold for umami taste was significantly increased (P < 0.01) in CHC patients compared with controls, indicating reduced ability to identify umami. In addition, the perception of sweet taste was significantly heightened (P < 0.05). These alterations were more pronounced in patients with advanced fibrosis. A similar trend was noted for salty taste recognition (P = 0.075), while the intensity of sour taste perception was lower. In summary, the authors reported alterations across all taste modalities except bitter (39).

There is a connection between liver cirrhosis and taste disorders which often include sweet taste aversion and salty taste intolerance. Sturniolo et al. (40) presented, in spite of impaired perception of sweet and salty taste, some abnormalities in sour taste perception among a liver cirrhosis group.

An animal model study, conducted by Fernandes et al. (41), on fourteen male Wistar rats with liver cirrhosis showed some morphological changes in the structure of the tongue. There have been some differences related to a significant reduction in the foliate papillae (not responsible for the sense of taste), papillae narrowing particularly in the base diameter and the apical region. It has been found that some rats in the cirrhosis group had only one taste bud per field, whereas others contained no taste buds. The presence of taste buds per field ranged from two to six in the control group. There was also positive immunoreactivity for the T1R3 receptor (belonging to the T1R family, responsible for the proper perception of sweet taste) in controls, not observed in the study group.

MASLD is currently the most prevalent chronic liver disease worldwide, affecting over 30% of the global population and closely associated with obesity and type 2 diabetes mellitus (42, 43). Appetite regulation and energy balance play central roles in MASLD pathogenesis. Glucagon-like peptide-1 (GLP-1) receptor agonists are the most promising therapeutic targets, which improves the metabolic dysfunction in MASLD (44). These agents reduce food intake, promote weight loss, and improve glucose tolerance through both central and peripheral mechanisms (45–47). Recent studies have also identified an additional, less recognized role of GLP-1 - signaling in modulating taste perception. The presence of GLP-1 receptors on gustatory nerve fibers suggests the involvement in sensory regulation (48). Supporting this notion, animal models lacking these receptors show significantly diminished responses to sweet stimuli, implicating GLP-1 pathways in the maintenance of sweet taste sensitivity and potentially influencing food preferences and intake behavior (49).

In an observational study conducted by Dallio et al. (15) the prevalence of dysgeusia in patients with advanced chronic liver disease (ACLD) related to MASLD was assessed, comparing its severity to stage of liver function. Dysgeusia increased with liver disease progression. Only 5% of patients without liver fibrosis were affected, comparing to 33% of patients with advanced stages of liver impairment. Taste disturbances increased from 7% in compensated (cACLD) to 59% in decompensated (dACLD). No significant difference was found between dACLD patients with active vs. past decompensation, suggesting dysgeusia is linked to liver injury stage rather than current symptoms. Dysgeusia was most commonly observed in both ascites and hepatic encephalopathy group. Importantly, 90.2% of dACLD patients with dysgeusia also had appetite loss, while none of them showed appetite loss without dysgeusia, thus indicating that dysgeusia may contribute to reduced appetite.

Emelyanov and Petrushanko (50) examined the oral and sensory alterations in a cohort of 258 patients with non-alcoholic fatty liver disease (NAFLD), a condition recognized as part of the broader MASLD spectrum. The study demonstrated that 82.6% of the patients experienced taste disturbances, primarily in the form of dysgeusia manifesting as a reduced or altered perception of taste. These alterations were frequently accompanied by signs of oral mucosal inflammation, dry mouth, and other dental pathologies, suggesting a multifactorial origin linked to both local (oral) and systemic metabolic dysfunction. The authors emphasized that such sensory impairments may negatively influence dietary patterns and food preferences, potentially contributing to further metabolic deterioration in patients with NAFLD/MASLD. Their findings underscore the importance of recognizing taste disorders as a relevant clinical feature in liver disease, particularly given their possible implications for nutritional status and disease progression.

In a Polish study (10) involving 84 individuals with NAFLD and 120 healthy controls, it was shown that most common taste alterations involve sweet and umami tastes. A significantly increased recognition threshold and decreased intensity of perception for these tastes were observed. Patients reported a reduced pleasure from consuming sweet products and increased enjoyment of foods rich in umami (e.g., fish, dairy). These changes were more pronounced in individuals with advanced liver fibrosis and steatosis. Additionally, the study found that taste disturbances may influence patients' food preferences and contribute to overweight and metabolic disorders.

In the searched databases there is only one research investigating taste dysfunction among patients with Wilson’s disease (WD) (51). WD is a rare autosomal recessive, metabolic dysfunction contributing to abnormal copper accumulation in organs involving liver, brain and others. Pathomechanism involves impaired secretion of copper into bile which clinically presents as hepatic, psychiatric and neurological symptoms. A predominance of hepatic symptoms may lead to mild liver dysfunction, chronic hepatitis, cirrhosis or a rare acute liver failure. WD patients are treated with copper chelators trientine and penicillamine. The second group of medications is zinc which lowers intestinal copper absorption (52).

In the research Salmon et al. (51), the patients were stratified into two symptom subtypes: hepatic and neurologic predominant of WD. Regarding the obtained results, the patients with WD regardless of subtype had no decrease in taste function while a significant decrease in olfactory function were observed compared to healthy controls. Nonetheless, the factory and gustatory test scores were weakly correlated in both WD and control subjects. It is unclear whether WD, especially liver symptoms severity influences gustation. Also, the pathophysiologic mechanism responsible for test and smell disorders in this group remains unclear. Further research is required on larger cohorts.

Taste disorders during treatment of liver diseases

In the study conducted by Klimacka-Nawrot et al. (26) the correlation between pegylated interferon-alpha, ribavirin therapy and taste acuity in patients with chronic type C hepatitis was assessed. After 12 weeks of therapy, sensitivity to salty and sweet was significantly decreased (p < 0.05), and sensitivity to bitter was described as being more unpleasant than before therapy (p < 0.05). The findings demonstrated that taste disturbances during therapy are multidirectional. No significant changes in food preferences were reported; however, a decrease in appetite was noted.

In order to evaluate the potential effects of adding boceprevir to the above-mentioned therapy, a double-blind study was conducted. The results showed that dysgeusia was reported more than twice as frequently in the boceprevir-treated groups compared to the control groups (24). Also in the study assessed by Bacon et al., dysgeusia was observed more frequently in the boceprevir groups than in the controls (25).

The literature also includes a comparison of treatment strategies for amebic liver abscess using metronidazole versus satranidazole. It has been demonstrated that a metallic taste occurred less frequently in patients treated with satranidazole. Furthermore, satranidazole was associated with significantly better tolerability compared to metronidazole, while maintaining similar therapeutic efficacy. Patients receiving satranidazole reported fewer adverse effects overall (27).

In a larger randomized clinical trial conducted in India (53), the efficacy and tolerability of metronidazole and tinidazole (derivatives of 5-nitroimidazole, like satranidazole) were compared in 150 patients with amoebic liver abscess. Patients were divided into two equal groups receiving either metronidazole or tinidazole. Taste disturbances in the form of a metallic taste were reported in 13.3% of patients in the metronidazole group and in 2.6% of patients in the tinidazole group (p = 0.03).

On the other hand, a meta-analysis conducted in 2021 (54) found that the incidence of metallic taste as an adverse effect was slightly lower with metronidazole compared to tinidazole. Although the difference was not statistically significant, switching from tinidazole to metronidazole could potentially reduce the incidence of metallic taste by 5.1%, while also offering broader antimicrobial coverage than tinidazole.

A summary of literature data regarding taste disorders in selected liver diseases and administered drugs is presented in Table 1.

Table 1. Comparison between taste disorders in selected liver diseases and administered drugs.

Type of liver disease	Type of study	Characteristics of groups	A type of taste disorder	N (%) of disorder	References
Hepatitis C virus	Double-blinded randomized controlled trial	Group 1 (control group = 363): peginterferon alfa-2b ribavirin for 4 weeks next placebo plus peginterferon–ribavirin for 44 weeks Group 2 (N = 368): peginterferon alfa-2b–ribavirin for 4 weeks next boceprevir plus peginterferon–ribavirin for 24 weeks, and patients with a detectable HCV RNA level between weeks 8 and 24 administered placebo plus peginterferon-ribavirin for an extra 20 weeks Group 3(N = 366): peginterferon alfa-2b–ribavirin for 4 weeks next boceprevir plus peginterferon–ribavirin for 44 weeks	Dysgeusia Dysgeusia Dysgeusia	64 (18%) 137 (37%) 156 (43%)	Poordad et al. 2011(24)
	Single-blinded randomized controlled trial	Group 1 (control group, N = 80) peginterferon alfa-2b ribavirin for 4 weeks next placebo plus peginterferon–ribavirin for 44 weeks Group 2 (N = 162)): peginterferon alfa-2b–ribavirin for 4 weeks next boceprevir plus peginterferon–ribavirin for 32 weeks, and patients with a detectable HCV RNA level at week 8 administered placebo plus peginterferon–ribavirin for an extra 12 weeks Group 3(N = 161): peginterferon alfa-2b–ribavirin for 4 weeks next boceprevir plus peginterferon–ribavirin for 44 weeks	Dysgeusia Dysgeusia Dysgeusia	9 (11%) 69 (43%) 72 (45%)	Bacon et al. 2011 (25)
Chronic hepatitis C	Non-randomized controlled trial	Group 1 (N=19) pegylated interferon-alpha 2b and ribavirin	Sensitivity to salty and sweet was decreased. Bitter was more unpleasant than before the therapy.	19 (100%)	Klimacka-Nawrot et al. 2009 (26)
Amebic Liver Abscess	Single-blinded randomized controlled trial with placebo	Group 1 (N=25) Metronidazole Group 2 (placebo, N=24) Satranidazole	Metallic taste Metallic taste	18 (72%) 3 (12.5%)	Muzaffar et al. 2006 (27)
	A randomized control trial	Group M- Metronidazole (N=75) Group T- Tynidazole (N=75)	Metallic taste Metallic taste	10 (13.3%) 2 (2.6%)	Sudhakar et al. 2018 (53)

Nutrients deficiency in liver diseases

The liver plays a crucial role in nutrient metabolism. Therefore, cirrhosis significantly impairs metabolic pathways, negatively impacting patient prognosis (55). Malnutrition is a common complication in liver cirrhosis and is frequently accompanied by nutritional deficiencies, including zinc deficiency (22, 56).

Zinc participates in protein structures formation, enzymes, transcription factors and homeostasis. It also has anti-inflammatory, anti-oxidant and anti- apoptotic properties, thus inhibiting cirrhosis-related fibrosis by modulating the function of hepatic stellate cells. Zinc deficiency may be responsible for the development or even intensify malnutrition with hypoalbuminemia and hypogeusia. Clinically, zinc deficiency may present as worsening of appetite, hair loss, testicle atrophy, abnormal taste and smell, immunology or even neurology defects (57).

It has been proven that lower zinc serum level occurs more often in patients with chronic liver disease and liver cirrhosis, responding with its severity and hepatic encephalopathy (56, 58, 59).

Patients with serum zinc concentrations under 60 µg/dL are at elevated risk for covert hepatic encephalopathy, independent of their ammonia levels, and are also more likely to progress to overt hepatic encephalopathy (60). One of the presented mechanisms of zinc deficiency in alcoholic liver disease is its increased excretion in the urine and reduced absorption in the intestine caused by chronic alcohol consumption (61). Similarly, in acute hepatitis, reduced serum zinc levels have been observed as a result of increased renal excretion (36).

A randomized clinical trial conducted by Juárez-Hernández et al. (62) evaluated the effects of a 6-month regimen of zinc supplementation (100 mg/day). The study demonstrated a 55% increase in the likelihood of improved taste perception for salty, sweet, sour, and umami flavors among patients receiving zinc. The recognition of umami taste improved specifically by 59%. However, no significant changes were observed in the perception of bitter taste.

Another deficiency found in patients with alcoholic liver disease was vitamin A deficiency. In line with prior research, the potential role of vitamin A in modulating taste perception was explored; however more recent literature on this topic remains scarce. There are only two studies in the searched databases regarding the influence of vitamin A on the perception of taste in liver cirrhosis patients (23, 63). In the first study, Madden et al. (23) found no correlation between vitamin A and taste acuity. However, they did report a significant negative association between serum magnesium levels and both salt detection thresholds and overall gustatory scores. The second study conducted by Garrett-Laster (63) examined 37 patients with alcoholic liver cirrhosis and vitamin A deficiency, 11 of those had co-existing zinc deficiency. Patients were treated with oral vitamin A (10.000 µg/day) for 4 weeks. Comparing to 21 healthy controls, all study group presented a significant improvement (P<0.01) in detection and mean recognition level for salty and bitter taste, with no relation with zinc status. As a result of the improvement in the concentration of vitamin A in the serum, there was a better perception of taste. The mechanism of vitamin A on salty and bitter taste modalities remains unknown.

Nagao et al. (64) evaluated the effects of a supplement enriched with branched-chain amino acids (BCAA) on taste sensitivity and zinc levels in a small group of patients (9 subjects) with HCV-related liver disease. After 90 days of supplementation, improvements in sour and sweet taste sensitivity as well as increased zinc levels were observed, thus indicating the effectiveness of BCAA in treating taste disorders.

Numerous studies have described the individual effects of vitamins such as B3, B6, B12, C, D3, E and folic acid on the progression of liver diseases or taste disturbances (65–67). However, there is a lack of research specifically assessing the combined or interrelated impact of these factors.

Comparison available data from the literature correlating between nutrient and taste disorders among patients with liver diseases are presented in Table 2.

Table 2. Correlation between nutrient deficiency and taste disorders among patients with liver diseases.

Nutrient deficiency	Type of liver disease	Connection with taste disorder	References
Zn	Cirrhosis	Yes	Zalewski 2005 (57)
	Cirrhosis	No	Sturniolo 1992 (40)
	Cirrhosis	No	Madden 1997 (23)
	Cirrhosis	Yes	Juárez-Hernández 2022 (34)
	Cirrhosis	Yes	Juárez-Hernández 2024 (62)
	HCV infected liver disease	Yes	Nago 2010 (64)
	Chronic/acute liver disease	No	Smith 1976 (38)
	Chronic liver disease	Yes	Ozeki 2020 (67)
Vitamin A	Alcoholic liver cirrhosis	Yes	Garrett-Laster 1984 (63)
	Cirrhosis	No	Madden 1997 (23)
Mg	Cirrhosis	Yes	Madden 1997 (23)

Discussion

Taste disturbances represent a multifactorial and clinically relevant problem in patients with liver diseases. As outlined in the introduction, proper gustatory function is an important determinant of appetite regulation, dietary habits, and overall health. Findings reported in our review confirm the fact that alterations in taste perception occur both in acute and chronic liver conditions, and that their severity often typically follows the course of liver injury (31, 33). These findings point out that taste disorders are not only a consequence of severe disease, but also may act as modifiers of nutritional status, thus creating a vicious cycle of malnutrition, sarcopenia, and reduced quality of life.

The repeated outcome of studies is a disruption of salty and umami taste modalities. These changes are particularly significant, because both taste qualities are involved in food preference, appetite stimulation, and protein intake. For example, patients with chronic hepatitis C exhibited increased umami recognition thresholds, as well as impaired perception of sweet taste. Similarly, a reduced sensitivity to salty taste was found in cirrhosis and it was often accompanied by aversion to sodium-containing foods (39). Findings suggest that gustatory dysfunction may directly influence food choices and contribute to nutrient imbalances commonly reported in chronic liver disease, including hypoalbuminemia and protein-energy malnutrition.

Several pathophysiological mechanisms are likely responsible for these taste disorder alterations. Zinc deficiency remains the most consistently reported factor, with evidence of reduced serum zinc concentrations in cirrhosis and hepatitis, often related to impaired absorption, altered transport, or increased urinary loss. Zinc plays an essential role in the structure and function of taste buds, and supplementation trials have demonstrated improved sensitivity for salty, sweet, and umami tastes (36, 56, 58, 59, 62). Similarly, vitamin A deficiency, particularly in alcoholic liver disease, has been associated with changes in bitter and salty taste perception, although available data remain limited, and studies are outdated (63). Recent studies also point to vitamin D deficiency as an indirect contributor, through its role in oral pathology such as oral lichen planus, which may exacerbate gustatory dysfunction (19, 20). Our analysis suggests that micronutrient deficiencies as a cause of taste disturbances should be considered in the context of overall nutritional disorders and their clinical consequences in patients with liver diseases, including an increased risk of oral pathologies that may themselves exacerbate gustatory dysfunction. However, it should be emphasized that this hypothesis requires confirmation by further studies specifically targeting this patient population. Oral health itself emerges as a key factor. Periodontitis and halitosis, as noted in epidemiological studies, may influence taste perception through local inflammatory mechanisms and altered saliva composition (32). The bidirectional association between periodontal disease and liver dysfunction provides further support for the role of oral health in modulating gustation in this population. In our review, most recent studies on MASLD and NAFLD highlighted the frequent coexistence of taste disturbances with oral dryness and mucosal inflammation, indicating that oral pathology is not only a comorbidity but also a potential mediator of altered taste perception, thereby reinforcing the hypothesis proposed earlier (15, 30).

Another dimension of taste impairment in liver disease relates to pharmacological treatment. Interferon-based regimens, as well as antiviral therapies with boceprevir, have consistently been associated with dysgeusia, often described as metallic or bitter sensations (24–26). These alterations, although usually reversible, may significantly impact appetite and adherence to therapy. Likewise, antimicrobial treatments such as metronidazole frequently induce metallic taste, whereas newer agents like satranidazole or tinidazole appear to have a more favorable profile (53, 54). Beyond these adverse effects, recent data have suggested a more complex role of pharmacotherapy, particularly with GLP-1 receptor agonists. Originally developed for diabetes and now increasingly used in MASLD, these drugs not only improve metabolic outcomes, but also interact with gustatory nerve pathway receptors, enhancing sweet sensitivity. This newly recognized mechanism of action requires further investigation; however, it offers promising potential in the treatment of taste disturbances that may contribute to the development of MASLD.

Importantly, our synthesis reveals that the majority of studies investigating taste disturbances in liver disease are outdated, limited in sample size, and often restricted to viral hepatitis or alcoholic liver disease. Only a few recent observational studies have assessed dysgeusia in MASLD, despite it being the most common chronic liver disease worldwide. The reported prevalence of dysgeusia in MASLD ranged from 7% in compensated to nearly 60% in decompensated stages, underlining the strong relationship between disease severity and gustatory dysfunction (15). However, heterogeneity in testing methods and the lack of standardized taste assessment protocols remain major obstacles to drawing firm conclusions.

The interpretation of our findings is limited by several important factors. Firstly, a considerable proportion of the cited literature was published decades ago and focused primarily on viral liver diseases. This restricts the applicability of conclusions to the current epidemiology of MASLD and modern therapeutic strategies. Secondly, numerous studies relied on small patient cohorts or single-case descriptions, which increases the risk of bias and limits generalizability. Thirdly, methodological heterogeneity – including variability in tools and protocols used to assess taste perception – complicates reliable comparisons across studies and synthesis of evidence. In addition, there is a lack of long-term prospective and interventional data, particularly the data regarding the impact of supplementation or emerging treatments, such as GLP-1 receptor agonists on gustatory function in liver disease.

Given the high prevalence of MASLD and cirrhosis worldwide, and the demonstrated connection between gustatory alterations, nutritional status, and disease outcomes including oral health, there is an urgent need for further research. Future studies should employ standardized and validated methods for assessing taste disturbances, include larger cohorts with longer follow-up, and cover different stages of liver disease. In-depth investigation of molecular mechanisms underlying taste alterations, including the role of GLP-1 receptors and other metabolic mediators, is also warranted. Finally, the comprehensive impact of nutrient deficiencies and medications used in liver disease therapy on taste perception should be systematically evaluated.

Conclusions

Taste disturbances are under-recognized in hepatology. Taste perception modulated by pharmacological treatments, oral health and nutritional status, plays a crucial role in appetite regulation and is significantly altered in patients with liver diseases. Zinc deficiency is the most studied nutritional factor contributing to altered taste perception. Taste modulators, including GLP-1 receptor agonists, by altering eating habits leading to weight loss, may prove beneficial in the treatment of MASLD. Addressing taste disorders may help combat malnutrition or obesity; improve the quality of life and prognosis in patients with liver diseases. Further research is needed.