Metabolic dysfunction-associated steatotic liver disease (MASLD), which was previously called non-alcoholic fatty liver disease (NAFLD), is a significant global public health problem due to its relationship with obesity, insulin resistance, type 2 diabetes mellitus, dyslipidaemia, and cardiovascular disease.[1] MASLD is diagnosed as liver fat accumulation in the absence of alcohol abuse and with at least one cardiometabolic risk factor.[2] It can manifest as simple hepatic steatosis, metabolic dysfunction-associated steatohepatitis (MASH), advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC).[3] According to global estimates, MASLD is seen in around 30% of the adult population, but with variable prevalence in different geographical regions and populations.[4]

Sarcopenic obesity is an emerging body composition disorder defined as a combination of excess adiposity and decreased skeletal muscle mass and function.[5] Sarcopenic obesity differs from the typical obesity assessment, which is mainly based on body mass index (BMI); it is an unfavorable combination of increased fat accumulation and diminished muscular health.[5] Skeletal muscle is an important site for glucose disposal and insulin sensitivity, energy expenditure, and whole-body metabolic regulation.[6] Therefore, the loss of muscle mass and function in individuals with excess adiposity may intensify insulin resistance, chronic low-grade inflammation, and metabolic dysfunction.[7] These mechanisms may play a role in the deposition of fat within liver tissue and the development of liver injury.[7, 8]

Evidence increasingly supports an association between skeletal muscle abnormalities and MASLD. A systematic review and meta-analysis published in 2024 that included 29 studies and 63,330 participants found a pooled prevalence of 23.5% of sarcopenia in patients with MASLD. Moreover, significantly higher odds of MASLD were observed with sarcopenia (adjusted OR: 2.08, 95% CI: 1.58–2.74). Moreover, sarcopenia was linked to higher overall mortality rates in patients with MASLD, suggesting that muscle health decline may be of prognostic importance.[9]  A recent systematic review and meta-analysis of 13 studies found that 63.4% of people with sarcopenic obesity had MASLD. Compared with individuals without sarcopenic obesity, those with this phenotype had higher odds of MASLD (odds ratio: 4.45, 95% CI: 2.57–7.72) and MASLD-related fibrosis (OR: 2.34, 95% CI: 1.78–3.08).[10]

Although these discoveries have surfaced, a major clinical question is whether sarcopenic obesity is linked not only with having MASLD, but with the severity of the condition. There are different disease burden components, including hepatic steatosis, steatohepatitis and liver fibrosis, which can be different and may not be consistent across muscle depletion and excess adiposity. Furthermore, most of what is known about MASLD has been on the presence or absence of this disease, but not on a systematic approach to comparing the severity of disease between sarcopenic obesity and non-sarcopenic obesity patients. There is also variation in the definition of different kinds of diagnostics, and limited representation of diverse populations further underscores the need for context-specific clinical evidence. Thus, the present study hypothesizes that the severity of MASLD is associated with sarcopenic obesity. This study could help determine if sarcopenic obesity is a higher-risk phenotype and help guide the incorporation of body-composition assessments into the workup of patients with MASLD. The present study aimed to determine the association between sarcopenic obesity and MASLD severity.

A hospital-based analytical cross-sectional study was conducted in the Department of Medicine, Faryal Dental College, Sheikhupura, Pakistan, over six months, from 1 August 2025 to 31 January 2026. The sample size was calculated using the OpenEpi online calculator for a single population proportion based on a prevalence of 23.5% for sarcopenia among patients with MASLD, a 95% confidence interval, and an absolute precision of 8%, the minimum required sample size was 120 patients.[11] A non-probability consecutive sampling technique was used. Patients aged ≥18 who had been diagnosed with MASLD based on hepatic steatosis (as evidenced by ultrasonography or another imaging modality accepted by the authors) and had at least one cardiometabolic risk factor were included. Patients of both sexes who were willing to participate and were informed consenters were included. Participants had to have clinical and anthropometric data that allowed for the assessment of sarcopenic obesity and severity of MASLD. Patients with other known liver diseases, such as chronic viral hepatitis and significant alcohol intake, were excluded. Patients who had other conditions associated with secondary muscle wasting, such as active malignancy, advanced neuromuscular disease, or other serious illnesses, were excluded. Patients with severe fluid retention, such as heavy ascites and/or peripheral edema, which may significantly affect body-composition measurements, were also excluded. Further, patients who did not have complete clinical records or were unable to complete the anthropometric and muscle-function evaluations were excluded. Eligible patients who consented to participate in the study on a written informed consent form were enrolled after approval from the IRB of the relevant institutions. A structured proforma was used to collect data. Demographic data such as age and sex, as well as clinical data such as the duration of diabetes mellitus, hypertension, dyslipidaemia, medication use, and other metabolic risk factors were collected. Standardized procedures were used to collect anthropometric data (height, weight, body mass index [BMI] and waist circumference). Blood pressure was recorded using a suitable clinical instrument, and relevant laboratory parameters such as fasting blood glucose, glycated haemoglobin (HbA1c), lipid profile, liver enzymes, and platelets were obtained from clinical assessment or investigations carried out as part of routine health care. MASLD was recognized when liver steatosis was evident on ultrasound or any other accepted imaging technique, and the patient had cardiometabolic risk factors. MRI-based imaging was used to classify the severity of hepatic steatosis, based on the prespecified imaging criteria. If ultrasonography was used, patients were categorized into mild, moderate, and severe steatosis according to the reported hepatic echogenicity and visualization of intrahepatic structures. If available, liver stiffness measurements or validated non-invasive fibrosis scores could also be noted to assess fibrosis risk. Steatosis grade and fibrosis stage were considered as independent endpoints and not as synonyms of the severity of the disease. Sarcopenic obesity was defined using pre-established criteria that include excess adiposity and skeletal muscle impairment.[12] Body composition was measured by a validated technique, DEXA.[13] To measure muscular strength, a handgrip dynamometer was used, and to measure the quantity of muscle, the selected body-composition method was used. Prespecified thresholds of body fat and/or anthropometric measurements were used for obesity classification, and the consensus-based definition was used for classifying sarcopenia. Participants who fell into both categories of obesity and sarcopenia were considered to have sarcopenic obesity. Patients were then divided into the sarcopenic obesity and non-sarcopenic obesity groups, and the distribution of severity of MASLD was compared between the two groups. Data collected were analyzed using IBM SPSS Statistics 26.0. Shapiro–Wilk test was used to test all continuous variables for normality. Data presented as normally distributed variables were shown as mean ± standard deviation, while data for non-normally distributed variables were shown as median and interquartile range. The frequencies and percentages of categorical variables such as sex, diabetes mellitus, hypertension, sarcopenic obesity status, and MASLD severity categories were summarized. The association between sarcopenic obesity and MASLD severity was assessed using the chi-square test. An independent-samples t-test was performed for normally distributed continuous variables between patient and non-patient groups of sarcopenic obesity, and the Mann–Whitney U test was performed for non-normally distributed continuous variables. When severity of MASLD was treated as an ordinal outcome, an appropriate ordinal logistic regression model was considered if its assumptions were met. After controlling for potential confounding factors such as age, sex, diabetes mellitus, and other metabolic risk factors, multivariable regression analysis was performed to determine the independent association between sarcopenic obesity and MASLD severity. The 95% confidence intervals were reported for effect estimates. The significance value used was P < 0.05

In total, 120 patients were included in the study, whose mean age was 47.1 ± 11.2 years, with a diagnosis of MASLD. Most participants were aged 40–59 years (55.0%), and 52.5% were male. Among the participants, 45.0% had type 2 diabetes mellitus, 55.0% had dyslipidemia, and 35.0% had hypertension. The mean duration of MASLD was 3.2 ± 2.1 years (Table 1).

The incidence of sarcopenic obesity was 30.0% (36 participants), and 70.0% (84 participants) did not meet the criteria. Sarcopenic obesity participants had a significantly increased BMI, waist circumference, body fat percentage, and systolic blood pressure, and decreased skeletal muscle mass and handgrip strength when compared to non-Sarcopenic obesity participants. The difference in diastolic blood pressure was not statistically significant (Table 2).

The biochemical profile presented less favorable metabolic parameters in sarcopenic obesity participants. Fasting blood glucose, HbA1c, total cholesterol, triglycerides, LDL cholesterol, ALT, and AST were higher, whereas HDL cholesterol was lower in this group. The platelet count difference was not significant (Table 3).

The prevalence of the different severity grades of MASLD varied significantly between the different sarcopenia obesity groups (χ² = 13.02, p = 0.0015). Sarcopenic obesity was associated with severe steatosis, and the absence of sarcopenic obesity was associated with mild steatosis. These results showed that there was a strong correlation between sarcopenic obesity and higher ultrasound-defined severity of steatosis (Table 4).

Sarcopenic obesity, T2DM, and dyslipidemia were significantly higher in participants with severe MASLD when compared to those with mild-to-moderate MASLD. The association was the same for older age, which was borderline significant, but not for the other factors, such as sex, hypertension, and HbA1c ≥ 7% in diabetics (Table 5).

Sarcopenic obesity remained significantly associated with severe MASLD in the multivariable logistic regression model (adjusted OR 3.25, 95% CI 1.24–8.51, p = 0.016) after adjustment for age, sex, diabetes mellitus, hypertension, and dyslipidemia. The relationships of age, sex, diabetes mellitus, hypertension, and dyslipidemia were not significant on adjustment (Table 6).

Table 1. Demographic and clinical characteristics of the study population (n = 120)

Table 2. Anthropometric and body-composition characteristics according to sarcopenic obesity status

Table 3. Biochemical and metabolic characteristics according to sarcopenic obesity status

Table 4. Distribution of MASLD severity according to sarcopenic obesity status

Table 5. Clinical and metabolic characteristics by severe versus mild/moderate MASLD

Table 6. Multivariable logistic regression for severe MASLD

The present study evaluated the association between sarcopenic obesity and metabolic dysfunction-associated steatotic liver disease (MASLD) severity among 120 patients. There was a significant relationship between sarcopenic obesity and a higher percentage of severe ultrasound-defined hepatic steatosis, as seen in 30.0% of participants. The association between sarcopenic obesity and severe steatosis was generally similar to that of Wijarnpreecha et al. (2021), who examined 1,925 individuals from the US National Health and Nutrition Examination Survey (NHANES). Using transient elastography, they reported that sarcopenic obesity was associated with higher odds of hepatic steatosis and significant liver fibrosis, including an adjusted odds ratio of 2.22 (95% CI: 1.03-4.80) for significant fibrosis.[14] Likewise, Song et al. (2023) investigated 2191 Korean adults and discovered that the occurrence of fatty liver disease and liver fibrosis rose with every category of body composition. Sarcopenic obesity showed higher odds of fatty liver disease compared with obesity or sarcopenia alone. The relevance of the assessment of muscle and adipose tissue together was supported by these studies, though the results varied from the degree of severity assessed by ultrasound in the present study, and the methods used differed from the present study.[15] Zhou et al. (2023) reported further evidence on 2,223 adults, using body-composition measurements, magnetic resonance imaging (MRI) based proton density fat fraction (PD-FF), and shear-wave elastography. They discovered that men with metabolic-associated fatty liver disease who had a lower skeletal muscle mass-to-weight ratio were linked to moderate to severe steatosis. The association was different depending on the method of assessment of muscle mass, emphasizing the need to choose the proper body-composition indices.[16] This is important for the present research because patients categorised into the sarcopenic obese group had lower skeletal muscle mass and higher adiposity. However, there is some difficulty in comparison due to the fact that the measurements are taken in different ways and ultrasound is used instead of quantitative imaging. In 2023, an NHANES-based study of 2,422 people also studied the relationship between sarcopenia and more advanced liver disease. The prevalence of significant fibrosis and advanced fibrosis was higher than that of people without fatty liver disease or sarcopenia. The authors found significant fibrosis in 18.3% of the patients with sarcopenic fatty liver disease and advanced fibrosis in 7.1% of them, while in patients without either condition there was significant fibrosis in 3.2% and advanced fibrosis in 0.2%. [17] The results here are compatible with a muscle-health/steatosis/fibrosis connection, but cannot be directly linked to the present finding of severe ultrasound-defined steatosis. Fat accumulation and fibrosis of the liver are two aspects of liver disease and should be considered independently. A related multicenter retrospective study by Kim and colleagues in 2023 examined 23,889 patients who had fatty liver disease and looked into risk stratification for patients with sarcopenic obesity. The study highlighted the need to identify people with additional fibrosis and cardiovascular risk, with 5.4% of participants showing signs of sarcopenic obesity.[18] This difference in prevalence rate from the 30.0% in our current study could be due to variations in population, selection, and definitions of sarcopenia and obesity. This explains the necessity of not comparing prevalence estimates without taking into account how body composition determination is classified. A systematic review and meta-analysis was performed by Malik et al. in 2024 that included 25 studies, finding that sarcopenia was more prevalent in MASLD cases than in controls. They also observed increased risk of liver fibrosis in MASLD patients with sarcopenia (OR 1.49, 95% CI: 1.03-2.14).[19] A cross-sectional NHANES study of 2,087 adults examined the association between skeletal muscle mass-to-visceral fat area ratio, a measure of sarcopenic obesity, and MASLD in that same year. These studies collectively suggest that the muscle-to-adipose ratio can offer further clues into metabolic liver disease.[20] Recent studies have further fueled interest in the connection between liver fibrosis and muscle health. Zhang et al. (2025) analyzed two cohorts comprising 821 patients from the United States and 3,405 from China. They found that, in both cohorts, sarcopenia correlated with significant fibrosis, advanced fibrosis and cirrhosis, assessed by transient elastography, which measures hepatic steatosis and liver stiffness. The decrease in the appendicular skeletal muscle mass index was also related to higher fibrosis risk.[21]These results were similar to the overall trend of the current study but were associated with fibrosis and not ultrasound (US) steatosis grade. They also do not indicate that sarcopenic obesity itself was responsible for the progression of liver disease. Xia et al. also conducted a systematic review and meta-analysis of studies published up to March 2024 to explore the link between MASLD and sarcopenia in 2025.[22] In 2025, an updated review was published that included 41 studies and 185,575 participants, with a pooled prevalence of sarcopenia of 23% in patients with fatty liver disease vs. 15% in controls. It also identified a relationship between sarcopenia and liver fibrosis.[23] The combined results offer stronger evidence for a relationship between lower muscle health and liver disease, yet there is significant heterogeneity in the diagnostic criteria and populations studied in these analyses, which restricts the applicability of the results to a given hospital-based study. Some particularly relevant evidence comes from a Middle Eastern population in the study by Elsabaawy et al. (2025). Sarcopenic visceral obesity was detected in 42.5% of 334 patients with MASLD, and was linked to poorer metabolic features and increased fibrosis risk. Multivariable analysis identified sarcopenic visceral obesity as being associated with fibrosis stage (OR 2.5, p = 0.002).[24] The metabolic difference in the current study is also worthy of consideration. Sarcopenic obese participants showed higher fasting glucose, HbA1c, triglycerides, LDL cholesterol, ALT, and AST levels, and lower HDL cholesterol levels. This pattern fits with the metabolic abnormalities seen with excess adiposity and decreased skeletal muscle health. The loss of skeletal muscle mass could be related to decreased glucose disposal and obesity with insulin resistance and lipid dysregulation. However, the cross-sectional design would not determine whether these abnormalities led to the onset of sarcopenic obesity, would exacerbate hepatic steatosis, or would occur simultaneously. The results presented should thus be considered as associations and not as evidence for a causal pathway. The proposed findings should be interpreted with a number of limitations in mind: The sample of 120 patients represents a small population from a single center and may not be generalizable. Selection bias can also creep in with consecutive sampling. Steatosis grading using ultrasound is not reliable for determining the stage of fibrosis or steatohepatitis and is operator-dependent. Moreover, the definition of sarcopenic obesity is influenced by the body composition approach and thresholds for muscle mass, muscle strength, and adiposity. Physical activity, dietary patterns, medication, and other metabolic factors might also account for the observed associations, as these factors may be residual or have not been measured. Lastly, the temporal relationship between sarcopenic obesity and severity of MASLD cannot be established using a cross-sectional study. Finally, the results indicate that sarcopenic obesity may have a significant relationship with the severity of ultrasound-defined MASLD and a negative metabolic profile. This interpretation aligns fairly well with observed associations of muscle dysfunction and excess adiposity with fatty liver disease. The importance and independence of these relationships, however, need to be verified with empirical study data. Additional studies that combine standardized measures of body composition and validated fibrosis markers will better elucidate the clinical implications of sarcopenic obesity among people with MASLD.

Sarcopenic obesity may represent an important body-composition phenotype associated with greater MASLD severity. The findings demonstrated a higher frequency of severe hepatic steatosis among patients with sarcopenic obesity, alongside less favorable metabolic characteristics. These observations highlight the potential value of assessing skeletal muscle health and adiposity together rather than relying exclusively on conventional anthropometric measures. Incorporating standardized body-composition assessment into MASLD evaluation may help identify patients who warrant closer metabolic and hepatic risk assessment.