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World J Hepatol. Jun 27, 2025; 17(6): 107931 Published online Jun 27, 2025. doi: 10.4254/wjh.v17.i6.107931
Dietary ω-3 polyunsaturated fatty acid intake improves skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease: A nationwide cross-sectional study
Li-Zhan Bie, Department of Cardiology, Affiliated Hospital 6 of Nantong University, Yancheng Third People’s Hospital, Yancheng 224000, Jiangsu Province, China
Chao Wu, Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200020, China
Jia-Lu Wang, Department of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai 200032, China
Author contributions: Wang JL and Bie LZ designed the study, analysis and interpretation, and were primarily responsible for drafting and revising the manuscript; Wang JL, Wu C and Bie LZ were responsible for statistical analysis and methodology; Bie LZ and Wu C were deeply involved in data analysis and interpretation; Wang JL providing significant review and editing contributions. All authors were involved in data interpretation, reviewed the manuscript, and approved the final version.
Supported by The National Natural Science Foundation of China, No. 82103356.
Institutional review board statement: This study was approved by the National Center for Health Statistic Ethics Review Board.
Informed consent statement: This study was approved by the National Center for Health Statistic Ethics Review Board.
Conflict-of-interest statement: The authors declare no conflict of interest.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement- checklist of items.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Received: March 31, 2025 Revised: April 22, 2025 Accepted: June 4, 2025 Published online: June 27, 2025 Processing time: 86 Days and 0.5 Hours
Abstract
BACKGROUND
Improving our understanding of whether increased dietary intake of ω-3 polyunsaturated fatty acids (PUFAs) is beneficial for increasing skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease (MAFLD) could provide an important clinical evidence base for the development of relevant nutritional guidelines.
AIM
To investigate the effect of total dietary ω-3 PUFAs and their subtypes on skeletal muscle mass in MAFLD.
METHODS
This cross-sectional study involved 2316 participants from four National Health and Nutrition Examination Survey cycles between 2011 and 2018. Dietary intake of ω-3 PUFAs was collected through 24-hour dietary recall interviews. Appendicular skeletal muscle mass index (ASMI) was calculated by dividing ASM in kilograms by height squared.
RESULTS
The multiple linear regression model showed significant relationships for dietary intake of total ω-3 PUFAs with higher ASMI (β: 0.06, 95%CI: 0.01–0.11) in MAFLD patients. Dietary a-linolenic acid (ALA) (β: 0.06, 95%CI: 0.01–0.12), docosapentaenoic acid (β: 1.28, 95%CI: 0.01–2.54), and docosahexaenoic acid (DHA) (β: 0.19, 95%CI: 0.01–0.37) were significantly associated with higher ASMI, while intake of stearidonic acid and eicosapentaenoic acid did not improve ASMI. In patients with high probability of liver fibrosis, dietary intake of ALA was associated with higher ASMI (β: 0.11, 95%CI: 0.03–0.18). Stratified analysis found that DHA was associated with higher ASMI in patients with obesity and higher metabolic risk.
CONCLUSION
Increasing dietary intake of ω-3 PUFAs improved skeletal muscle health in patients with MAFLD. Patient with obesity and higher metabolic risk were more likely to benefit from intake of DHA.
Core Tip: This study found that dietary intake of ω-3 polyunsaturated fatty acids improved skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease, and patients with obesity and higher metabolic risk were more likely to benefit from supplementation with docosahexaenoic acid. These results fill a gap in muscle nutrient metabolism in patients with fatty liver disease.
Citation: Bie LZ, Wu C, Wang JL. Dietary ω-3 polyunsaturated fatty acid intake improves skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease: A nationwide cross-sectional study. World J Hepatol 2025; 17(6): 107931
Metabolic dysfunction-associated fatty liver disease (MAFLD) is the name proposed by an international panel of experts in 2020 that is more suitable for describing liver disease associated with metabolic dysfunction, replacing the existing non-alcoholic fatty liver disease (NAFLD)[1]. The new terminology is thought to better reflect the strong link between fatty liver diseases and metabolic diseases such as type 2 diabetes, obesity and dyslipidemia. The global prevalence of MAFLD is about 30% of the general population, placing a huge global economic and public health burden[2].
In recent years, an increasing number of studies have shown that lifestyle factors such as unhealthy diet, physical inactivity and reduced skeletal muscle mass are important risk factors for the development of MAFLD. Reduced skeletal muscle mass is not only an important early risk factor for MAFLD, but also an adverse outcome of abnormal fat distribution in MAFLD. A meta-analysis conducted by Cai et al[3] noted that patients with MAFLD had significantly lower muscle mass than healthy subjects had. Nutrient deficiencies have been found to be part of the common underlying pathogenesis of MAFLD and sarcopenia[4], and nutrition is thought to play a crucial role in lipid muscle metabolism. A cross-sectional study investigating the association between nutrient intake and sarcopenia found that participants with adequate daily total energy and protein intake had a significantly lower risk of developing sarcopenia compared with those with inadequate intake[5]. Malnutrition reduces muscle protein synthesis and is a major cause and predictor of the onset and progression of sarcopenia. Addressing malnutrition is a critical intervention to improve skeletal muscle mass[6-8].
ω-3 polyunsaturated fatty acids (PUFAs) have been shown to be critical to human health, and increased intake may reduce the risk of cardiovascular disease[9,10]. Recently, increasing attention has focused on the association between ω-3 PUFA intake and skeletal muscle disease, and the roles of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in muscle health remain unclear[11]. Several clinical intervention studies have revealed that EPA and DHA are key supportive nutrients for skeletal muscle health in specific populations, such as older adults and subjects with low skeletal muscle mass[12,13], whereas some studies have reported no benefits of ω-3 PUFAs for skeletal muscle health[14]. In view of this, it is unclear whether and by how much dietary ω-3 PUFA intake increases skeletal muscle mass in subjects with MAFLD. There is currently no consensus on nutritional recommendations for dietary intake of ω-3 PUFAs to promote skeletal muscle health. To this end, using data from National Health and Nutrition Examination Survey (NHANES) 2011–2018, we investigated the effect of dietary intake of ω-3 PUFAs on skeletal muscle mass in patients with MAFLD to provide dietary nutrition guidance for patients with MAFLD combined with reduced skeletal muscle mass.
MATERIALS AND METHODS
Data source and study population
NHANES is a comprehensive cross-sectional survey conducted by the National Center for Health Statistics to provide statistical data on population health and nutrition issues. More detailed information can be found at www.cdc.gov/nchs/nhanes/irba98.htm. The NHANES protocol was approved by the National Research Ethics Committee on Health Statistics with signed consent forms. We followed the guidelines for the use of research data, ensuring that the data were only used for statistical analysis and that all experiments followed current standards and protocols. We extracted data from four NHANES cycles from 2011 to 2018 (2011–2012, 2013–2014, 2015–2016 and 2017–2018), which included 39156 participants. We excluded 6363 participants with missing data on dietary intake of ω-3 PUFAs; 15978 participants with missing data on dual-energy X-ray absorptiometry (DXA); and 6242 participants with missing data on diagnosis of fatty liver. We further excluded 7559 participants without fatty liver disease, and 698 with missing data on covariates. Finally, 2316 subjects were left in the current analysis (Figure 1).
Figure 1 Flowchart of study design and exclusion criteria for adults from National Health and Nutrition Examination Survey 2011–2018.
NHANES: National Health and Nutrition Examination Survey; PUFAs: Polyunsaturated fatty acids; MAFLD: Metabolic-dysfunction-associated fatty liver disease; FLI: Fatty liver index; BMI: Body mass index; ASMI: Appendicular skeletal muscle mass index.
Dietary assessment of ω-3 PUFAs
Daily intake of ω-3 PUFAs was obtained from the average of two 24-hour dietary recalls. The first recall was conducted face-to-face at the Mobile Examination Center, while the second recall was obtained via telephone 3–10 d afterwards. A total of five types of ω-3 PUFAs were collected, namely a-linolenic acid (ALA, 18:3), stearidonic acid (SDA, 18:4), EPA (20:5), docosapentaenoic acid (DPA, 22:5) and DHA (22:6). As well as calculating the total daily intake of ω-3 PUFAs, the average daily intake of each of the five ω-3 PUFAs was calculated separately.
Measurement of appendicular skeletal muscle mass index
DXA scan was carried out to collect the bone and soft tissue measurements of the entire body. Appendicular skeletal muscle mass (ASM) was defined as the sum of lean muscle mass in both arms and legs. ASM index (ASMI) (kg/m2) was calculated by dividing the ASM by the height squared.
Assessment of MAFLD and fibrosis evaluated by noninvasive markers
Fatty liver was diagnosed by a previously validated fatty liver index (FLI) with the following formula: FLI = ey/(1 + ey) × 100, where y = 0.953 × loge (triglycerides) + 0.139 × body mass index (BMI) + 0.718 × loge (γ-glutamyl transpeptidase) + 0.053 × waist circumference - 15.745.
According to the definition of the international expert consensus statement[1], MAFLD was diagnosed through the above formula in combination with the presence of any of the following three conditions: Overweight/obesity, diabetes or metabolic dysregulation. Metabolic dysregulation was defined as the presence of two or more of the following risk factors for metabolic abnormalities: (1) Waist circumference ≥ 90 cm in men and ≥ 80 cm in women; (2) Blood pressure ≥ 130/85 mmHg or specific medical treatment; (3) Triglycerides ≥ 1.70 mmol/L or specific medical treatment; (4) High density lipoprotein cholesterol < 1.0 mmol/L for men and < 1.3 mmol/L for women or specific medical treatment; (5) Prediabetes (fasting plasma glucose 5.6–6.9 mmol/L, or 2-hour plasma glucose 7.8–11.0 mmol or glycated hemoglobin A1c 5.7%–6.4%); and (6) Homeostatic model assessment of insulin resistance index ≥ 2.5.
NAFLD fibrosis score (NFS) was applied to evaluate the severity of fibrosis and a higher probability of fibrosis was defined as NFS ≥ −1.455. The NFS score was calculated according to the published formula: NFS = −1.675 + 0.037 × age (years) + 0.094 × BMI (kg/m2) + 1.13 × impaired fasting glucose or diabetes (yes = 1, no = 0) + 0.99 × aspartate aminotransferase / alanine transaminase ratio − 0.013 × platelet count (× 109/L) − 0.66 × albumin (g/dL)[15]. The missing NFS value is replaced by the mean value.
Covariates
Demographic variables were collected by in-person interview, including age, sex, race and survey cycles. Socioeconomic status included education level, marital status (married or living with partner; divorced, separated, or widowed; never married) and family income to poverty ratio (PIR) (low income, PIR ≤ 1.3; middle income, 1.3 < PIR < 3.5; high income, PIR ≥ 3.5). BMI was calculated.
Statistical analysis
All analyses used examination sample weights, encompassing those who participated in an examination in a mobile examination center. As there were four consecutive cycles of NHANES, the 2-year sample weights divided by four were used to ensure representativeness of the population. We described continuous variables by means with 95%CI or medians (25% quartile-75% quartile), and categorical variables by frequencies with weighted percentages. We used analysis of variance to compare continuous values and adjusted χ2 tests to compare categorical variables grouped in different sex groups.
Weighted multiple linear regression was used to evaluate relationship (β and 95%CI) between different dietary ω-3 PUFA intake and ASMI. Model 1 was unadjusted, while model 2 was adjusted for age, sex and BMI. Model 3 was further adjusted for race and ethnicity, education status, marital status, PIR, current smoker and current drinker.
We further evaluated the association between dietary ω-3 PUFAs intake and ASMI according to the probability of liver fibrosis. As mentioned above, NFS was used to assess the probability of liver fibrosis. Additionally, stratified analyses were performed in subgroups of subtypes of MAFLD, such as obesity (BMI ≥ 30), more than two metabolic risk factors, diabetes and hypertension. All statistical analyses were performed using R 4.3.3 (http://www.r-project.org/) and SAS version 9.4 (SAS Institute Inc., Cary, North Carolina). All analyses were two-sided and P < 0.05 was considered statistically significant.
RESULTS
Study population
The study included 2316 participants with MAFLD aged ≥ 20 years and < 60 years, and their baseline characteristics are shown in Table 1. The average age of participant was 40.5 ± 11.0 years, and 53% were male. The ASMI of the total study participants was 9.1 ± 1.6 kg/m2 and the ω-3 PUFA daily intake was 1.9 ± 1.2 g. We further divided the study participants into two groups by sex. The male participants exhibited older age, higher financial income, lower BMI and a greater prevalence of hypertension. There were notable disparities in ethnic distribution based on gender. Additionally, male participants had higher ASMI and consumed more daily ω-3 PUFAs compared to females. Table 2 shows the dietary intake of different ω-3 PUFAs, and male participants had higher intakes of each of the PUFAs than females had.
Table 1 Baseline characteristics of adults by gender from National Health and Nutrition Examination Survey 2011–2018, n (%)/mean ± SD.
Association between dietary ω-3 PUFA intake and ASMI
The association between dietary ω-3 PUFA intake and ASMI are presented in Table 3. Univariate linear regression analysis found a linear association between ω-3 PUFA intake and ASMI (β: 0.19, 95%CI: 0.11–0.27). After adjusting for potential confounders, this linear association remained significant (β: 0.06, 95%CI: 0.01–0.11). A daily intake of 1 g ω-3 PUFAs increased ASMI by about 0.06 kg/m2. We further analyzed the correlation between different ω-3 PUFA components and ASMI. After adjusting for potential confounders, intake of ALA (β: 0.06, 95%CI: 0.01–0.12), DPA (β: 1.28, 95%CI: 0.01-2.54) and DHA (β: 0.19, 95%CI: 0.01–0.37) significantly improved ASMI, while intake of SDA and EPA did not.
Table 3 Relationship between different ω-3 polyunsaturated fatty acids intake and appendicular skeletal muscle mass index from National Health and Nutrition Examination Survey 2011-2018 using weighted multiple linear regression analyses1.
Model 1, β (95%CI)
Model 2, β (95%CI)
Model 3, β (95%CI)
ω-3 PUFAs (n = 2316)
0.19 (0.11, 0.27)
0.07 (0.02, 0.12)
0.06 (0.01, 0.11)
ALA, 18:3 (n = 2316)
0.19 (0.11, 0.28)
0.07 (0.01, 0.12)
0.06 (0.01, 0.12)
SDA, 18:4 (n = 1720)
1.40 (-0.23, 3.10)
0.63 (-0.57, 1.83)
0.53 (-0.69, 1.80)
EPA, 20:5 (n = 2252)
0.49 (-0.34, 1.32)
0.20 (-0.50, 0.90)
0.12 (-0.56, 0.80)
DPA, 22:5 (n = 2278)
4.13 (0.94, 7.41)
1.50 (0.27, 2.73)
1.28 (0.01, 2.54)
DHA, 22:6 (n = 2225)
0.32 (0.04, 0.61)
0.23 (0.05, 0.41)
0.19 (0.01, 0.37)
We classified the risk of liver fibrosis according to NFS in patients with MAFLD into high and low probability fibrosis groups. Intake of ω-3 PUFAs improved ASMI in the group with higher probability of fibrosis (β: 0.11, 95%CI: 0.03–0.18) (Table 4). After adjusting for potential confounders, a daily intake of 1 g ALA increased ASMI by about 0.11 kg/m2. However, such associations were not noted in the low probability fibrosis group.
Table 4 Relationship between different ω-3 polyunsaturated fatty acids intake and appendicular skeletal muscle mass index in different probability of advanced liver fibrosis from National Health and Nutrition Examination Survey 2011–2018 using weighted multiple linear regression analyses.
Model 1 β (95%CI)
Model 2 β (95%CI)
Model 3 β (95%CI)
NFS ≥ 1.455 (n = 975)
ω-3 PUFAs
0.28 (0.15, 0.41)
0.16 (0.07, 0.24)
0.11 (0.03, 0.18)
ALA, 18:3
0.29 (0.15, 0.43)
0.17 (0.08, 0.26)
0.11 (0.03, 0.18)
SDA, 18:4
0.87 (-2.30, 4.10)
0.61 (-1.60, 2.80)
0.74 (-1.10, 2.60)
EPA, 20:5
0.85 (-1.10, 2.80)
0.45 (-0.92, 1.80)
0.63 (-0.82, 2.10)
DPA, 22:5
3.50 (-0.31, 7.20)
1.50 (-0.21, 3.10)
1.60 (-0.44, 3.60)
DHA, 22:6
0.33 (-0.02, 0.68)
0.18 (-0.03, 0.39)
0.12 (-0.01, 0.53)
NFS < 1.455 (n = 1341)
ω-3 PUFAs
0.15 (0.07, 0.24)
0.02 (-0.04, 0.08)
0.01 (-0.04, 0.07)
ALA, 18:3
0.14 (0.05, 0.23)
0.01 (-0.05, 0.07)
0.01 (-0.06, 0.07)
SDA, 18:4
2.20 (0.16, 4.30)
1.20 (-0.62, 3.10)
0.60 (-1.10, 2.30)
EPA, 20:5
0.39 (-0.47, 1.20)
0.23 (-0.86, 1.30)
0.08 (-0.61, 0.77)
DPA, 22:5
5.50 (1.10, 9.80)
1.60 (-0.49, 3.70)
1.50 (-0.75, 3.80)
DHA, 22:6
0.32 (-0.16, 0.79)
0.26 (-0.04, 0.56)
0.19 (-0.06, 0.44)
Figure 2 presents the effect of dietary ω-3 PUFAs (PUFAs, ALA, DPA and DHA) on ASMI in different metabolic abnormalities subgroups. In stratification of BMI ≥ 30 kg/m2, intake of total ω-3 PUFAs (β: 0.06, 95%CI: 0.01– 0.11), ALA (β: 0.06, 95%CI: 0.01– 0.12) and DHA (β: 0.59, 95%CI: 0.02–1.20) improved ASMI significantly. In the higher metabolic risk factors group (≥ 2), only DHA was associated with higher ASMI (β: 0.48, 95%CI: 0.10–0.86). However, we did not find that ω-3 PUFAs increased ASMI in the diabetes group. In contrast, we found that total ω-3 PUFAs (β: 0.07, 95%CI: 0.01–0.12), ALA (β: 0.06, 95%CI: 0.01–0.11), DPA (β: 4.40, 95%CI: 1.90–7.0) and DHA (β: 0.53, 95%CI: 0.12–0.95) intake was associated with higher ASMI in the nondiabetic group.
Figure 2 Association between dietary ω-3 polyunsaturated fatty acids intake and appendicular skeletal muscle mass index was stratified by body mass index, metabolic risk factors, diabetes status and hypertension status for adults from National Health and Nutrition Examination Survey 2011–2018. Adjusted for age, sex, body mass index race and ethnicity, education status, marital status, income to poverty ratio, current smoker and current drinker.aThe correlation results were statistically significant. PUFAs: Polyunsaturated fatty acids; ASMI: Appendicular skeletal muscle mass index; ALA: α-Linolenic acid; DPA: Docosapentaenoic acid; DHA: Docosahexaenoic acid; BMI: Body mass index; PIR: Income to poverty ratio.
DISCUSSION
In this United States nationwide cross-sectional population-based study of 2316 participants, we found that dietary intake of ω-3 PUFAs and their subtypes (ALA, DPA and DHA) was significantly associated with higher ASMI in individuals diagnosed with MAFLD. ALA was only observed to be effective in increasing ASMI in individuals with high probability of liver fibrosis. In analyses stratified according to the classification of MAFLD subgroups, DPA and DHA were significantly associated with higher ASMI in the nondiabetic MAFLD population. These findings highlight the critical role of ω-3 PUFAs in the improvement of ASMI and further identify the importance of specific subtypes in certain populations, providing an important basis for individualized nutritional management of MAFLD.
MAFLD, formerly known as NAFLD, is caused by excessive accumulation of fat in > 5% of hepatocytes and may lead to a range of liver pathologies including simple steatosis, metabolic dysfunction-associated steatohepatitis, liver fibrosis, cirrhosis and hepatocellular carcinoma[16]. It is worth noting that the definitions of fatty liver disease, such as MAFLD and metabolic dysfunction-associated steatotic liver disease (MASLD), are being more widely researched. MASLD is a new concept proposed by Kim et al[17] in 2023. It is intended to replace NAFLD and MAFLD. At present, the definition of NAFLD really does lag behind clinicians' and researchers' understanding of the disease. However, there are many different opinions as to whether MAFLD or MASLD is an accurate definition of fatty liver disease, and there is no definitive answer[18]. It is generally accepted that the "exclusion of excessive alcohol intake" should be removed. It is also recognized that metabolic dysfunction is a central factor in the diagnosis of fatty liver disease. The new definition of MAFLD emphasizes the importance of cardiovascular–metabolic risk factors.
In recent years, research focusing on the potential role of ω-3 PUFAs in skeletal muscle health has been ongoing. Previous studies have demonstrated that ω-3 PUFAs could protect mitochondrial function in several organs or tissues, such as the brain, liver, and skeletal muscle[19]. Skeletal muscle mitochondrial dysfunction has been implicated in the pathogenesis of many diseases, including aging-related sarcopenia[20]. Reactive oxygen species are products of normal oxygen metabolism within the mitochondrial matrix. It has been found that with aging or other factors, the production of reactive oxygen species exceeds the scavenging capacity of the intracellular antioxidant system, contributing to oxidative damage to mitochondrial structure and function, whereas EPA and DHA could mitigate oxidative damage to skeletal muscle by balancing the production and scavenging capacity of reactive oxygen species[21,22]. However, debate remains about the role of ω-3 PUFAs in the development of skeletal muscle mass[23]. A study conducted in Korea using Korea National Health and Nutrition Examination Survey database reported that EPA and DHA intake was inversely associated with low lean body mass and positively correlated with muscle mass among older Korean women[24]. Conversely, another study based on NHANES 2011–2012 data found no significant relationship between ω-3 PUFAs and their subtypes with skeletal muscle mass in young and middle-aged populations[25]. In this study, we focused on patients with MAFLD and identified that augmentation of ω-3 PUFA intake was significantly associated with higher ASMI. In further subgroup analyses of ω-3 PUFAs, we found that ALA, DPA and DHA played an important role. w-3 PUFAs belong to the family of essential fatty acids that are involved in the mediation of numerous biological processes. w-3 PUFAs have been found to have anti-inflammatory properties and to enhance the fluidity of muscle cell membranes, which facilitates amino acid uptake and consequently increases muscle protein synthesis, independent of age[26,27]. Supplementation with ω-3 PUFAs has been demonstrated to reduce liver fat accumulation and liver enzyme levels, improve insulin sensitivity and diminish inflammation and fibrosis[28]. However, no studies have specifically examined the impact of ω-3 PUFAs on skeletal muscle mass in patients with MAFLD. A review of current research suggests that MAFLD and skeletal muscle health are mutually reinforcing. Some studies have found that a reduction in skeletal muscle mass may contribute to the progression of MAFLD[29,30]. In this context, our study adds to the gap of ω-3 PUFAs in the field of skeletal muscle health in MAFLD, finding that consuming more ω-3 PUFAs in the diet improves skeletal muscle mass in patients with MAFLD.
We specifically observed an important role for DPA in promoting skeletal muscle health; a nutrient that has often been overlooked in previous studies. DPA is closely related to other common ω-3 PUFAs such as EPA and DHA. An early study by Kaur et al[29] found that short-term supplementation with DPA resulted in increased blood levels of EPA, DHA and DPA, suggesting that DPA can be optimally absorbed and converted to EPA or DHA. Due to the difficulty in obtaining pure DPA, few studies have been conducted to systematically investigate its function.
Considering that reduced skeletal muscle mass in MAFLD is significantly associated with an increased risk of advanced liver fibrosis[31], this study aimed to investigate whether the subtypes of ω-3 fatty PUFAs could improve skeletal muscle mass in patients with liver fibrosis. We found that only ALA was associated with higher ASMI in the group with a high probability of liver fibrosis. This finding may be due to the essential role of ALA, as the major component of ω-3 PUFAs, in increasing mitochondrial oxidative capacity and protein synthesis, while reducing protein degradation, thereby reducing inflammation and improving insulin sensitivity[32].
We also investigated the associations of ω-3 PUFAs and their subtypes with ASMI based on MAFLD subgroup classifications. Our study found that DHA supplementation in MAFLD improved ASMI in obese and higher metabolic risk individuals. The mechanism by which DHA improves skeletal muscle mass remains unclear. Studies have shown that DHA supplementation in rats can improve muscle mitochondrial function, increase muscle oxygen consumption and improve muscle endurance capacity[33]. DHA can delay muscle wasting by inhibiting proteasomes[34]. Our study demonstrated the important role of DHA in increasing skeletal muscle mass in obese or metabolically impaired American adults with MAFLD, providing a new idea to prevent early muscle loss in such individuals.
The main strengths of our study were the use of data from NHANES (a large national survey), which was used for the first time to show the relationship between ω-3 PUFAs and ASMI and to ensure that the results were representative. Secondly, we present beneficial subtypes of ω-3 PUFAs in different metabolic risk populations. However, we also recognize some limitations. First, our study was conducted as a cross-sectional analysis from NHANES 2011–2018 and could not explain the causal relationship between ω-3 PUFAs and ASMI. Therefore, further prospective studies are needed. Second, the data on ω-3 PUFA intake were obtained using a 24-h dietary recall questionnaire, which may be subject to recall bias. However, questionnaires are still considered the mainstay of established surveys. Third, high-sensitivity C-reactive protein was not included in the definition of MAFLD in our study.
CONCLUSION
In this cross-sectional study of American adults, we observed that higher intake of ω-3 PUFAs was associated with higher ASMI in adults with MAFLD. More importantly, ALA was found to increase ASMI in subjects with a high likelihood of liver fibrosis, while DHA was found to increase ASMI in those with obesity or metabolic dysfunction. These findings highlight the importance of dietary intake of ω-3 PUFAs for skeletal muscle health in people with liver disease. The results suggest that increasing dietary intake of ω-3 PUFAs will have a significant public health and clinical impact, with major implications for the management of muscle-skeletal health across the lifespan.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Gastroenterology and hepatology
Country of origin: China
Peer-review report’s classification
Scientific Quality: Grade B
Novelty: Grade A
Creativity or Innovation: Grade B
Scientific Significance: Grade A
P-Reviewer: Avudaiappan AP S-Editor: Liu H L-Editor: A P-Editor: Zhao YQ
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