Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with an increased risk of multisystemic complications, including muscle changes such as sarcopenia and myosteatosis that can reciprocally affect liver function. We conducted a systematic review to highlight innovative assessment tools, pathophysiological mechanisms and metabolic consequences related to myosteatosis in MASLD, based on original articles screened from PUBMED, EMBASE and COCHRANE databases. Forty-six original manuscripts (14 pre-clinical and 32 clinical studies) were included. Microscopy (8/14) and tissue lipid extraction (8/14) are the two main assessment techniques used to measure muscle lipid content in pre-clinical studies. In clinical studies, imaging is the most used assessment tool and included CT (14/32), MRI (12/32) and ultrasound (4/32). Assessed muscles varied across studies but mainly included paravertebral (4/14 in pre-clinical; 13/32 in clinical studies) and lower limb muscles (10/14 in preclinical; 13/32 in clinical studies). Myosteatosis is already highly prevalent in non-cirrhotic stages of MASLD and correlates with disease activity when using muscle density assessed by CT. Numerous pathophysiological mechanisms were found and included: high-fat and high-fructose diet, dysregulation in fatty acid transport and ketogenesis, endocrine disorders and impaired microRNA122 pathway signalling. In this review we also uncover several potential consequences of myosteatosis in MASLD, such as insulin resistance, MASLD progression from steatosis to metabolic steatohepatitis and loss of muscle strength. In conclusion, data on myosteatosis in MASLD are already available. Screening for myosteatosis could be highly relevant in the context of MASLD, considering its correlation with MASLD activity as well as its related consequences.

Background and aims: Lifestyle factors could influence the development of metabolic dysfunction–associated steatotic liver disease (MASLD). However, there is a lack of data including the consumption of ultra-processed foods (UPF) within the broad field of steatotic liver disease. Methods: Dietary intake and physical activity were assessed using standardized questionnaires in patients with MASLD, ALD and healthy controls. Liver disease severity was quantified by transient elastography and liver histology. Results: One hundred and fifty-two patients with MASLD were recruited and compared with 95 patients with ALD and 31 controls. Patients with MASLD consume significantly less total calories than patients with ALD (1620 vs. 2290 kcal/day, p < 0.0001), primarily due to lower alcohol intake, despite a higher body mass index. ALD patients consume lower proportions of proteins, lipids, carbohydrates, and dietary fibres than MASLD and control groups. Fibre intake is higher in the control group compared with the MASLD and ALD groups. In the biopsied MASLD subgroup, significant fibrosis is associated with a lower fibre intake (15 vs. 19 g/day, p = 0.03). No differences in NOVA category distribution are observed between MASLD and control groups, and UPF intake is not associated with liver histological severity. Controls devote a greater proportion of leisure-time physical activity (54% vs. 11% in MASLD and 17% in ALD, p < 0.0001). Conclusions: Patients with MASLD and ALD exhibit lower dietary fibre intake and reduced leisure-time physical activity compared with controls. Fibre intake, but not UPF consumption, is associated with fibrosis severity in MASLD.