The Visceral Fat-Muscle Trade-off in Obese Chronic Liver Disease: Insights From SMA-Level Periportal VAT
Atsushi Nakamura1, Takeshi Ichikawa1, Keiji Okuyama1
1Gastroenterological Liver Disease Center, Nippon Koukan Hospital, Kawasaki, Japan.
Background And Aims:
Visceral adipose tissue (VAT) contributes to MASLD pathophysiology via the portal circulation, and weight loss is a cornerstone of treatment; however, its effect on skeletal muscle remains unclear. This study evaluated intra-abdominal area (IAA) at the superior mesenteric artery (SMA) level-a site capturing periportal adipose tissue-and examined the association between weight loss and muscle loss in non-cirrhotic obese chronic liver disease (CLD).
Methods:
IAA and paraspinal muscle area were quantified by MRI at the SMA level. Longitudinal changes in IAA, muscle mass, proton density fat fraction (PDFF), ALT, and liver stiffness (LS) were annualized. Cross-sectional associations were evaluated in the overall cohort (BMI ≥ 25 kg/m2, n = 286); longitudinal relationships were assessed in CLD undergoing lifestyle intervention (n = 141, median follow-up: 36 months).
Results:
In the cohort (MASLD 60%), IAA was independently associated with lower muscle mass and higher LS beyond FIB-4. In the longitudinal cohort, IAA reduction was independently associated with improvements in PDFF and LS, whereas muscle mass declined nonlinearly with greater IAA reduction (R2 = 0.336, p < 0.001). In MASLD, a ≥ 4% IAA reduction significantly improved PDFF, ALT, and LS but was accompanied by muscle loss (-3.9%/y), whereas albumin remained unchanged (p = 0.968).
Conclusions:
In obese CLD, IAA at the SMA level serves as a practical marker of periportal VAT. Although its reduction benefits the liver, it may be accompanied by muscle loss. Preserved serum albumin does not exclude ongoing skeletal muscle catabolism. Enhanced protein intake during weight loss may help mitigate muscle catabolism.
