Slim Limbs But Protruding Belly? Check for Fatty Liver Disease

Prof. Lee Han-a, Department of Gastroenterology, Chung-Ang University Hospital

Fatty liver is diagnosed when fat accounts for more than 5% of total liver tissue. For fatty liver disease, waist circumference matters more than body weight. Even if you appear slim on the outside, if your waist has grown or you have thin limbs but a protruding belly, there is a high likelihood of excessive visceral fat. While subcutaneous fat safely stores excess energy in our body, visceral fat sends fatty acids and inflammatory signals directly to the liver through the portal vein, accumulating fat in the liver and worsening inflammation.

Even with normal weight, "insulin resistance" can develop if muscle mass is low or there is a genetic predisposition. When insulin resistance develops, the liver produces more fat and burns less, tilting metabolism toward fat accumulation. As this process repeats, triglycerides build up in the liver, leading to fatty liver progression.

Muscles are not simply attached to bones to enable movement—they are the metabolic organs that process the most glucose in our body. When muscle mass decreases, blood sugar rises more easily even with the same food intake, requiring more insulin. As insulin resistance worsens, excess energy more easily converts to visceral and liver fat. Multiple studies have already shown that sarcopenia and fatty liver share common pathophysiology with insulin resistance and chronic inflammation. In other words, the distribution and function of fat—particularly visceral fat and ectopic fat—have a greater impact on the liver than weight alone. This means that even those who appear thin can develop fatty liver deposits if they have high visceral fat or ectopic fat accumulation in the liver, pancreas, or muscles.

The risk of fatty liver complications varies depending on whether it is simple steatosis, whether inflammation and ballooning degeneration are present, and the degree of fibrosis progression. Even fatty liver occurring at normal weight can progress if left untreated, and some reports suggest the risk of severe liver disease is actually higher than in fatty liver accompanied by obesity. According to large-scale prospective multicenter cohort studies from the UK and China, normal-weight fatty liver patients showed significantly higher risks for liver-related events and mortality, cardiovascular mortality, and all-cause mortality compared to obese fatty liver patients. The liver is central to various metabolic processes in the body. When fat accumulates in the liver, triglycerides and remnant lipoproteins increase, inflammatory responses occur, vascular endothelial function deteriorates, and coagulation tendency worsens, raising the risk of systemic atherosclerosis. This is why fatty liver also increases cardiovascular metabolic complication risks.

The European Association for the Study of Obesity recently proposed a new concept of "clinical obesity" beyond defining obesity by body mass index (BMI), calculated by dividing weight (kg) by height (m) squared. The position is that even at normal weight, if waist circumference increases and metabolic complications such as diabetes, hypertension, and fatty liver, mechanical complications such as sleep apnea and degenerative arthritis, or psychological complications such as obesity-related depression are present, active treatment is needed for clinical obesity. This perspective warns of the dangers of normal-weight fatty liver, where fat pathologically accumulates in the liver or blood vessels despite appearing slim. The key point is that obesity should be understood not as a matter of external weight but as a chronic metabolic disease that determines organ damage and prognosis.

Currently, no treatments are specifically designed for normal-weight fatty liver. In the United States, resmetirom is used to treat fatty liver with inflammation or fibrosis regardless of weight. For glucagon-like peptide (GLP)-1 receptor agonists such as Wegovy and Mounjaro, there is not yet sufficient evidence for use in normal-weight individuals. The key is reducing visceral fat and fibrosis risk and improving insulin resistance, muscle mass, and strength rather than weight itself. Lifestyle modification is most important for this. If comorbidities such as diabetes, dyslipidemia, or hypertension are present, active pharmacotherapy helps improve fatty liver and prognosis.

Even at normal weight, increased visceral fat, ectopic fat accumulation, and sarcopenia clinically carry the same risks as obesity. Therefore, evaluation considering both waist circumference and body composition (muscle and fat) is necessary. Increasing muscle mass and strength through resistance training is a core strategy for improving insulin resistance. For diet, minimizing refined carbohydrates and sugars based on a balanced diet with essential nutrients helps reduce de novo lipogenesis in the liver. Fatty liver can be hidden even if liver enzyme levels are normal on health checkups. If metabolic signals such as elevated triglycerides, decreased HDL cholesterol, borderline fasting glucose or HbA1c levels, or elevated blood pressure are present, fatty liver should be suspected. Hidden metabolic diseases should be actively identified and treated, and for those with fatty liver risk factors, evaluation of liver fibrosis degree—an important prognostic factor—through liver fibrosis testing or blood tests via specialist consultation is recommended.