Background <p>Obesity includes a wide range of metabolic conditions. Some patients remain metabolically healthy despite excess body weight (MHO phenotype), while others develop metabolic syndrome and metabolic dysfunction–associated fatty liver disease (MAFLD). These differences may determine the risk of diabetes and cardiovascular disease. The present study compared clinical and biochemical characteristics between people with MHO and those with MetS combined with MAFLD, and evaluated the effects of six months of metformin therapy in the latter group.</p> Methods <p>A total of 78 adults with obesity (BMI ≥ 30&#xa0;kg/m<sup>2</sup>) were examined. Participants were classified as MHO (n = 26) or as having metabolic syndrome with MAFLD (n = 52). Anthropometric data, glucose and lipid metabolism indicators, liver enzymes, and non-invasive measures of hepatic steatosis and fibrosis (CAP, FIB-4, HSI) were recorded. Patients with MetS + MAFLD were randomized to lifestyle modification (Mediterranean diet and moderate exercise) or the same program plus metformin (500&#xa0;mg twice daily) for six months.</p> Results <p>After six months, patients in the metformin group showed significant improvements in fasting glucose (− 0.9 ± 0.4&#xa0;mmol/L, p &lt; 0.001), HbA1c (− 0.5 ± 0.2%, p &lt; 0.001), and HOMA-IR (p &lt; 0.001), accompanied by modest weight reduction (− 1.6 ± 0.8&#xa0;kg, p = 0.02). ALT and AST decreased (p = 0.001 and p = 0.003, respectively), and CAP values fell by 9% (p = 0.004). Fibrosis indices FIB-4 and HSI both improved (p &lt; 0.001). Triglycerides (p = 0.01) and blood pressure (p &lt; 0.05) decreased, while HDL-cholesterol increased (p = 0.02).</p> Conclusions <p>People with MHO showed preserved metabolic function and no signs of fatty liver despite similar BMI. In patients with metabolic syndrome and MAFLD, metformin treatment for six months led to meaningful improvement in glucose control, liver function, and lipid profile.</p>

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Metabolic profiling of healthy vs. syndrome-associated obesity and effects of six-month metformin therapy

  • Iryna Halabitska,
  • Iryna Kamyshna,
  • Pavlo Petakh,
  • Inna Krynytska,
  • Denis Putilin,
  • Oleksandr Kamyshnyi

摘要

Background

Obesity includes a wide range of metabolic conditions. Some patients remain metabolically healthy despite excess body weight (MHO phenotype), while others develop metabolic syndrome and metabolic dysfunction–associated fatty liver disease (MAFLD). These differences may determine the risk of diabetes and cardiovascular disease. The present study compared clinical and biochemical characteristics between people with MHO and those with MetS combined with MAFLD, and evaluated the effects of six months of metformin therapy in the latter group.

Methods

A total of 78 adults with obesity (BMI ≥ 30 kg/m2) were examined. Participants were classified as MHO (n = 26) or as having metabolic syndrome with MAFLD (n = 52). Anthropometric data, glucose and lipid metabolism indicators, liver enzymes, and non-invasive measures of hepatic steatosis and fibrosis (CAP, FIB-4, HSI) were recorded. Patients with MetS + MAFLD were randomized to lifestyle modification (Mediterranean diet and moderate exercise) or the same program plus metformin (500 mg twice daily) for six months.

Results

After six months, patients in the metformin group showed significant improvements in fasting glucose (− 0.9 ± 0.4 mmol/L, p < 0.001), HbA1c (− 0.5 ± 0.2%, p < 0.001), and HOMA-IR (p < 0.001), accompanied by modest weight reduction (− 1.6 ± 0.8 kg, p = 0.02). ALT and AST decreased (p = 0.001 and p = 0.003, respectively), and CAP values fell by 9% (p = 0.004). Fibrosis indices FIB-4 and HSI both improved (p < 0.001). Triglycerides (p = 0.01) and blood pressure (p < 0.05) decreased, while HDL-cholesterol increased (p = 0.02).

Conclusions

People with MHO showed preserved metabolic function and no signs of fatty liver despite similar BMI. In patients with metabolic syndrome and MAFLD, metformin treatment for six months led to meaningful improvement in glucose control, liver function, and lipid profile.