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. 2025 Jun 1;17(11):1908.
doi: 10.3390/nu17111908.

Liver Fibrosis Is Positively and Independently Associated with Leptin Circulating Levels in Individuals That Are Overweight and Obese: A FibroScan-Based Cross-Sectional Study

Nicole Cerabino  1 , Martina Di Chito  1 , Davide Guido  2 , Vincenza Di Stasi  1 , Caterina Bonfiglio  2 , Giuseppe Lisco  3 , Endrit Shahini  4 , Marianna Zappimbulso  4 , Raffaele Cozzolongo  4 , Valeria Tutino  5 , Arianna Diciolla  5 , Rosanna Mallamaci  6 , Dolores Stabile  7 , Anna Ancona  7 , Sergio Coletta  7 , Pasqua Letizia Pesole  7 , Gianluigi Giannelli  8 , Giovanni De Pergola  1
Affiliations

Liver Fibrosis Is Positively and Independently Associated with Leptin Circulating Levels in Individuals That Are Overweight and Obese: A FibroScan-Based Cross-Sectional Study

Nicole Cerabino et al. Nutrients. .

Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly correlated with the severity of obesity, and the extent of liver fibrosis is associated with a higher risk of liver-related complications, cardiovascular events, and overall mortality. Leptin circulating levels are directly correlated with the amount of adipose tissue. Aims: In the present study, we investigated the association between circulating leptin levels and liver steatosis and fibrosis. Methods: Eighty-six patients (41.7 ± 12.6 yrs, 35 men, 41%), naïve to medications, who attended the Nutrition Center for the Research and Care of Obesity and Metabolic Diseases at the National Institute of Gastroenterology "Saverio de Bellis" for weight management, were cross-sectionally evaluated. Demographic, anthropometric, clinical, and laboratory data were collected and analyzed. All patients underwent liver ultrasonographic assessment by FibroScan to diagnose liver steatosis (controlled attenuation parameter, CAP > 275 dBm) and fibrosis (liver stiffness measurement, LSM > 8.2 kPa). Results: Sixty-three individuals (73.3%) had liver steatosis, and 17 (19.8%) had liver fibrosis. The mean leptin levels were 22.3 ± 14.1 ng/mL, while the BMI and waist circumference were 36.7 ± 7.2 kg/m2 and 114.5 ± 16.4 cm, respectively. CAP values exhibited no correlation with leptin (r = 0.09, p = 0.436), while a significant connection was seen between leptin and LSM (β = 0.065; p = 0.038). Specifically, for each unit increase in leptin, LSM values were varied by +0.065 units (p = 0.038). This association was independent of gender, age, insulin resistance, adiponectin, RBP4, and visfatin. This is the first study showing these results by using FibroScan assessment in patients naïve to medications. Conclusions: Circulating leptin concentrations are independently correlated with hepatic fibrosis in individuals with a BMI ≥ 25 kg/m2. These findings indicate a function for leptin in promoting liver fibrosis; however, longitudinal studies are required to elucidate the causal nature of this interaction.

Keywords: FibroScan; leptin; liver fibrosis; liver steatosis; obesity; overweight.

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Conflict of interest statement

The authors declare that they have no competing financial interests or personal relationships that could have influenced the work reported in this paper.

Figures

Figure 1
Figure 1
Scatter plots in the first row, contour plots in the second row: joint distributions of leptin (x-axis) and ultrasonographic features of liver steatosis (CAP) and fibrosis (LSM). In the scatter plots are also shown the regression lines.
Figure 2
Figure 2
Plots of the post hoc power analysis for Pearson correlation coefficients between leptin and CAP and LSM.
See this image and copyright information in PMC

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