The Journal of clinical endocrinology and metabolism · 2026
Pancreatic Fat and Stiffness Reflect Distinct Features of Pancreatic Remodeling and β-Cell Function.
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De Lucia Sara Sofia, Ciccarelli Gea, Gliozzo Giulia, Di Giuseppe Gianfranco, Soldovieri Laura, Gentile Emanuele, Genco Enza, Gallo Lorenzo, Zocco Maria Assunta, Ainora Maria Elena, Esposto Giorgio, Sposato Paolo, Bizzotto Roberto, Pontecorvi Alfredo, Giaccari Andrea, Gasbarrini Antonio, Nista Enrico Celestino, Mezza Teresa
Аннотация
CONTEXT: Fatty pancreas is associated with obesity and metabolic alterations and may coexist with pancreatic structural remodeling. However, its contribution to β-cell dysfunction remains unclear.
OBJECTIVE: We investigated the relationship between pancreatic fat, tissue remodeling, and β-cell function.
DESIGN: We conducted a cross-sectional study in individuals with ultrasound-detected pancreatic hyperechogenicity without prior diagnosis of diabetes. Pancreatic fat was quantified by MRI-derived proton density fat fraction (PDFF), while tissue stiffness was assessed by shear-wave elastography. Metabolic phenotyping was based on oral glucose tolerance test (OGTT).
PARTICIPANTS: We recruited 29 individuals with ultrasound-detected fatty pancreas (F/M 16/13, age 54 ± 10.4 years) and assessed glucose tolerance with OGTT: 75.9% exhibited normal glucose tolerance (NGT; n=22), while 24.1% had impaired glucose tolerance (IGT; n=7).
RESULTS: MRI-derived pancreatic fat fraction was positively correlated with anthropometric measures (BMI ρ=0.43, p=0.02) and β-cell function (β-cell glucose sensitivity ρ=0.40, p=0.03). Pancreatic stiffness correlated negatively with body weight (ρ= -0.38, p=0.04), did not correlate with pancreatic fat fraction (ρ= -0.15, p= 0.44) and was correlated inversely with the potentiation factor ratio (PFR1; ρ= -0.44, p= 0.02), a measure of non-glucose-dependent amplification of insulin secretion.
CONCLUSIONS: Intrapancreatic fat and pancreatic stiffness appear to reflect distinct pathophysiological processes, with potentially different relationships to systemic metabolic status and β-cell function. These findings support a more nuanced view of pancreatic structural alterations as heterogeneous markers of metabolic dysfunction.
OBJECTIVE: We investigated the relationship between pancreatic fat, tissue remodeling, and β-cell function.
DESIGN: We conducted a cross-sectional study in individuals with ultrasound-detected pancreatic hyperechogenicity without prior diagnosis of diabetes. Pancreatic fat was quantified by MRI-derived proton density fat fraction (PDFF), while tissue stiffness was assessed by shear-wave elastography. Metabolic phenotyping was based on oral glucose tolerance test (OGTT).
PARTICIPANTS: We recruited 29 individuals with ultrasound-detected fatty pancreas (F/M 16/13, age 54 ± 10.4 years) and assessed glucose tolerance with OGTT: 75.9% exhibited normal glucose tolerance (NGT; n=22), while 24.1% had impaired glucose tolerance (IGT; n=7).
RESULTS: MRI-derived pancreatic fat fraction was positively correlated with anthropometric measures (BMI ρ=0.43, p=0.02) and β-cell function (β-cell glucose sensitivity ρ=0.40, p=0.03). Pancreatic stiffness correlated negatively with body weight (ρ= -0.38, p=0.04), did not correlate with pancreatic fat fraction (ρ= -0.15, p= 0.44) and was correlated inversely with the potentiation factor ratio (PFR1; ρ= -0.44, p= 0.02), a measure of non-glucose-dependent amplification of insulin secretion.
CONCLUSIONS: Intrapancreatic fat and pancreatic stiffness appear to reflect distinct pathophysiological processes, with potentially different relationships to systemic metabolic status and β-cell function. These findings support a more nuanced view of pancreatic structural alterations as heterogeneous markers of metabolic dysfunction.