Pancreatic Fat and Stiffness Reflect Distinct Features of Pancreatic Remodeling and β-Cell Function

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.

We investigated the relationship between pancreatic fat, tissue remodeling, and β-cell function.

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).

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).

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.

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.