Association between interlobular pancreatic adipose tissue and low glucose-induced insulin secretion by β-cells.

The potential role of pancreatic fat on human β-cell dysfunction and its association with fibrosis are controversial. From the PANC-DB database, we estimated β-cell function with glucose-stimulated insulin secretion (GSIS) and quantified fat infiltration and fibrosis using pancreatic histology sections from 45 organs from cadaveric organ donors. In the donors without diabetes, high fat infiltration and adipocyte size in the pancreatic septum were associated with lower GSIS. Low GSIS in fatty pancreas was confirmed in living pancreatic tissue slices. This association is dependent on age and global adiposity and independent of fibrosis. These results suggest that the localization and phenotype of fat infiltration in the pancreas are important factors to determine the role of adipose tissue on pancreatic endocrine function.NEW & NOTEWORTHY Adipose tissue infiltration in the pancreas and its potential implication in the development or maintenance of diabetes has been and is still intensively investigated. In this short communication, we showed negative association between pancreatic fat infiltration and glucose-stimulated insulin secretion (GSIS), specifically in T2D. In addition, interlobular adipocyte size correlated positively with body mass index, age, and HbA1c, and negatively with GSIS. This suggests that adipocyte phenotype, rather than fat quantity alone, may influence β-cell function.