We appreciate the insightful comments by Kwok et al. on our manuscript.[1, 2] In their commentary, they discuss important caveats regarding the radiographic evaluation and quantification of pancreatic fat content. Although liver fat content estimation by proton-density-fat-fraction (PDFF) using magnetic resonance imaging (MRI) has been validated by comparison with MR spectroscopy-determined liver fat content and liver histology-determined steatosis grade,[3, 4] we agree that estimation of pancreatic PDFF using MRI has not been validated using pancreatic histology, and further studies are needed to determine the threshold at which pancreatic fat accumulation leads to adverse outcomes.
In addition, Kwok et al. point out that the inverse association between pancreatic fat and liver fibrosis may be related to patient selection and due to the use of insulin-sensitising agents amongst diabetic patients. Previous studies have shown that diabetes is associated with increased risk of non-alcoholic steatohepatitis (NASH) and advanced fibrosis. In the present study, although more patients with grade 1 steatosis had diabetes, the increased risk of fibrosis in diabetic patients and the inverse relationship between liver steatosis and fibrosis may also explain this finding.
As Kwok et al. pointed out, pancreatic biopsy is not possible to document presence of pancreatic fibrosis, so we were not able to provide information regarding pancreatic fibrosis. In future, advanced MRI techniques may become available to identify and quantify pancreatic fibrosis. These advanced imaging techniques may help in improving our understanding of the long-term consequences of fat deposition in the pancreas and whether pancreatic fat deposition leads to pancreatic fibrosis. We agree that additional longitudinal studies are needed to provide further insights into this area.