Pancreatic fat is related to the longitudinal decrease in the increment of C-peptide in glucagon stimulation test in type 2 diabetes patients

Aims/Introduction The relationship between pancreatic fatty infiltration and diabetes is widely known, whereas the causal relationship is not clear. Furthermore, it is uncertain whether pathogenesis of pancreatic fat is similar to that of liver fat. We aimed to clarify the contribution of this type of fat to glucose metabolism in type 2 diabetes patients by cross-sectional and longitudinal analyses. Material and Methods A total of 56 patients with type 2 diabetes who had been hospitalized twice were analyzed. We evaluated the mean computed tomography values of the pancreas (P), liver (L) and spleen (S). Lower computed tomography values indicate a greater fat content. We defined indices of pancreatic or liver fat content as the differences between P or L and S. We assessed the associations among fat content for the two organs (P-S, L-S) and clinical parameters at the first hospitalization, and then analyzed the associations between these fat contents and changes in glycometabolic markers (the second data values minus the first). Results In the cross-sectional study, P-S negatively correlated with the increment of C-peptide in the glucagon stimulation test (r = -0.71, P < 0.0001) and body mass index (r = -0.28, P = 0.034). L-S negatively correlated with homeostasis model assessment of insulin resistance (r = -0.73, P < 0.0001), body mass index (r = -0.62, P < 0.0001) and some other obesity-related indicators, but not with the increment of C-peptide in the glucagon stimulation test. In the longitudinal study, P-S positively correlated with the change of the increment of C-peptide in the glucagon stimulation test (r = 0.49, P = 0.021). Conclusions In type 2 diabetes patients, pancreatic fat was less associated with obesity-related indicators than liver fat, but was more strongly associated with the longitudinal decrease in endogenous insulin-secreting capacity.