Aims/IntroductionThe 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 MethodsA 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).ResultsIn 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).ConclusionsIn 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.
IntroductionChronic inflammation is observed in type 2 diabetes islets, and fat deposition in the pancreas affects insulin secretion and glucose tolerance. However, the relationship between this inflammation and pancreatic fat deposition has not been elucidated.Research design and methodsWe examined pancreatic sections from 60 Japanese patients obtained by pancreatectomy. We evaluated pancreatic fat-cell area (%) and CD68-positive (CD68+) cells per islet histologically and examined the relationships between these histological findings and various clinical parameters.ResultsThe number of CD68+ cells per islet in the diabetes group was significantly higher than that in the normal glucose tolerance group (p=0.026). Moreover, CD68+ cells per islet were significantly correlated with body mass index (r=0.33, p=0.0080), fasting C-peptide immunoreactivity (r=0.46, p=0.0042), homeostasis model assessment insulin resistance (r=0.38, p=0.016), C-peptide index (r=0.38, p=0.018), the area under the glucose concentration curve (AUCglucose) at the 75 g oral glucose tolerance test (r=0.49, p=0.0065) and fat-cell area (r=0.51, p<0.0001). In multiple regression analyses, fat-cell area (β=0.600, p=0.0027) and AUCglucose (β=0.453, p=0.0042) were the independent and significant determinants of CD68+ cells per islet.ConclusionThe inflammation of islets is associated with pancreatic fatty infiltration and hyperglycemia, which may further aggravate glucose tolerance.
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