The University of Osaka · Medicine
Professor Junji Kozawa's research lab focuses on the pathophysiological role of ectopic fat deposition—particularly in the pancreas, liver, muscle, and heart—in the development and progression of type 2 diabetes and its complications. The lab investigates how pancreatic fat accumulation, islet inflammation, and β-cell dysfunction contribute to impaired insulin secretion and glucose intolerance. Using clinical and metabolic assessments, including F-CPR, U-CPR, and imaging techniques, the lab explores the dynamic changes in islet cell populations and endocrine function over time in diabetic patients. Their work highlights the interplay between ectopic fat, insulin resistance, and organ-specific dysfunction, aiming to identify early biomarkers and therapeutic targets for diabetes management.
Figures are computed from collected data and may differ slightly.
Insulin secretion evaluated by F-CPR, CPI, I.I., U-CPR and the duration of type 2 diabetes were useful parameters for predicting the efficacy of liraglutide in patients with type 2 diabetes. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00168.x, 2011).
Type 2 diabetes patients had high LD accumulation in β cells, which was associated with insulin resistance, hyperglycemia, aging and β cell dysfunction involving decreased mature insulin granules.
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.
The inflammation of islets is associated with pancreatic fatty infiltration and hyperglycemia, which may further aggravate glucose tolerance.
The pancreatic α/β increases after type 2 diabetes onset and correlates with diabetes duration. This change might occur through α-cell proliferation and phenotypic changes in pancreatic endocrine cells.
Ectopic fat is found in liver, muscle, and kidney and is known to accumulate as visceral fat. In recent years, ectopic fat has also been observed in the pancreas, and it has been said that pancreatic fat accumulation is related to the pathophysiology of diabetes and the onset of diabetes, but the relationship has not yet been determined. In the heart, epicardium fat is another ectopic fat, which is associated with the development of coronary artery disease. Ectopic fat is also observed in the my
Immune checkpoint inhibitors (ICIs) could cause type 1 diabetes (T1D). However, the underlying mechanism remains unclear. We immunohistochemically analyzed pancreatic specimens from three individuals with ICI-related T1D, and their histopathological data were compared those from three patients who had received ICI therapy but did not develop T1D (non-T1D) and seven normal glucose-tolerant subjects as control subjects. All ICI-related T1D patients had susceptible HLA haplotypes. In ICI-related T1
Insulin sensitizers were effective in type 2 diabetic patients with high insulin resistance estimated by the ITT. The ITT could be useful to predict the effectiveness of insulin sensitizers.
These results indicate that HB-EGF gene transduction into adult pancreatic duct cells not only promotes the proliferation of pre-existing beta cells but also leads to beta-cell differentiation from duct cells, and the resulting increase in beta-cell mass improves glucose tolerance.
Postprandial glucagon secretion was shown to be dysregulated in patients with type 2 diabetes. However, the differences in secretory patterns between obese and non-obese patients and their physiological effects on plasma glucose levels are not fully understood. This study population consisted of 21 (10 obese and 11 non-obese) consecutive patients with type 2 diabetes admitted for glycemic control. A 3-hour mixed-meal tolerance test was performed after glycemic control improved. Six non-diabetic
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