Expression and Correlation of Serum PTH, Trx, Txnip and 25(OH)D3 in Patients with Type 2 Diabetes Mellitus
Type 2 diabetes occurs during asymptomatic impaired glucose tolerance. In many patients with glucose intolerance, blood glucose is in the normal range on an empty stomach, and hyperglycemia occurs only after a meal. We examined whether pancreatic B-cell function changes during acute hyperglycemia caused by oral glucose load. METHODS: We calculated the proinsulin index as an indicator of pancreatic B cell function and measured serum thioredoxin (Trx), thioredoxin interacting protein (Txnip), 25 hydroxyvitamin D3 (25-OH) D3 ), serum parathyroid hormone (PTH). In 45 oral 75 g glucose tolerance tests, 24 patients with normal glucose tolerance, 14 patients with intolerance and 7 patients with type 2 diabetes underwent stress testing. Trx levels decreased after glucose loading 66.1 ± 23.7, 59.3 ± 22.4, 49.3 ± 21.2 and 37.7 ± 18.0 ng / mL, fasted for 0 minutes, 30, 60 and 120 minutes. P < 0.001 compared to fasting. Conversely, the concentration of Txnip peaked at 30 minutes and then gradually decreased (0.402 ± 0.123, 0.440 ± 0.120, 0.362 ± 0.119 and 0.355 ± 0.131 ng / mL, P < 0.05 compared with fasting, P < 0.01, fasting for 30 minutes). Proinsulin index was associated with changes in thioredoxin levels (r = 0.34, P < 0.05). However, it is independent of the change in Txnip level from 0 to 30 minutes. Hyperglycemia in response to oral glucose impairs islet B cell function and reduces thioredoxin levels. Hyperglycemia-induced enhancement of oxidative stress may affect cellular redox status. These findings strongly suggest that repeated postprandial hyperglycemia may play an important role in the development and progression of type 2 diabetes.