Diabetes & Metabolism Journal

Original Articles

Role of Glucocorticoid Receptor on Insulin Secretion and Synthesis in INS-1 Cells.: Ju Yeon Yang, Myong Su Kang, Tak Ho Song, In Kook Jeong, Pyong Ju Seo, Hee Jin Kim; Korean Diabetes J. 2006;30(6):428-434. Published online November 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.6.428

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Abstract PDF: BACKGROUND
Glucocorticoids play important roles in the regulation of glucose homeostasis. It is well known that glucocorticoids reduce hepatic and peripheral tissue sensitivity to insulin, but the roles of glucocorticoids on insulin secretion and synthesis in pancreatic beta cells are still unclear. We have investigated the direct effects of glucocorticoids on insulin secretion and synthesis in rat insulinoma (INS-1) cells. METHODS: Insulin content and 11.2 mM glucose-stimulated insulin secretion (GSIS) were measured in INS-1 cells after culture with or without 1 micrometer dexamethasone (DEX). Preproinsulin mRNA levels were analyzed by real-time RT-PCR and normalized to the internal control. Effect of RU486 on DEX-induced inhibition of GSIS and preproinsulin mRNA synthesis was evaluated. RESULTS: Insulin content of INS-1 cells cultured in RPMI containing 11.2 mM glucose in the presence of DEX was not different from that of control cells. After 1-h preincubation in 2.8 mM glucose, basal insulin secretion from cells treated with DEX did not differ from that of controls, but GSIS was significantly reduced in the cells treated with DEX in comparison to control cells. The expression of preproinsulin mRNA relative to beta-actin mRNA was also lower in the cells treated with DEX. Glucocorticoid receptor antagonist improved DEX-induced inhibition of GSIS and preproinsulin mRNA synthesis. CONCLUSION: DEX inhibited GSIS and preproinsulin mRNA synthesis in INS-1 cells. Glucocorticoid receptor antagonist ameliorated the reduced GSIS and preproinsulin mRNA synthesis induced by DEX.

The Effects of Dexamethasone on the Expansion and Transdifferentiation of Transplanted Porcine Neonatal Pancreas Cell Clusters into beta-cells in Normal Nude Mice.: Ji Hun Yang, Sun Hee Suh, Sung Yoon Jeon, Oak Kee Hong, Kun Ho Yoon; Korean Diabetes J. 2004;28(5):356-366. Published online October 1, 2004

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Abstract PDF: BACKGROUND
Several studies have suggested that glucocorticoid has an influence on the development and function of the -cells. Thus, we undertook this study to determine whether exposure to dexamethasone (Dx) has an influence on the expansion or transdifferentiation of transplanted porcine NPCCs. METHODS: After transplantation (Tx) of 4,000 islet equivalents (IEQs) of porcine NPCCs into normal nude mice, Dx (1mg/kg) or the control vehicle were injected daily for 10 weeks. To clarify the effects of timing and duration of the Dx, one group was treated by Dx at the first 2 weeks (n=10) and the other group was treated later 8 weeks (n=10) during the 10 weeks treatment period. Thr total graft and beta-cell masses were determined by morphometric analysis. We preformed semi-quantitative RT-PCR for evaluating the pancreas transcription factors. RESULTS: The relative volume and absolute mass of the beta-cells and the total graft were significantly decreased by 10 weeks Dx treatment. Moreover, Dx treatment at thr first 2 weeks (n=10) also significantly decreased the total graft mass and absolute mass of the beta-cells. The relative volume of the beta-cells was negatively correlated and the area of the duct cysts was positively correlated with the duration of the Dx treatment. Pancreas transcription factors including PDX1, Ngn 3, ISL1 and NKx6.1 were decreased in the graft by 2 days treatment of Dx. CONCLUSION: These results suggest that Dx treatment suppresses the expansion and transdifferentiation of transplanted pancreas precursor cells into beta-cell.

The Role of Chromium as an Insulin Sensitizer in Rats Receivieng Corticosteroid.: Dong Sun Kim, Chang Beom Lee, Yong Soo Park, You Hern Ahn, Tae Wha Kim, Ho Soon Choi, Il Kyu Park, Hyun Jin Shin, Ju Seop Kang; Korean Diabetes J. 2001;25(3):211-217. Published online June 1, 2001

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Abstract PDF: BACKGROUND
Chromium (Cr) has been known to be essential for the regulation of insulin action. Recently it has been reported that corticosteroid increases urinary loss of Cr, and that Cr supplementation recovers steroid induced diabetes mellitus. METHODS: Rats were daily treated with dexamethasone (0.2 mg/kg, ip) for first 7 days and were further treated daily with dexamethasone plus either chromium picolinate (30 mg/kg) or a placebo for a period of 14 days. RESULTS: At the end of experiment (Day 21), the control rats treated only with dexamethasone weighed 320 gram (80% of initial weight) in average, but the Cr treated rats weighed 364 gram (91% of initial weight. p<0.05). An insulin sensitivity test [subcutaneous injection of insulin (5 U/kg) plus intraperitoneal injection of glucose (30 minutes after insulin injection)] were conducted. During the insulin sensitivity tests, the area under curves (AUC(0->120 min)) of the time-glucose concentrations curves in the Cr-treated group were decreased compared to those in the control group (5250 vs 15883 mg-min/dL, p<0.01). Fasting serum insulin levels in the Cr-treated rats were clearly decreased by 46.9% compared to those in the control group (2.98 vs 5.60 ng/mL, p<0.05). CONCLUSIONS: We conclude that chromium supplementation reverse a catabolic state, and increase insulin sensitivity in dexamethasone treated rats.

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