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Original Articles
- Clinical Care/Education
- Diabetes Camp as Continuing Education for Diabetes Self-Management in Middle-Aged and Elderly People with Type 2 Diabetes Mellitus
- So Young Park, Sun Young Kim, Hye Mi Lee, Kyu Yeon Hur, Jae Hyeon Kim, Moon-Kyu Lee, Kang-Hee Sim, Sang-Man Jin
- Diabetes Metab J. 2017;41(2):99-112. Published online March 3, 2017
- DOI: https://doi.org/10.4093/dmj.2017.41.2.99
- 7,962 View
- 52 Download
- 4 Web of Science
- 3 Crossref
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Abstract
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Supplementary Material
PubReader 
ePub Background Despite the established benefits of diabetes camps for the continuing education of children with type 1 diabetes mellitus, little is known about the long-term metabolic benefits of diabetes camps for middle-aged and elderly people with type 2 diabetes mellitus (T2DM), especially in terms of glycosylated hemoglobin (HbA1c) variability.
Methods The 1-year mean and variability of HbA1c before and after the diabetes camp was compared between the participants of the diabetes camp (
n =57; median age 65 years [range, 50 to 86 years]; median diabetes duration 14 years [range, 1 to 48 years]). Additional case-control analysis compared the metabolic outcomes of the participants of the diabetes camp and their propensity score-matched controls who underwent conventional diabetes education (n =93).Results The levels of HbA1c during the first year after the diabetes camp were comparable to those of the matched controls (
P =0.341). In an analysis of all participants of the diabetes camp, the 1-year mean±standard deviation (SD) of HbA1c decreased (P =0.010 andP =0.041) after the diabetes camp, whereas the adjusted SD and coefficient of variance (CV) of HbA1c did not decrease. The adjusted SD and CV significantly decreased after the diabetes camp in participants whose 1-year mean HbA1c was ≥6.5% before the diabetes camp (n =40) and those with a duration of diabetes less than 15 years (n =32).Conclusion The 1-year mean and SD of HbA1c decreased after the diabetes camp, with significant reduction in the adjusted SD and CV in those with higher baseline HbA1c and a shorter duration of diabetes.
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Citations
Citations to this article as recorded by
- Camp-style lifestyle modification program (CAMP) for diabetes prevention among rural women with prior GDM: study protocol for a three-arm cluster hybrid type 2 randomized controlled trial
Yao Chen, Qinyi Zhong, Wencong Lv, Qing Long, Man Ping Wang, Jyu-Lin Chen, James Allen Willey, Robin Whittemore, Jia Guo
BMC Public Health.2024;[Epub] CrossRef - Older adults’ experiences of being at a senior summer camp—A phenomenographic study
Veronika Wallroth, Kjerstin Larsson, Agneta Schröder
Qualitative Social Work.2022; 21(5): 956. CrossRef - Pushing for miracles, pulling away from risk: An ethnographic analysis of the force dynamics at Senior Summer Camps in Sweden
Gabriella Nilsson, Lisa Ekstam, Janicke Andersson
Journal of Aging Studies.2018; 47: 96. CrossRef
- Camp-style lifestyle modification program (CAMP) for diabetes prevention among rural women with prior GDM: study protocol for a three-arm cluster hybrid type 2 randomized controlled trial
- The Role of cAMP/PKA Activation on Exendin-4-Induced Cyclin D1 Expression in INS-1 Cell.
- Gyeong Ryul Ryu, Jung Hoon Kang, Hwa In Jang, Seung Hyun Ko, In Kyung Jeong, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Yang Hyeok Jo, Myung Suk Kim, Myung Jun Kim
- Korean Diabetes J. 2005;29(4):295-303. Published online July 1, 2005
- 2,068 View
- 29 Download
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Abstract
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- BACKGROUND
Glucagon-like peptide-1(GLP-1) and exendin-4(EX-4) have been known to induce pancreatic islet proliferation and increases in the betacell mass. Cyclin D1 is a key protein responsible for the entry of the G into the S phase, thereby contributing to cell proliferation. Therefore, the effect of EX-4 on the expression of cyclin D1 in INS-1 cells, a rat pancreatic betacell line, was investigated. The involvement of either mitogen-activated protein kinases(MAPKs) or cyclic adenosine 5'-monophosphate/protein kinase A(cAMP/ PKA) in the EX-4-induced cyclin D1 expression was also examined. METHODS: INS-1 cells were treated with EX-4 (10 nM), and the cyclin D1 protein levels then determined by Western blot. To investigate the involvement of MAPKs in the EX-4- induced cyclin D1 expression, either a combined treatment of MAPKs inhibitors or transient transfection of extracellular signal-regulated kinase-1 (ERK1) was performed. The effect of cAMP on the EX-4-induced cyclin D1 expression was also examined by treatments with forskolin, an adenylyl cyclase activator, and H-89, a PKA inhibitor. RESULTS: EX-4 increased the expression of cyclin D1 protein in a dose-dependent manner. Although EX-4 induced phosphorylation of ERK1/2, the treatment with PD 98059 or the overexpression of ERK1 had no effect on the EX-4-induced cyclin D1 expression. However, forskolin significantly induced the expression of cyclin D1, whereas the pretreatment of H-89 inhibited the EX-4-induced cyclin D1 expression. CONCLUSION: These results suggest that EX-4 induce cyclin D1 expression in INS-1 cells via cAMP/PKA pathway, but this is not due to ERK activation.
- The Effect of cAMP-Elevating Agents on High Glucose-Induced Apoptosis of Isolated Islets of Rat Pancreas.
- Gwan Pyo Koh, Kwang Sik Suh, Suk Chon, Seung Joon Oh, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Sun Hee Kwon
- Korean Diabetes J. 2004;28(6):490-500. Published online December 1, 2004
- 1,983 View
- 23 Download
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Abstract
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- BACKGROUND
High glucose-induced apoptosis has been implicated in the loss of beta-cells of the pancreatic islets in animal models of type 2 diabetes. GLP-1 has been shown to reduce apoptosis by the cAMP-dependent mechanism in beta-cells. Other studies have also shown that elevated levels of intracellular cyclic AMP delayed apoptosis in other types of cells. We investigated whether cAMP-elevating agents could suppress the high glucose-induced apoptosis of isolated rat islets. METHODS: Pancreatic islets were isolated from Sprague-Dawley (SD) rats. The expression of phosphodiesterase (PDE) 3 subtypes was investigated by using extracts of freshly isolated islets and analyzing them by RT-PCR. After 2 days of isolation, the islets were cultured in RPMI-1640 media containing 5% FBS with various glucose concentrations (11.1, 16.7 and 27.8 mM), 5x10-6 M forskolin, 2x10-4 M 3-isobutyl-1-methylxanthine (IBMX), 10-5 M cilostazol, and 10-6, 5x10-6 and 10-5 M H-89 for 5 days. The islet apoptosis was measured by a sandwich enzyme-immunoassay using antihistone antibody. RESULTS: Apoptosis was lowest at 11.1 mM glucose concentration, and increased at higher glucose concentrations (1.00 +/- 0.04 A.U. (arbitrary unit) at 11.1 mM, 1.17 +/- 0.12 A.U. at 16.7 mM, and 1.65 +/-0.13 A.U. at 27.8 mM (P <0.05 for 11.1 mM). Both PDE 3A and 3B mRNA were expressed in the islet extracts. In 16.7 and 27.8 mM glucose concentrations, forskolin (P <0.01), IBMX (P <0.05) and cilostazol (P < 0.05) suppressed apoptosis of the islet cells. Protein kinase A (PKA) nhibitor, H-89, did not prevent the inhibition of apoptosis by forskolin. CONCLUSION: These results show that high glucose-induced apoptosis of the cells in rat islet is attenuated by such cAMP-elevating agents as cilostazol. However, cyclic AMP regulation of islet apoptosis may occur via a PKA-independent signaling pathway.
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