Diabetes & Metabolism Journal

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Diabetes and Osteoporosis.: Ki Won Oh; Korean Diabetes J. 2009;33(3):169-177. Published online June 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.3.169

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Increased life expectancy and increased obesity have contributed to an increasing incidence of osteoporosis and diabetes mellitus. Recent meta-analyses and cohort studies confirm that diabetes is associated with a higher risk of fracture. Patients with type 2 diabetes exhibit increased fracture risks despite a higher bone mass, which are mainly attributable to non-skeletal risk factors. Patients with type 1 diabetes may have impaired bone formation because of absence of the anabolic effects of insulin and insulin-like growth factor I (IGF-I) system. Several clinical studies have reported adverse skeletal actions of peroxisome proliferator-activated receptor gamma (PPARgamma) agonist in humans. Obesity regulates bone metabolism not only by increasing weight loading but also by modulating adipokines that are known to affect bone remodeling.

Citations

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Original Article

Mitogenic Effects and Signaling Pathway of Insulin-Like Growth Factor-I (IGF-I) in the Rat Beta Cell Line (INS-1).: In Kyung Jeong, Ja Young Kim, Hyung Joon Yoo, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim; Korean Diabetes J. 2004;28(6):478-489. Published online December 1, 2004

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Abstract PDF: BACKGROUND
Nutrients and growth factors are known to stimulate pancreatic beta cell mitogenesis. IGF-I acts as a survival factor by limiting apoptosis and stimulating proliferation in many cell types. However, the appropriate mitogenic signaling pathways have not been defined. The aim of this study is to elucidate the mitogenic effect and signaling pathways of IGF-I in the rat beta cell line (INS-I). METHODS: The studies were performed using the rat pancreatic beta cell line, INS-1. INS-1 cells were cultured in RPMI 1640 containing serum-free, 0.2% BSA and 11.1 mmol/L glucose media for 24 hours, and the cells were then treated with IGF-I and different concentrations of glucose or tyrosine phosphorylation inhibitors, or insulin. The cell proliferation was measured by the [3H]thymidine uptake and MTT assay. The cell cycle was analyzed by a flow cytometer by using propidium iodide staining. Western blot analyses were performed using antibodies against PY20 and phospho-MAPK. RESULTS: 1) MTT assay and the [3H]thymidine uptake showed that IGF-I stimulated the INS-1 cell proliferation in a dose dependent manner. Glucose was noted to independently increase the INS-1 cell proliferation. A combination of IGF-I and glucose has a synergistic effect on the proliferation of INS-I cells. Insulin did not influence on the mitogenic effect of IGF-I. 2) The S fraction of INS-1 cells treated with IGF-I was increased in a dose dependent manner. IGF-I stimulated the exit from G1 into the S phase of the cell cycle. 3) Investigation of the role of the PI3K and MAPK, by using of the inhibitors LY294002, wortmannin, and PD98059, demonstrated that the activation of MAPK, but not PI3K, required to stimulate the proliferation of INS-1 cells. 4) IGF-I stimulated the phosphorylation activation of pp60 and phospho-MAPK in the INS-1 cells. IGF-I induced the beta cell proliferation, and this was mediated via a signaling mechanism that was facilitated by MAPK. CONCLUSION: The proliferative effect of IGF-I on pancreatic beta cell seems to be mediated through MAPK signaling pathway.

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