• Korean Journal of Psychosomatic Medicine
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• v.30 no.2
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• pp.155-164
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• 2022

Objectives : A growing body of evidence links type 2 diabetes (T2D) with a neurodegenerative disease (ND) such as Alzheimer's disease and Parkinson's disease. The purpose of this study is to investigate the relationship between NDs and the development of T2D by comparing the incidence of T2D in a group of various NDs (ND group) and control group. Methods : A population-based 10-year follow-up study was conducted using the Korean National Health Information Database for 2002-2015. We used a retrospective cohort study design to investigate the association of ND with T2D occurrence. The study population included ND (n=8,814) and control (n=37,970) groups, all aged 60 years or over. The Kaplan-Meier method was used to estimate the risk of developing T2D as a function of time. Cox proportional hazards regression models were used to evaluate the relationship between ND and T2D. Results : T2D was developed in a significantly higher percentage of patients in the ND group (53.6%) than in the control group (44.7%). The ND group increased the risk of T2D (HR, 1.43; 95% CI, 1.38-1.47). About one-third of patients in both groups were additionally diagnosed with another ND before the occurrence of T2D during a 10-year follow-up period. When compared to those who did not have another ND during the follow-up period, the incidence of T2D in those who were additionally diagnosed with another ND was higher in both the ND and control groups. Conclusions : The ND group had about 1.4 times higher risk of developing T2D than the control group. Our results showed a positive association between ND and T2D.

• Journal of Life Science
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• v.21 no.7
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• pp.961-968
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• 2011

The formation of reactive lipid aldehydes, 4-hydroxynonenal (HNE) is shown to be derived from fatty acid hydroperoxides through the oxidative process. Among its known effects in cytotoxicity, HNE has been implicated in apoptotic cell death. To delineate its putative role as a potential mediator, we investigated the mechanism by which HNE induces apoptosis of endothelial cells (ECs). The anti-proliferative effects of HNE were tested through MTT assay after exposure to various concentrations ($5\sim15\;{\mu}M$) of HNE. We observed apoptotic bodies with propidium iodide staining, and measured the HNE induction of endothelial apoptosis by flow cytometry assay. We observed that cells exposed to HNE for 24 hr resulted in increased poly(ADP-ribose) polymerase cleavage and up-regulation of Bax. Data on the HNE action strongly indicated the involvement of reactive species, namely, intracellular ROS, nitrite, and peroxynitrite. To obtain evidence on the implication of ROS and peroxynitrite in HNE-induced apoptosis, a ROS scavenger, N-acetylcysteine (NAC), and a peroxynitrite scavenger, penicillamine, were tested. Results clearly indicate that the induction of apoptosis by HNE was effectively inhibited by NAC and penicillamine. Based on the present data, we conclude that the endothelial apoptosis induced by HNE involves both ROS generation and peroxynitrite activity. Our new data could lead to a redefinition of HNE action on apoptosis in ECs.