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전염증성 사이토카인에 의해 유도된 베타세포 자연사에 대한 유비퀴틴화를 통한 GLP-1의 보호효과
임동미,김주영,이강우,박근용,김병준 대한내분비학회 2011 Endocrinology and metabolism Vol.26 No.2
Background: Proinflammatory cytokines are one of the causes of diabetes mellitus. However, the exact molecular mechanism by which proinflammatory cytokines induce β-cell death remains to be clearly elucidated. Glucagon-like peptide-1 (GLP-1) affects the stimulation of insulin secretion and the preservation of β-cells. Additionally, it may exert an antiapoptotic effect on β cells; however,the mechanism underlying this effect has yet to be demonstrated. Therefore, we investigated the protective effects of GLP-1 in endoplasmic reticulum (ER)-mediated β-cell apoptosis using proinflammatory cytokines. Methods: To induce ER stress, hamster insulin-secreting tumor (HIT)-T15 cells were treated using a mixture of cytokines. Apoptosis was evaluated via MTT assay, Hoechst 33342 staining, and annexin/propidium iodide (PI) flow cytometry. The mRNA and protein expression levels of ER stress-related molecules were determined via PCR and Western blotting, respectively. Nitric oxide was measured with Griess reagent. The levels of inducible nitric oxide synthase (iNOS) mRNA and protein were analyzed via real-time PCR and Western blot, respectively. iNOS protein degradation was evaluated via immunoprecipitation. We pretreated HIT-T15 cells with exendin (Ex)-4 for 1 hour prior to the induction of stress. Results: We determined that Ex-4 exerted a protective effect through nitric oxide and the modulation of ER stress-related molecules (glucose-regulated protein [GRP]78, GRP94, and CCAAT/enhancer-binding protein homologous protein [CHOP]) and that Ex-4stimulates iNOS protein degradation via the ubiquitination pathway. Additionally, Ex-4 also induced the recovery of insulin2 mRNA expression in β cells. Conclusion: The results of this study indicate that GLP-1 may protect β cells against apoptosis through the ubiquitination pathway.
제2형 당뇨병환자에서 각 대사증후군의 정의(WHO, NCEP-ATP III, IDF)에 따른 심혈관질환의 예측능 비교
임동미,고관표,박근용 대한당뇨병학회 2008 Diabetes and Metabolism Journal Vol.32 No.2
Background: Metabolic syndrome (MetS) is constellation of cardiovascular risk factors. There are three typically used definitions of MetS proposed by WHO, IDF and NCEP-ATP III. We conducted this study to compare the associations of MetS by WHO, IDF and NCEP-ATP III definition to various metabolic markers of coronary heart diseases in Korean type 2 diabetes patients.Methods: We enrolled 151 Korean type 2 diabetes patients in one hospital. Anthropometric and biochemical parameters, including high-sensitivity C-reactive protein (hsCRP), homocysteine, uric acid were measured. And then, we divided MetS group from non-MetS group according to three other definitions.Results: Serum hsCRP level was higher in those with MetS group than non-MetS group by WHO definition (0.33 ± 0.36 mg/dL vs 0.18 ± 0.26 mg/dL, P < 0.001). But, there are no difference in MetS group and non-MetS group by IDF and NCEP-ATPIII definition. (By IDF, 0.28 ± 0.31 mg/dL vs 0.25 ± 0.34 mg/dL, P = 0.64; By NCEP-ATP III, 0.28 ± 0.33 mg/dL vs 0.22 ± 0.32 mg/dL, P = 0.41). Uric acid and homocysteine levels were higher in those with MetS by WHO definition (P < 0.05). Similarly, analyses according to IDF and NCEP ATP III definition showed no significant difference.Conclusion: In conclusion, WHO definition of MetS has a stronger relationship with the biochemical markers of coronary heart disease in Korean type 2 diabetes patients. (KOREAN DIABETES J 32:157~164, 2008)
제2형 당뇨병환자에서 대사증후군의 정도에 따른 심혈관질환 위험도
임동미 ( Dong Mee Lim ),박근용 ( Keun Young Park ),김병준 ( Byung Joon Kim ),이강우 ( Kang Woo Lee ),이명준 ( Myung Jun Lee ),염윤식 ( Yoon Shick Yom ),고관표 ( Gwan Pyo Koh ) 대한당뇨병학회 2009 임상당뇨병 Vol.10 No.3
연구배경: 대사증후군은 한 개인에서 죽상동맥경화성 심혈관질환 위험인자들이 무리지어 발생하는 현상을 말한다. 그러나 제2형 당뇨병환자에서도 대사증후군이 관상동맥질환의 발생위험을 증가시키는지 확실치 않다. FRS는 관상동맥질환의 10년 위험도를 계산하는 전통적인 방법이다. 저자는 제2형 당뇨병에서 대사증후군 및 FRS와 관상동맥질환예측인자들의 연관성을 분석하여 대사증후군이 관상동맥질환 위험도를 증가시키는지 간접적으로 알아보고자 하였다. 대상 및 방법: 제2형 당뇨병으로 진단 받은 78명을 대상으로 하였고(남자: 29명, 여자: 49명) 심혈관질환의 과거력, 고지혈증 약제의 복용력, 감염이 있는 환자는 제외하였다. 복부둘레는 남자 90 cm, 여자 85 cm을 적용하였고 나머지는 NCEP 기준에 따라 대사증후군을 진단하였다. 관상동맥질환의 예측인자로서는 hsCRP, 호모시스테인, 피브리노겐, 지단백(a), 요산, 감마지티를 측정하였다. 결과 및 결론: 전체 대상의 71.8%는 대사증후군을 가지고 있었다. 모든 관상동맥질환 예측인자들의 수치는 대사증후군을 가진 군과 없는 군 사이에 차이가 없었다. 대사증후군 각 진단인자 수에 따라 5개 군으로 나누어 비교하여도 차이가 없었다. 그러나 예측인자 중 호모시스테인(r=0.317; P<0.05), 피브리노겐(r=0.332; P<0.05), 요산 (r=0.268; P<0.05)는 FRS수와 의미 있는 양의 상관관계를 보였다. FRS를 크기에 따라 5군으로 나누어 비교하였을 때도 호모시스테인(6.6±1.7, 11.0±3.7, 10.2±3.7, 14.0±6.1 and 11.3±2.9 mmol/L; P<0.001)과 요산(3.2±0.5, 4.6±1.5, 5.4±2.3, 7.1±3.9 and 5.2±2.2 mg/dL; P<0.05)는 유의한 차이를 보였다. 제2형 당뇨병환자에서 대사증후군은 어떤 관상동맥질환 예측인자와도 관련이 없었으나 FRS는 일부 예측인자들과 유의한 연관성이 있었다. 이는 제2형 당뇨병에서 대사증후군은 관상동맥질환의 발생과 상관관계가 없다는 가능성을 시사한다. The metabolic syndrome (MetS) is a constellation of interrelated risk factors to promote the development of atherosclerotic cardiovascular disease (CVD). In type 2 diabetes mellitus (T2DM), however, it has not yet been clarified whether the identification of the MetS improves the prediction of cardiovascular (CV) events. Framingham risk score (FRS) is an established predicting model for CVD. In the present study, we compared the impact of MetS with FRS on CV predictors in patients with T2DM. Seventy eight patients with T2DM (29 males and 49 females) were enrolled. Patients with history of CVD, any inflammatory disease and anti-hyperlipidemic medication were excluded. MetS was defined by modified NCEP-ATP III criteria. High-sensitivity C-reactive protein (hsCRP), homocysteine, lipoprotein(a), fibrinogen, uric acid and γ-glutamy transferase were regarded as CV predictors. 71.8% of total patients had the MetS. Diabetic patients with or without MetS were well matched in terms of the levels of all CV predictors. The CV factors were also not significantly different between numbers (1, 2, 3, 4 and 5) of components of the MetS. However, homocysteine (r=0.317; P<0.05), fibrinogen (r=0.332; P<0.05) and uric acid (r=0.268; P<0.05) levels were positively correlated with FRS. The levels of homocysteine (6.6±1.7, 11.0±3.7, 10.2±3.7, 14.0±6.1 and 11.3±2.9 mmol/L; P<0.001) and uric acid (3.2±0.5, 4.6±1.5, 5.4±2.3, 7.1±3.9 and 5.2±2.2 mg/dL; P<0.05) were significantly different to increasing quintiles of FRS. It suggests that categorizing type 2 diabetic subjects as having or not having the MetS does not provide further prediction of CVD. Collectively, these results suggest that the prediction of CVD was not related to the possession of the MetS in categorizing type 2 diabetic patients. (Korean Clinical Diabetes J 10:196-203, 2009)
양측성 알도스테론 생성 선종으로 오인될 수 있었던 특발성 고알도스테론증 1예
임동미 ( Dong Mee Lim ),박근용 ( Keun Yong Park ) 대한내과학회 2008 대한내과학회지 Vol.75 No.1
저자들은 난치성 고혈압과 저칼륨혈증을 보인 환자에서 원발성 알도스테론증의 원인을 조사하던 중 부신 전산화 단층 촬영에서 양측성 알도스테론 생성 선종의 소견이었으나, 알도스테론의 체위변화 검사와 부신정맥 도자술을 통하여 양측성의 특발성 알도스테론증으로 진단한 증례를 경험하였기에 보고하는 바이다. In most cases, primary aldosteronism is due to a unilateral adrenal adenoma or bilateral hyperplasia of the adrenal cortex. However, a few bilateral adrenal tumors have also been reported in primary aldosteronism. In such cases, it is important to differentiate bilateral aldosterone-producing adenomas from bilateral adrenal hyperplasia so as to develop the optimal treatment plan. We report a case of idiopathic hyperaldosteronism due to bilateral adrenal hyperplasia that could have been misdiagnosed as a bilateral aldosterone-producing adenoma. An adrenal CT scan revealed bilateral adrenal tumors (1.5 cm [right] and 3.6 cm [left] in diameter). Idiopathic hyperaldosteronism was properly diagnosed using a posture test and selective adrenal venous sampling.(Korean J Med 75:93-97, 2008)