http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
제2형 당뇨병 환자에서 혈관합병증과 Lipoprotein(a)와의 관계
김현각,박지현,류완희,박태선,백홍선 대한당뇨병학회 2001 임상당뇨병 Vol.2 No.2
연구배경: Lipoprotein(a) [Lp(a)]는 LDL-콜레스테롤과 크기와 지질 구성이 유사하지만 표면에 apo B100와 disulfide 결합을 하고있는 apo(a)라는 당단백을 갖고 있는 것이 특징이다. 이 혈장 성분은 심혈관 질환의 독립적인 위험인자로 알려져 있으며, 최근에 당뇨병이 없는 일반 환자에서 경동맥 죽상동맥경화증과 만성 신장질환과의 관련도 제시되고 있다. 본 연구는 죽상동맥경화증의 고 위험군인 제2형 당뇨병 환자에서 Lp(a)농도를 측정하고, 경동맥 내중막두께와 그 밖의 만성 합병증과의 관계를 알아보고자 하였다. 방법: 대상 환자는 1998년 3월부터 1999맨 12월까지 본원 내분비내과에 내원한 150명의 제2형 당뇨병 환자를 대상으로 하였고 환자의 연령분포는 31세부터 77세까지, C-peptide 평균농도는 1.27pmol/㎖ 이었다. 고해상도 B-mode 초음파기기로 경동맥 내중막두께와 죽전을 측정하였고, two-site sandwich enzyme-linked immunosorbent assay를 이용하여 Lp(a)를 측정하였다. 결과: 혈장 Lp(a) 농도는 경동맥 내중막두께가 두꺼울수록 증가하였고(24.5±17.6, 22.8±20.2, 40.2±37.0 ㎎/㎗ respectively; p=O.003), 죽전이 있는 환자에서 증가되어 있었다(35.4±26.5, 24.8±17.5㎎/㎗, p=0.019). 미세혈관 합병증과의 관계를 보면 망막증이 있는 환자에서 Lp(a)가 증가해 있었고, 정상 단백뇨를 보이는 환자보다 미세 단백뇨와 거대 단백뇨를 보이는 환자에서 Lp(a)가 증가해 있음을 알 수 있었다. 결론: Lp(a)는 제2형 당뇨병 환자에서 경동맥 죽상동맥경화증, 미세혈관 합병증과 관련이 있을 것으로 사료되며 Lp(a)가 당뇨병의 혈관합병증에 미치는 작용을 규명하기 위해서는 전향적 연구가 필요하리라 생각된다. Background: Lipoprotein(a) [Lp(a)] is a plasma particle, similar in size and lipid composition, to LDL, which, in addition to apo B1OO, contains a second glycoprotein, apo(a), which bears a strong resemblance to plasminogen. Many reports have indicated that Lp(a) is an independent risk factor for ischemic heart disease. Furthermore, recent studies have suggested an association between elevated Lp(a) levels and carotid atherosclerosis and chronic renal insufficiency in nondiabetic subjects. Thus we investigated the relationship between Lp (a) level and carotid intima-media thickness (IMT) and the other vascular complications in type 2 diabetes subjects. Method: A total of 150 diabetic patients with type 2 diabetes were examined. The carotid artery IMT and plaque formation were measured by high-resolution ultrasonography. The subjects were divided into tertiles according to IMT values. Serum Lp (a) level was measured by two-side sandwich enzyme-linked immunosorbent assay. Results: Serum Lp (a) increased with increasing IMT (24.5±17.6, 22.8±20.2, 40.2±37.0 ㎎/㎗, respectively; p=0.003) and was higher in subject with carotid artery plaques than without carotid artery plaques (35.4±26.5, 24.8±17.5 ㎎/㎗, p=0.019). Furthermore, serum LP(a) was increased with increasing proteinuria and was higher in subject with retinopathy than without retinopathy. Conclusions : From our study, we suggest that Lp(a) level is associated with carotid atherosclerosis and microvascular diabetic complications in subjects with type 2 diabetes mellitus. Prospective studies will be needed to confirm the effect of Lp(a) an the development of vascular complications in type 2 diabetes.
김현각,김종주,김영생 의과학연구소 2000 全北醫大論文集 Vol.24 No.2
It has been reported that NAD induces apototic cell death of T cells through ADP-ribosylation o fCD38 by arginine-specific ADP-ribosyltransferase. In this study, it was investigated whether the T cell lines can be apoptosed by the addition of NAD using EL-4 and CTLL-2 cell lines originated from murine lymphoma and cytotoxic T cell leukemia from mice, respectively. The T cell lines did not show apoptosis, but rather showed proliferation by the treatment or NAD. The reason why the two T cell lines were resistant to the NAD-dependent apoptosis was that CTLL-2 cells and EL-4 cells did not express CD38 and arginine-specific ADP-ribosyltransferase, respectively. In order to examine the mechanism of proliferative effect of NAD, we tested the effect of NAD metabolites on their proliferation. ADP-ribose, ATP and AMP induced proliferation of these cell lines of NAD metabolites on their proliferation. ADP-ribose, ATP and AMP induced proliferation of these cell lines in dose-dependent and time dependent manner. 8-cyclopentyl-1, 3-dipropylxanthine (CPX), an adenosine receptor antagonist, inhibited the NAD- and NAD metabolites-dependent proliferation of the cell lines, suggesting that the proliferative effect of the NAD metabolites may be through the actions of adenosine derived from the NAD metabolites on adenosine receptor. (Key words : EL-4 cell, CTLL-2, NAD, Adenosine receptor)