http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Ciaraldi, (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
-
-
사람 골격근 세포에서 글리코겐 합성효소 유전자 억제가 대사표현형에 미치는 영향
김정미,박경수,이홍규,고재준,Ciaraldi, TP,Henry, RR 대한당뇨병학회 2000 Diabetes and Metabolism Journal Vol.24 No.3
Background: Glycogen synthase (GS) is the rate-limiting enzyme controlling nonoxidative glucose disposal in skeletal muscle. Reduction in GS activity and impaired insulin responsiveness are characteristic features of skeletal muscle in type 2 diabetes that contribute to glucose intolerance. These properties also exist in human skeletal muscle cell cultures from type 2 diabetic subjects. The aim of study is to determine the effect of an isolated reduction in GS on glucose metabolism and if this change can generate a diabetes-like state. Methods: Cultured skeletal muscle cells from non-diabetic subjects were treated with antisense oligodeoxynucleotides (ODN) to GS to interfere with expression of the gene for b days. GS activity, protein expression, glycogen synthesis and cellular glycogen content were measured. Results: Treatment with antisense ODN reduced GS protein expression by 70% compared to control (scrambled) ODN (p$lt;0.01). Both total GS activity and that measured at 0.1 mM G-6-P were reduced by antisense ODN treatment. Insulin responsiveness of GS was also halved. Basal GS FV_(0.1), was decreased in both antisense ODN and control ODN treated cells and antisense treated cells did not show increase in GS FV0.1 in response to insulin stimulation. Glucose incorporation into glycogen under basal conditions was unaltered after antisense ODN treatment, though no further stimulation in response to insulin was observed. Yet both cellular glycogen content and glycogen synthesis were lower in antisense ODN treated cells compared to control ODN treated cells. Conclusions: Reduction in GS expression in human skeletal muscle cell impair GS activity and insulin responsiveness but does not replicate the abnormalities of glycogen synthesis found in cultured diabetic skeletal muscle cells.
-
-
Lovastatin이 골격근 세포의 지방산 산화에 미치는 영향
김동림 ( Dong Lim Kim ),송기호 ( Kee Ho Song ),김숙경 ( Suk Kyeong Kim ),김해림 ( Hae Rim Kim ),( Theodore P. Ciaraldi ),( Robert R. Henry ) 대한내과학회 2007 대한내과학회지 Vol.72 No.6
목적: Statin이 혈당을 감소시키고 인슐린 저항성을 개선시킨다고 보고되었다. 본 연구는 statin이 인슐린 저항성의 주 조직인 골격근에서 지방산의 산화에 어떤 영향을 미치는지를 알아보고자 하였다. 방법: 정상 혈당군 7명과 제2형 당뇨병 환자 7명에서 근육 생검으로 골격근 조직을 얻었다. 골격근 세포를 배양하여 분화 후 lovastatin (0, 20 μM)을 배지에 첨가하고 2일 후 [9,10-3H] palmitate 와 [8-3H] octanoate를 이용하여 지방산 산화를 측정하였다. 유리 지방산 산화를 조절하는 기전을 알아보고자 AMPK와 ACC 인산화를 관찰하였다. 결과: Lovastatin 처리 후 대조군과 비교하여 palmitate의 산화 및 (44.2±12.1 nmol/mg protein/3h, 271.2±32.7% 증가 vs 15.5±3.0 nmol/mg protein/3h, p<0.01) octanoate의 산화가 유의하게 증가하였다(10.0±4.6 nmol/mg protein/3h, 158.3±21.9% 증가 vs 5.0±1.4 nmol/mg protein/3h, p<0.05). 이런 반응은 정상 혈당군과 제2형 당뇨병 환자의 골격근 세포 모두에서 유사하였다. Lovastatin 처리 후 AMPK의 인산화는 관찰되지 않았지만 AMPK 단백은 감소하였다(73.6±6.2% of control, p<0.01). ACC의 인산화는 통계적으로 유의하게 증가하였다(149.5±20.6% of control, p<0.05). 결론: ACC 인산화를 통한 지방산 산화의 증가가 lovastatin이 골격근에 침착된 지방 농도를 감소 시키고 인슐린 저항성을 호전시킬 것으로 생각된다. Background: Recent clinical studies have suggested that statins improve insulin resistance and glucose metabolism in the skeletal muscle of diabetic patients. To evaluate a possible component of this action, we measured free fatty acid oxidation in cultured human skeletal muscle cells (HSMC). Methods: Seven normal controls and 7 type 2 diabetic patients underwent quadriceps muscle biopsy. The HSMCs (n=14) were treated with or without lovastatin (Lova, 20 μM) for 2 days, and the free fatty acid (FFA) oxidation was measured. Results: Lova increased the oxidation of the long-chain FA palmitate to 271.2±32.7% of the control (p<0.01). Oxidation of the medium chain FA octanoate also increased after treatment of Lova (158.3±21.9%, p<0.05). One pathway of regulation of FFA is through AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation. Following Lova treatment, AMPK phosphorylation did not show a significant change while the total protein expression of AMPK was decreased (73.6±6.2% of the control, p<0.01). Lova treatment significantly increased ACC phosphorylation (149.5±20.6% of the control, p<0.05). Conclusion: Lova increased FFA oxidation by increasing the ACC phosphorylation in human skeletal muscle cells. Stimulation of skeletal muscle FFA oxidation may be one mechanism by which statins act to lower intramyocellular triglyceride and improve insulin action on glucose metabolism. (Korean J Med 72:600-606, 2007)
KCI
KISS연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
