Duodenal-jejunal bypass surgery does not increase skeletal muscle insulin signal transduction or glucose disposal in Goto-Kakizaki type 2 diabetic rats.

Duodenal-jejunal bypass surgery does not increase skeletal muscle insulin signal transduction or glucose disposal in Goto-Kakizaki type 2 diabetic rats.
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DOI:
10.1007/s11695-010-0304-y
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发表时间:
2011-02
期刊:
影响因子:
2.9
通讯作者:
Dohm, G. Lynis
Dohm, G. Lynis
中科院分区:
医学3区
文献类型:
--
作者:
Gavin, Timothy P.;Sloan, Ruben C., III;Lukosius, Eric Z.;Reed, Melissa A.;Pender, John R.;Van Boghossian;Carter, Jacqueline J.;McKernie, Robert D.;Parikh, Kushal;Price, J. William;Tapscott, Edward B.;Pories, Walter J.;Dohm, G. Lynis

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十二指肠-空肠搭桥术(DJB)可逆转非肥胖型T2 DM啮齿动物模型Goto-Kakazaki(GK)大鼠的T2 DM。骨骼肌胰岛素抵抗是2型糖尿病患者胰岛素抵抗的标志。本研究的目的是研究DJB对骨骼肌胰岛素信号转导和葡萄糖代谢的影响。推测DJB能增加GK大鼠骨骼肌胰岛素信号转导和葡萄糖代谢。对GK大鼠进行DJB治疗。对GK大鼠和非糖尿病Wistar-京都(WKY)大鼠进行假手术。DJB后2周测定口服葡萄糖耐量(OGTT)。DJB后3周,检测骨骼肌胰岛素诱导的信号转导和葡萄糖处理情况。在GK大鼠模型上,与假手术组相比,DJB不能:1)改善空腹血糖或胰岛素;2)改善OGTT;或3)增加骨骼肌胰岛素信号转导或葡萄糖处置。有趣的是,骨骼肌糖代谢在WKY-Sham、GK-Sham和GK-DJB之间相似。搭桥近端小肠并不会增加骨骼肌葡萄糖的处置。GK大鼠骨骼肌胰岛素抵抗的缺乏,质疑这种动物模型是否足以研究T2 DM的病因和治疗。此外,在T2 DM的其他动物模型和T2 DM患者中,绕过前肠可能会导致不同的结果。
Duodenal-jejunal bypass (DJB) has been shown to reverse type 2 diabetes (T2DM) in Goto-Kakazaki (GK) rats, a rodent model of non-obese T2DM. Skeletal muscle insulin resistance is a hallmark decrement in T2DM. The aim of the current work was to investigate the effects of DJB on skeletal muscle insulin signal transduction and glucose disposal. It was hypothesized that DJB would increase skeletal muscle insulin signal transduction and glucose disposal in GK rats. DJB was performed in GK rats. Sham operations were performed in GK and non-diabetic Wistar-Kyoto (WKY) rats. At two weeks post-DJB, oral glucose tolerance (OGTT) was measured. At three weeks post-DJB, insulin-induced signal transduction and glucose disposal were measured in skeletal muscle. In GK rats and compared to Sham operation, DJB did not: 1) improve fasting glucose or insulin; 2) improve OGTT; or 3) increase skeletal muscle insulin signal transduction or glucose disposal. Interestingly, skeletal muscle glucose disposal was similar between WKY-Sham, GK-Sham, and GK-DJB. Bypassing of the proximal small intestine does not increase skeletal muscle glucose disposal. The lack of skeletal muscle insulin resistance in GK rats questions whether this animal model is adequate to investigate the etiology and treatments for T2DM. Additionally, bypassing of the foregut may lead to different findings in other animal models of T2DM as well as in T2DM patients.
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发表时间: 1993-01-15
影响因子: 4.1
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