Altered response of skeletal muscle to IL-6 in type 2 diabetic patients.
Altered response of skeletal muscle to IL-6 in type 2 diabetic patients.
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作者：
Jiang LQ;Duque-Guimaraes DE;Machado UF;Zierath JR;Krook A
白细胞介素-6（IL-6）在调节胰岛素敏感性方面具有双重作用，有证据表明这种细胞因子既是胰岛素作用的增强剂又是抑制剂。我们确定了IL-6暴露对正常糖耐量或2型糖尿病患者建立的培养肌管中葡萄糖和脂质代谢的影响。急性IL-6暴露增加糖原合成，葡萄糖摄取，和信号转导和转录激活因子3（STAT 3）磷酸化培养的肌管从正常的葡萄糖耐量的受试者。然而，在2型糖尿病患者中，IL-6对葡萄糖代谢和STAT 3信号传导没有影响，伴随着细胞因子信号传导抑制因子3（SOCS 3）表达的增加。IL-6增加2型糖尿病和正常葡萄糖耐量受试者肌管中的脂肪酸氧化。IL-6，IL-6受体（IL-6 R），或糖蛋白130的表达，以及IL-6的分泌，是从正常的葡萄糖耐量或2型糖尿病受试者培养的肌管之间不变。正常糖耐量和2型糖尿病受试者之间的循环血清IL-6浓度不变。总之，来自2型糖尿病患者的骨骼肌细胞显示对葡萄糖而不是脂质代谢的选择性IL-6抗性。总之，IL-6在2型糖尿病患者中与正常糖耐量受试者相比，在调节代谢方面似乎起着不同的作用。
Interleukin-6 (IL-6) has a dual role in modulating insulin sensitivity, with evidence for this cytokine as both an enhancer and inhibitor of insulin action. We determined the effect of IL-6 exposure on glucose and lipid metabolism in cultured myotubes established from people with normal glucose tolerance or type 2 diabetes. Acute IL-6 exposure increased glycogen synthesis, glucose uptake, and signal transducer and activator of transcription 3 (STAT3) phosphorylation in cultured myotubes from normal glucose tolerant subjects. However, in type 2 diabetic patients, IL-6 was without effect on glucose metabolism and STAT3 signaling, concomitant with increased suppressor of cytokine signaling 3 (SOCS3) expression. IL-6 increased fatty acid oxidation in myotubes from type 2 diabetic and normal glucose tolerant subjects. Expression of IL-6, IL-6 receptor (IL-6R), or glycoprotein 130, as well as IL-6 secretion, was unaltered between cultured myotubes from normal glucose tolerant or type 2 diabetic subjects. Circulating serum IL-6 concentration was unaltered between normal glucose tolerant and type 2 diabetic subjects. In summary, skeletal muscle cells from type 2 diabetic patients display selective IL-6 resistance for glucose rather than lipid metabolism. In conclusion, IL-6 appears to play a differential role in regulating metabolism in type 2 diabetic patients compared with normal glucose tolerant subjects.
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影响因子：
16.2
作者：
Ghanim H;Abuaysheh S;Sia CL;Korzeniewski K;Chaudhuri A;Fernandez-Real JM;Dandona P
通讯作者：
Dandona P
影响因子：
16.2
作者：
Deopurkar R;Ghanim H;Friedman J;Abuaysheh S;Sia CL;Mohanty P;Viswanathan P;Chaudhuri A;Dandona P
通讯作者：
Dandona P
影响因子：
7.7
作者：
Febbraio, MA;Hiscock, N;Pedersen, BK
通讯作者：
Pedersen, BK
影响因子：
5.9
作者：
O'Gorman, Donal J.;Krook, Anna
通讯作者：
Krook, Anna
影响因子：
6.3
作者：
Rune, A.;Salehzadeh, F.;Al-Khalili, L.
通讯作者：
Al-Khalili, L.