Stimulation of Islet Protein Kinase C Translocation by Palmitate Requires Metabolism of the Fatty Acid
Stimulation of Islet Protein Kinase C Translocation by Palmitate Requires Metabolism of the Fatty Acid
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棕榈酸酯刺激胰岛蛋白激酶 C 易位需要脂肪酸的代谢
DOI：
10.2337/diab.46.7.1153
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发表时间：
1997
期刊：
影响因子：
7.7
通讯作者：
J. Tamarit
中科院分区：
文献类型：
--
作者：
O. Alcáazar;Qiu;E. Giné;J. Tamarit
The secretory, metabolic, and signaling aspects of glucose/ palmitate interaction on β-cell function have been studied on rat islets. Palmitate potentiated the glucose-induced insulin response of perifused islets at suprathreshold (>3 mmol/1) sugar concentrations. This potentiating effect could be suppressed by 8-bromocGMP, which also blocks palmitate metabolism. Palmitate did not modify glucose utilization, but it slightly reduced glucose oxidation and concomitantly increased lactate production. The very low rate of palmitate oxidation (80-fold lower than that of 20 mmol/l glucose) might explain its lack of effect on glycolysis and hence that the glucose/fatty acid cycle is inoperative in islet cells. However, glucose determines the metabolic fate of exogenous palmitate, which is mainly diverted toward lipid synthesis at high sugar concentrations and might then generate lipid messengers for cell signaling. Palmitate did not increase glucose-induced production of inositol-l,4,5-trisphosphate, but it stimulated the translocation of protein kinase C activity from a cytosolic to a particulate fraction at 20 but not at 3 mmol/l glucose. This increased translocation was partially or completely blocked by hydroxycitrate or 8-bromo-cGMP, respectively, which are agents interfering with palmitate metabolism (inhibiting lipid synthesis). The metabolic interaction between glucose and palmitate might generate lipid messengers (diacylglycerol, phosphatidylserine) necessary for the activation of islet protein kinase C, which would in turn result in a potentiation of glucose-induced insulin secretion.
影响因子：
15.9
作者：
Stein, DT;Esser, V;McGarry, JD
通讯作者：
McGarry, JD
促分泌素诱导的二酰甘油在离体胰岛中积累。
影响因子：
2.9
作者：
Wolf,BA;Easom,RA;Hughes,JH;McDaniel,ML;Turk,J
通讯作者：
Turk,J
丙二酰辅酶A在葡萄糖刺激克隆胰腺β细胞分泌胰岛素中的作用。
DOI：
--
发表时间：
1989
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Corkey,BE;Glennon,MC;Chen,KS;Deeney,JT;Matschinsky,FM;Prentki,M
通讯作者：
Prentki,M