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首页> 外文期刊>Journal of Cellular Physiology >NAD(P)H oxidase participates in the palmitate-induced superoxide production and insulin secretion by rat pancreatic islets.
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NAD(P)H oxidase participates in the palmitate-induced superoxide production and insulin secretion by rat pancreatic islets.

机译:NAD (P) H氧化酶参与palmitate-induced过氧化物生产和通过大鼠胰岛细胞胰岛素分泌。

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Nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase complex has been shown to be involved in the process of glucose-stimulated insulin secretion (GSIS). In this study, we examined the effect of palmitic acid on superoxide production and insulin secretion by rat pancreatic islets and the mechanism involved. Rat pancreatic islets were incubated during 1 h with 1 mM palmitate, 1% fatty acid free-albumin, 5.6 or 10 mM glucose and in the presence of inhibitors of NAD(P)H oxidase (DPI--diphenyleneiodonium), PKC (calphostin C) and carnitine palmitoyl transferase-I (CPT-I) (etomoxir). Superoxide content was determined by hydroethidine assays. Palmitate increased superoxide production in the presence of 5.6 and 10 mM glucose. This effect was dependent on activation of PKC and NAD(P)H oxidase. Palmitic acid oxidation was demonstrated to contribute for the fatty acid induction of superoxide production in the presence of 5.6 mM glucose. In fact, palmitate caused p47(PHOX) translocation to plasma membrane, as shown by immunohistochemistry. Exposure to palmitate for 1 h up-regulated the protein content of p47(PHOX) and the mRNA levels of p22(PHOX), gp91(PHOX), p47(PHOX), proinsulin and the G protein-coupled receptor 40 (GPR40). Fatty acid stimulation of insulin secretion in the presence of high glucose concentration was reduced by inhibition of NAD(P)H oxidase activity. In conclusion, NAD(P)H oxidase is an important source of superoxide in pancreatic islets and the activity of NAD(P)H oxidase is involved in the control of insulin secretion by palmitate.
机译:烟酰胺腺嘌呤二核苷酸磷酸(NAD (P) H氧化酶)已被证明是复杂参与分子生物学的过程胰岛素分泌(GSIS)。研究了棕榈酸的影响过氧化物生产和胰岛素分泌大鼠胰岛细胞和所涉及的机制。大鼠胰岛细胞中孵化1 h与1毫米棕榈酸酯、脂肪酸free-albumin 1%5.6到10毫米葡萄糖的存在NAD (P) H氧化酶的抑制剂(DPI——diphenyleneiodonium), PKC (calphostin C)和肉毒碱棕榈酰transferase-I (CPT-I)(etomoxir)。hydroethidine化验。在5.6和过氧化物生产10毫米葡萄糖。激活PKC和NAD (P) H氧化酶。酸氧化了贡献过氧化物生产的脂肪酸诱导在5.6毫米葡萄糖。棕榈酸酯引起p47 (PHOX)易位等离子体膜,如图所示免疫组织化学。h上调的蛋白含量p47 (PHOX)和第22位(PHOX)的mRNA水平gp91 (PHOX),p47 (PHOX),胰岛素原和G protein-coupled受体40 (GPR40)。胰岛素分泌的高葡萄糖浓度降低了抑制NAD (P) H氧化酶活动。氧化酶超氧化物的重要来源胰腺胰岛和NAD (P) H的活动氧化酶参与胰岛素的控制由棕榈酸分泌。

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