PARTICIPATION OF ENDOGENOUS FATTY-ACIDS IN THE SECRETORY ACTIVITY OF THE PANCREATIC B-CELL
PARTICIPATION OF ENDOGENOUS FATTY-ACIDS IN THE SECRETORY ACTIVITY OF THE PANCREATIC B-CELL
复制标题
DOI：
10.1042/bj2270995
复制
发表时间：
1985-01-01
影响因子：
4.1
通讯作者：
HELLERSTROM, C
中科院分区：
文献类型：
--
作者：
MALAISSE, WJ;MALAISSELAGAE, F;HELLERSTROM, C
胰岛β细胞可能是燃料感受器，营养促分泌剂引起的胰岛素释放可归因于外源性和/或内源性底物的氧化增加。本文研究了内源性脂肪酸在大鼠胰岛分泌反应中的作用。长链脂肪酸氧化抑制剂棕榈酸甲酯(MCN-3716，0.1 mM)可抑制外源性[U-14C]棕榈酸酯的氧化，并抑制[U-14C]棕榈酸酯标记的胰岛产生的14CO_2。帕莫昔酸甲酯不影响外源性D-[U-14C]葡萄糖或L-[U-14C]谷氨酰胺的氧化，不影响L-[U-14C]谷氨酰胺标记的胰岛NH_4~+的产生和14CO_2的产生。在没有外源养分的情况下以及在.apprx的滞后期之后。60min时，帕莫昔拉酸甲酯使氧摄取量降低至对照组的69%。棕榈酸甲酯抑制D-葡萄糖、D-甘油醛、2-氧基异己酸、L亮氨酸、2-氨基双环[2.2.1]庚烷-2-羧酸盐或3-苯丙酮酸诱导的胰岛素释放。当内源性脂肪酸的氧化已经被抑制时，例如，在丙酮酸或L-谷氨酰胺存在的情况下，帕莫昔酸甲酯对胰岛素的释放没有影响。由营养促分泌剂引起的胰岛素释放紧密依赖于营养物质氧化的总体速率，包括内源脂肪酸的氧化速率。
The pancreatic beta-cell may represent a fuel-sensor organ, the release of insulin evoked by nutrient secretagogues being attributable to an increased oxidation of exogenous and/or endogenous substrates. The participation of endogenous fatty acids in the secretory response of isolated rat pancreatic islets was investigated. Methyl palmoxirate (McN-3716, 0.1 mM), an inhibitor of long-chain-fatty-acid oxidation, suppressed the oxidation of exogenous [U-14C]palmitate and inhibited 14CO2 output from islets prelabeled with [U-14C]palmitate. Methyl palmoxirate failed to affect the oxidation of exogenous D-[U-14C]glucose or L-[U-14C]glutamine, the production of NH4+ and the output of 14CO2 from islets prelabeled with L-[U-14C]glutamine. In the absence of exogenous nutrient and after a lag period of .apprx. 60 min, methyl palmoxirate decreased O2 uptake to 69% of the control value. Methyl palmoxirate inhibited insulin release evoked by D-glucose, D-glyceraldehyde, 2-oxoisohexanoate, L-leucine, 2-aminobicyclo[2.2.1]heptane-2-carboxylate or 3-phenylpyruvate. Methyl palmoxirate failed to affect insulin release when the oxidation of endogenous fatty acids was already suppressed, e.g., in the presence of pyruvate or L-glutamine. Insulin release evoked by nutrient secretagogues tightly depends on the overall rate of nutrient oxidation, including that of endogenous fatty acids.