Panten U
Naunyn Schmiedebergs Arch Pharmacol. 1975;291(4):405-20. doi: 10.1007/BF00501798.
In perifused isolated pancreatic islets alpha-ketoisocaproic acid (KIC) or alpha-ketocaproic acid (KC) induced a high insulin secretion rate and a steep increase of the fluorescence of reduced pyridine pyridine nucleotides [NAD(P)H] which fell again to almost prestimulatory levels 6 min after medium change. Insulin release in response to alpha-ketooctanoic (KO) acid started slowly and was accompanied by a decrease of the NAD(P)H-fluorescence trace. Beta-phenylpyruvate which is known to initiate insulin release also caused a fluorescence decrease. Alpha-keto-isovaleric (KIV) acid or pyruvate had no significant effects upon insulin secretion or NAD(P)H-fluorescence. In contrast to l-leucine, l-norleucine or l-valine did not enhance insulin release or fluorescence of NAD(P)H. KIV, alpha-keto-beta-methylvaleric acid (KMV), KIC and KC raised the production their corresponding amino acids by islet cells. From these results it is concluded that alpha-ketomonocarboxylic acids as such trigger insulin release by acting upon receptor sites which differ from those occupied by amino acids.
在灌流的分离胰岛中,α-酮异己酸(KIC)或α-酮己酸(KC)诱导了高胰岛素分泌率以及还原型吡啶核苷酸[NAD(P)H]荧光的急剧增加,在更换培养基6分钟后,荧光又再次降至几乎刺激前的水平。对α-酮辛酸(KO)的胰岛素释放开始缓慢,并伴有NAD(P)H荧光迹线的下降。已知能引发胰岛素释放的β-苯丙酮酸也导致荧光下降。α-酮异戊酸(KIV)或丙酮酸对胰岛素分泌或NAD(P)H荧光没有显著影响。与L-亮氨酸不同,L-正亮氨酸或L-缬氨酸不会增强胰岛素释放或NAD(P)H荧光。KIV、α-酮-β-甲基戊酸(KMV)、KIC和KC提高了胰岛细胞对其相应氨基酸的生成。从这些结果可以得出结论,α-酮单羧酸本身通过作用于与氨基酸所占据的受体位点不同的受体位点来触发胰岛素释放。