Panten U, Holze S, Lenzen S
Horm Metab Res Suppl. 1980;Suppl 10:27-30.
Evidence is presented that, to explain the insulin releasing capacity of L-leucine, b-BCH or alpha-ketoisocaproate (KIC), the following alternatives must be considered: 1. Interaction of the unchanged molecules with specific B-cell membrane receptors triggers insulin release. Stimulation of metabolism is a consequence of these events. 2. Primary enhancement of intramitochondrial hydrogen production triggers insulin secretion which could modulate metabolism. 3. Combination of mechanism 1 and 2: a) Additive effects of 1 and 2. b) Potentiation of 1 by 2. c) Potentiation of 2 by 1. 4. Different control of first phase or second phase of insulin release by 1, 2, or 3.
有证据表明，为了解释L-亮氨酸、β-羟基丁酸（b-BCH）或α-酮异己酸（KIC）的胰岛素释放能力，必须考虑以下几种可能性：1. 未改变的分子与特定的B细胞膜受体相互作用触发胰岛素释放。这些事件会刺激代谢。2. 线粒体内产氢的原发性增强触发胰岛素分泌，进而调节代谢。3. 机制1和2的组合：a) 1和2的相加作用。b) 2对1的增强作用。c) 1对2的增强作用。4. 1、2或3对胰岛素释放的第一阶段或第二阶段进行不同的调控。
