Abstract
In order to investigate the glucoreceptor mechanism involved in insulin release and the haracter, characterics of the mechanism we have studied the dynamics of insulin release from the perifusd isolated islets of rats under slow-rise stimulation with α and β-D-glucose (α and β anomers), which were kept at 4°C in solution to prevent anomerization we tried to analyze kinetically each dose response curve obtained from those dynamics.
At concentrations ranging from 5 to 9 mM greater release of insulin was stimulated by the β anomer than by the β anomer. Both dose response curves were sigmoid with the same maximal rate of insulin release (0.9μu/ml/islet/min) at around 11 mM glucose, but the value of Km for the, β anomer was higher than that (6-7 mM) for the α anomer with 2 mM glucose.
Since the Lineweaver-Burk, plots for the α and β anomers were not straight lines, but parabolic ones, those insulin responses seem to be represented as n-ordered reactions (n> 1).
The logalithmic values were -3.9±0.7 and -5.9±0.6 (mM-n, M±S. E. M.), respectively for the α and β anomers, and therefoer, the affinity of the glucorecepter for the α anomer seemed to be one hundred times as strong as that for the β anomer.
The Hill plot for the α anomer was represented as a single line (n=4.8), whereas that for the β anomer consisted of two straight lines (n=2.3 and 6.2) which had a breakdown at 8.3 mM glucose. Therefore, this result shows that the recepter-recepter interaction may be increased at concentrations of the β anomer over 8.3 mM.
In conclusion, we have been led to the following suggestions: that the pancreatic B cells contain common glucoreceptors on the plasma membrane permitted to bind both anomers of D-glucose, and that the substrate-recepter complex formed between the β anomer and glucoreceptor may be “an incompleted binding” to induce an insulin release less than that with the α anomer at concentrations lower than 8.3 mM. But, in accordance with the raising of the β anomer concentration, the β anomer caused the same amount of insulin release as the α anomer through a change of the glucoreceptor conformation.
