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Insulin release is glucose anomeric specific in the human.
The alpha-glucose anomer produces a greater insulin release than beta-glucose in various animal models. These glucose anomers were dissolved rapidly and administered intravenously to human volunteers at a high dose (0.5 g/kg) over a 3-min period or a low dose (3.5 g) over a 20-s period. Blood samples were obtained at frequent time intervals for measurement of whole blood glucose (ferricyanide), plasma glucose (beta-glucose oxidase) and serum immunoreactive insulin. The high-dose infusion test showed no differences between the anomers of either blood glucose or serum insulin levels. However, at the lower dose, the alpha-glucose anomer stimulated a significantly greater insulin release than did beta-glucose. It is concluded that the alpha-glucose anomer stimulates a greater insulin release than the beta-glucose anomer in human subjects at low but not at high doses intravenously and that this response is not apparently related to approximations of the degree of mutarotation. These results suggest that a steric specific glucose receptor site exists on the beta-cell as a rapid insulin release trigger, although the alpha-anomer does not exclusively produce this stimulation.[1]References
- Insulin release is glucose anomeric specific in the human. Rossini, A.A., Soeldner, J.S. J. Clin. Invest. (1976) [Pubmed]
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