Abstract

Rat brain cells were incubated at 9 °C (and occasionally at 37°C) in the presence of the anomers of d-[5- 3H]glucose, d-[U- 14C]glucose, d-[6- 14C]glucose and d-[1- 14C]glucose (1.0 mM). The utilization of β- d-[5- 3H]glucose was slightly higher than that of α- d-[5- 3H]glucose, a situation possibly attributable to the anomeric behaviour of hexokinase. However, the production of 14CO 2 from the α-anomer always largely exceeded that from the β-anomer. The anomeric difference in d-[U- 14C]glucose oxidation, relative to d-[5- 3H]glucose utilization, was suppressed in the presence of NH 4Cl. Even at anomeric equilibrium, the relative contribution of α- d-glucose to 14CO 2 output exceeded its relative abundance. The β/α ratio for d-[1- 14C]glucose oxidation (or d-[U- 14C]glucose oxidation) was higher than that for d-[6- 14C]glucose oxidation. Comparable observations were made in brain cells from albino rats and either lean or obese Zucker rats. It is concluded that d-glucose metabolism displays anomeric specificity in rat brain cells, even when the latter are exposed to equilibrated d-glucose. It is also speculated that anomeric differences in the phosphorylation of d-glucose by bound hexokinase may directly influence mitochondrial oxidative events.

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