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Overexpression of either liver type or pancreatic β cell type glucokinase via recombinant adenovirus enhances glucose oxidation in isolated rat hepatocytes
Author(s) -
Takeuchi Hideo,
Inoue Yasushi,
Ishihara Hisamitsu,
Oka Yoshitomo
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(96)00833-2
Subject(s) - glucokinase , hexokinase , biochemistry , chemistry , carbohydrate metabolism , recombinant dna , cell , enzyme , phosphorylation , pyruvate kinase , hepatocyte , medicine , biology , cell type , endocrinology , glycolysis , in vitro , gene
To elucidate a role of glucokinase in hepatic glucose metabolism, we overexpressed hexokinase I (HKI), liver type glucokinase (LGK), or β cell type glucokinase (βGK) in primary rat hepatocytes using a recombinant adenovirus vector system. Overexpression of HKI and LGK induced a 34‐ and 25‐fold increase, respectively, in glucose phosphorylation activity measured in cell homogenates. While HKI overexpression induced only a 1.3‐fold increase in glucose oxidation, LGK overexpression increased glucose oxidation by 2.9‐fold. Overexpression of βGK had essentially the same effect as LGK. The results indicate that glucokinase does indeed regulate the rate of hepatic glucose oxidation and that the liver‐specific sequence of this enzyme is not essential for this function.