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1 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: masakazu.shota{at}vanderbilt.edu.
Hepatic glucose fluxes and intracellular movement of glucokinase (GK) in response to increased plasma glucose and insulin were examined in 10 w old 6 h fasted conscious Zucker diabetic fatty (ZDF) rats and lean littermates. Under basal conditions, plasma glucose (mmol/l) and glucose turnover rate (GTR; µmol.kg-1.min-1) were slightly higher in ZDF (8.4 ± 0.3 and 53 ± 7, respectively) than in lean rats (6.2 ± 0.2 and 45 ± 4, respectively), while plasma insulin (pmol/l) was higher in ZDF (1800 ± 350) than lean rats (150 ± 14). The ratio of hepatic uridine 5'-diphosphate-glucose to plasma glucose [3H] specific activity ([3H]UDPG/G; %), total hepatic glucose output (µmol.kg-1.min-1) and hepatic glucose cycling (µmol.kg-1.min-1) were higher in ZDF (35 ± 5, 87 ± 16, and 33 ± 10, respectively) compared to lean rats (18 ± 3, 56 ± 6, and 11 ± 2, respectively). [3H]-glucose incorporation into glycogen (µmol glucose.g liver-1) was similar in lean (1.0 ± 0.7) and ZDF (1.6 ± 0.8) rats. GK was predominantly located in the nucleus in both rats. With elevated plasma glucose and insulin, GTR (µmol.kg-1.min-1), [3H]UDPG/G (%), and [3H]-glucose incorporation into glycogen (µmol glucose.g liver-1) were markedly higher in lean (191 ± 22, 62 ± 3, and 5.0 ± 1.4, respectively), but similar in ZDF rats (100 ± 6, 37 ± 3, and 1.4 ± 0.4, respectively), compared to basal conditions. GK translocation from the nucleus to the cytoplasm occurred in lean, but not in ZDF rats. The unresponsiveness of hepatic glucose flux to the rise in plasma glucose and insulin seen in pre-diabetic ZDF rats was associated with impaired GK translocation.
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