RGD Reference Report - Defect in glucokinase translocation in Zucker diabetic fatty rats. - Rat Genome Database

Send us a Message

Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Defect in glucokinase translocation in Zucker diabetic fatty rats.

Authors: Fujimoto, Y  Donahue, EP  Shiota, M 
Citation: Fujimoto Y, etal., Am J Physiol Endocrinol Metab. 2004 Sep;287(3):E414-23. Epub 2004 May 11.
RGD ID: 1582633
Pubmed: PMID:15138155   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpendo.00575.2003   (Journal Full-text)

Hepatic glucose fluxes and intracellular movement of glucokinase (GK) in response to increased plasma glucose and insulin were examined in 10-wk-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; micromol.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), whereas plasma insulin (pmol/l) was higher in ZDF (1,800 +/- 350) than in lean rats (150 +/- 14). The ratio of hepatic uridine 5'-diphosphate-glucose 3H specific activity to plasma glucose 3H specific activity ([3H]UDP-G/[3H]G; %), total hepatic glucose output (micromol.kg(-1).min(-1)), and hepatic glucose cycling (micromol.kg(-1).min(-1)) were higher in ZDF (35 +/- 5, 87 +/- 16, and 33 +/- 10, respectively) compared with lean rats (18 +/- 3, 56 +/- 6, and 11 +/- 2, respectively). [3H]glucose incorporation into glycogen (micromol glucose/g liver) 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 (micromol.kg(-1).min(-1)), [3H]UDP-G/[3H]G (%), and [3H]glucose incorporation into glycogen (micromol glucose/g liver) 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 with 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 prediabetic ZDF rats was associated with impaired GK translocation.

Disease Annotations    

Gene Ontology Annotations    

Biological Process

Cellular Component
cytoplasm  (IDA)
nucleus  (IDA)

Molecular Function

Molecular Pathway Annotations    
Objects Annotated

Genes (Rattus norvegicus)
Gck  (glucokinase)
Gckr  (glucokinase regulator)
Gys2  (glycogen synthase 2)
Hk1  (hexokinase 1)
Hk2  (hexokinase 2)
Hk3  (hexokinase 3)
Pygl  (glycogen phosphorylase L)

Genes (Mus musculus)
G6pc  (glucose-6-phosphatase, catalytic)
Gck  (glucokinase)
Gys2  (glycogen synthase 2)
Pygl  (liver glycogen phosphorylase)

Genes (Homo sapiens)
G6PC1  (glucose-6-phosphatase catalytic subunit 1)
GCK  (glucokinase)
GYS2  (glycogen synthase 2)
PYGL  (glycogen phosphorylase L)

Objects referenced in this article
Gene G6pc1 glucose-6-phosphatase catalytic subunit 1 Rattus norvegicus

Additional Information