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1 Exercise Science Research Institute, Arizona State University, Tempe, Arizona 85287; and 2 University of Colorado Health Sciences Center, Department of Medicine, Denver, Colorado 80262
High-fat (HFD) and
high-sucrose diets (HSD) reduce insulin suppression of glucose
production in vivo, increase the capacity for gluconeogenesis in vitro,
and increase glucose-6-phosphatase (G-6-Pase) activity in whole cell
homogenates. The present study examined the effects of HSD and HFD on
in vivo gluconeogenesis, the catalytic and glucose-6-phosphate
translocase subunits of G-6-Pase, glucokinase (GK) translocation, and
glucose cycling. Rats were fed a high-starch control diet (STD; 68%
cornstarch), HSD (68% sucrose), or HFD (45% fat) for 7-13 days.
The ratio of 3H in C6:C2 of glucose after
3H2O injection into 6- to 8-h-fasted rats was
significantly increased in HSD (0.68 ± 0.07) and HFD (0.71 ± 0.08) vs. STD (0.40 ± 0.10). G-6-Pase activity was
significantly higher in HSD and HFD vs. STD in both intact and
disrupted liver microsomes. HSD and HFD significantly increased the
amount of the p36 catalytic subunit protein, whereas the p46
glucose-6-phosphate translocase protein was increased in HSD only.
Despite increased nonglycerol gluconeogenesis and increased G-6-Pase,
basal glucose and insulin levels as well as glucose production were not
significantly different among groups. Hepatocyte cell suspensions were
used to ascertain whether diet-induced adaptations in glucose
phosphorylation and GK might serve to compensate for upregulation of
G-6-Pase. Tracer-estimated glucose phosphorylation and glucose cycling
(glucose 
glucose 6-phosphate) were significantly higher in cells
isolated from HSD only. After incubation with either 5 or 20 mM glucose
and no insulin, GK activity (nmol · mg
protein
1 · min1) in
digitonin-treated eluates (translocated GK) was significantly higher in
HSD (32 ± 4 and 146 ± 6) vs. HFD (4 ± 1 and 83 ± 10) and STD (9 ± 2 and 87 ± 9). Thus short-term, chronic
exposure to HSD and HFD increase in vivo gluconeogenesis and the
G-6-Pase catalytic subunit. Exposure to HSD diet also leads to
adaptations in glucose phosphorylation and GK translocation.
glucose-6-phosphatase; liver; glucose metabolism; glucokinase
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