It has been demonstrated in the conscious dog that portal glucose infusion
creates a signal that increases net hepatic glucose uptake and hepatic glyc
ogen deposition. Experiments leading to an understanding of the mechanism b
y which this change occurs will be facilitated if this finding can be repro
duced in the rat. Rats weighing 275-300 g were implanted with four indwelli
ng catheters (one in the portal vein, one in the left carotid artery, and t
wo in the light jugular vein) that were externalized between the scapulae.
The rats were studied in a conscious, unrestained condition 7 days after su
rgery, following a 24-h fast. Each experiment consisted of a 30- to 60-min
equilibration, a 30-min baseline, and a 120-min test period. In the test pe
riod, a pancreatic clamp was performed by using somatostatin, insulin, and
glucagon. Glucose was given simultaneously either through the jugular vein
to clamp the arterial blood level at 220 mg/dl (Pe low group) or at 250 mg/
dl (Pe high group), or via the hepatic portal vein (Po group; 6 mp.kg(-1).m
in(-1)) and the jugular vein to clamp the arterial blood glucose level to 2
20 mg/dl. In the test period, the arterial plasma glucagon and insulin leve
ls were not significantly different in the three groups (36 +/- 2, 33 +/- 2
, and 30 +/- 2 pg/ml and 1.34 +/- 0.08, 1.37 +/- 0.18, and 1.66 +/- 0.11 ng
/ml in Po, Pe low; and Pe high groups, respectively). The arterial blood gl
ucose levels during the test period were 224 +/- 4 mg/dl for Po, 220 +/- 3
for Pe low and 255 +/- 2 for Pe high group. The Liver glycogen content (mu
mol glucose/g liver) in the two Pe groups was not statistically different (
51 +/- 7 and 65 +/- 8, respectively), whereas the glycogen level in the Po
group was significantly greater (93 +/- 9, P < 0.05). Because portal glucos
e delivery also augments hepatic glycogen deposition in the rat, as it does
in the dogs, mechanistic studies relating to its function can now be under
taken in this species.