scholarly journals Intraportal glucose delivery enhances the effects of hepatic glucose load on net hepatic glucose uptake in vivo.

1991 ◽  
Vol 88 (1) ◽  
pp. 158-167 ◽  
Author(s):  
S R Myers ◽  
D W Biggers ◽  
D W Neal ◽  
A D Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Load ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

scholarly journals Nonhepatic response to portal glucose delivery in conscious dogs

2000 ◽  
Vol 279 (6) ◽  
pp. E1271-E1277 ◽  
Author(s):  
Mary Courtney Moore ◽  
Po-Shiuan Hsieh ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
The Difference ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Blood Glucose Concentrations ◽  
Hepatic Glucose Uptake

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg−1 · min−1 via a peripheral (Pe10, n = 5) or the portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were not different during the glucose infusion in Pe10 and Po10 (37 ± 6 and 43 ± 12 μU/ml, respectively), and glucagon concentrations declined similarly throughout the two studies. Arterial blood glucose concentrations during glucose infusion were not different between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and Po10, respectively). Portal glucose delivery made the hepatic glucose load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg−1 · min−1 in Pe10 vs. Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg−1 · min−1) and fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller ( P < 0.05) in Pe10 than in Po10. Nonhepatic (primarily muscle) glucose uptake was correspondingly increased in Pe10 compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg−1 · min−1, P < 0.05). Approximately one-half of the difference in NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the portal signal itself. Even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to alter partitioning of a glucose load among the tissues, stimulating NHGU and reducing peripheral glucose uptake.

Rapid reversal of the effects of the portal signal under hyperinsulinemic conditions in the conscious dog

1999 ◽  
Vol 276 (5) ◽  
pp. E930-E937 ◽  
Author(s):  
Po-Shiuan Hsieh ◽  
Mary Courtney Moore ◽  
Doss W. Neal ◽  
Maya Emshwiller ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Infusion Rate ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Conscious Dog ◽  
The Third ◽  
Hepatic Glucose ◽  
Rapid Reversal ◽  
Hepatic Glucose Uptake

Experiments were performed on two groups of 42-h-fasted conscious dogs ( n = 6/group). Somatostatin was given peripherally with insulin (4-fold basal) and glucagon (basal) intraportally. In the first experimental period, glucose was infused peripherally to double the hepatic glucose load (HGL) in both groups. In the second experimental period, glucose (21.8 μmol ⋅ kg−1⋅ min−1) was infused intraportally and the peripheral glucose infusion rate (PeGIR) was reduced to maintain the precreating HGL in the portal signal (PO) group, whereas saline was given intraportally in the control (CON) group and PeGIR was not changed. In the third period, the portal glucose infusion was stopped in the PO group and PeGIR was increased to sustain HGL. PeGIR was continued in the CON group. The glucose loads to the liver did not differ in the CON and PO groups. Net hepatic glucose uptake was 9.6 ± 2.5, 11.6 ± 2.6, and 15.5 ± 3.2 vs. 10.8 ± 1.8, 23.7 ± 3.0, and 15.5 ± 1.1 μmol ⋅ kg−1⋅ min−1, and nonhepatic glucose uptake (non-HGU) was 29.8 ± 1.1, 40.1 ± 4.5, and 49.5 ± 4.0 vs. 26.6 ± 4.3, 23.2 ± 4.0, and 40.4 ± 3.1 μmol ⋅ kg−1⋅ min−1in the CON and PO groups during the three periods, respectively. Cessation of the portal signal shifted NHGU and non-HGU to rates similar to those evident in the CON group within 10 min. These results indicate that even under hyperinsulinemic conditions the effects of the portal signal on hepatic and peripheral glucose uptake are rapidly reversible.

Factors Which Regulate Net Hepatic Glucose Uptake In Vivo

1991 ◽  
Vol 15 (3) ◽  
pp. 71S-73S ◽  
Author(s):  
Alan D. Cherrington ◽  
Michael J. Pagliassotti ◽  
Sharon R. Myers ◽  
Bess Adkins-Marshall ◽  
Owen P. Mcguinness
Keyword(s):  
Glucose Uptake ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

scholarly journals A physiological increase in the hepatic glycogen level does not affect the response of net hepatic glucose uptake to insulin

2009 ◽  
Vol 297 (2) ◽  
pp. E358-E366 ◽  
Author(s):  
Jason J. Winnick ◽  
Zhibo An ◽  
Mary Courtney Moore ◽  
Christopher J. Ramnanan ◽  
Ben Farmer ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glycogen Synthesis ◽  
Control Period ◽  
In Vivo Studies ◽  
Hepatic Glycogen ◽  
Glycogen Level ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Hepatic Glucose Uptake

To determine the effect of an acute increase in hepatic glycogen on net hepatic glucose uptake (NHGU) and disposition in response to insulin in vivo, studies were performed on two groups of dogs fasted 18 h. During the first 4 h of the study, somatostatin was infused peripherally, while insulin and glucagon were replaced intraportally in basal amounts. Hyperglycemia was brought about by glucose infusion, and either saline ( n = 7) or fructose ( n = 7; to stimulate NHGU and glycogen deposition) was infused intraportally. A 2-h control period then followed, during which the portal fructose and saline infusions were stopped, allowing NHGU and glycogen deposition in the fructose-infused animals to return to rates similar to those of the animals that received the saline infusion. This was followed by a 2-h experimental period, during which hyperglycemia was continued but insulin infusion was increased fourfold in both groups. During the initial 4-h glycogen loading period, NHGU averaged 1.18 ± 0.27 and 5.55 ± 0.53 mg·kg−1·min−1 and glycogen synthesis averaged 0.72 ± 0.24 and 3.98 ± 0.57 mg·kg−1·min−1 in the saline and fructose groups, respectively ( P < 0.05). During the 2-h hyperinsulinemic period, NHGU rose from 1.5 ± 0.4 and 0.9 ± 0.2 to 3.1 ± 0.6 and 2.5 ± 0.5 mg·kg−1·min−1 in the saline and fructose groups, respectively, a change of 1.6 mg·kg−1·min−1 in both groups despite a significantly greater liver glycogen level in the fructose-infused group. Likewise, the metabolic fate of the extracted glucose (glycogen, lactate, or carbon dioxide) was not different between groups. These data indicate that an acute physiological increase in the hepatic glycogen content does not alter liver glucose uptake and storage under hyperglycemic/hyperinsulinemic conditions in the dog.

Prior exercise increases net hepatic glucose uptake during a glucose load

1999 ◽  
Vol 276 (6) ◽  
pp. E1022-E1029 ◽  
Author(s):  
Pietro Galassetti ◽  
Robert H. Coker ◽  
Drury B. Lacy ◽  
Alan D. Cherrington ◽  
David H. Wasserman
Keyword(s):  
Portal Vein ◽  
Glucose Uptake ◽  
Control Period ◽  
Vena Cava ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Prior Exercise ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

The aim of these studies was to determine whether prior exercise enhances net hepatic glucose uptake (NHGU) during a glucose load. Sampling catheters (carotid artery, portal, hepatic, and iliac veins), infusion catheters (portal vein and vena cava), and Doppler flow probes (portal vein, hepatic and iliac arteries) were implanted. Exercise (150 min; n = 6) or rest ( n = 6) was followed by a 30-min control period and a 100-min experimental period (3.5 mg ⋅ kg−1⋅ min−1of glucose in portal vein and as needed in vena cava to clamp arterial blood glucose at ∼130 mg/dl). Somatostatin was infused, and insulin and glucagon were replaced intraportally at fourfold basal and basal rates, respectively. During experimental period the arterial-portal venous (a-pv) glucose gradient (mg/dl) was −18 ± 1 in sedentary and −19 ± 1 in exercised dogs. Arterial insulin and glucagon were similar in the two groups. Net hepatic glucose balance (mg ⋅ kg−1⋅ min−1) shifted from 1.9 ± 0.2 in control period to −1.8 ± 0.2 (negative rates represent net uptake) during experimental period in sedentary dogs (Δ3.7 ± 0.5); with prior exercise it shifted from 4.1 ± 0.3 ( P < 0.01 vs. sedentary) in control period to −3.2 ± 0.4 ( P < 0.05 vs. sedentary) during experimental period (Δ7.3 ± 0.7, P < 0.01 vs. sedentary). Net hindlimb glucose uptake (mg/min) was 4 ± 1 in sedentary animals in control period and 13 ± 2 during experimental period; in exercised animals it was 7 ± 1 in control period ( P < 0.01 vs. sedentary) and 32 ± 4 ( P < 0.01 vs. sedentary) during experimental period. As the total glucose infusion rate (mg ⋅ kg−1⋅ min−1) was 7 ± 1 in sedentary and 11 ± 1 in exercised dogs, ∼30% of the added glucose infusion due to prior exercise could be accounted for by the greater NHGU. In conclusion, when determinants of hepatic glucose uptake (insulin, glucagon, a-pv glucose gradient, glycemia) are controlled, prior exercise increases NHGU during a glucose load due to an effect that is intrinsic to the liver. Increased glucose disposal in the postexercise state is therefore due to an improved ability of both liver and muscle to take up glucose.

scholarly journals A Cyclic Guanosine Monophosphate-Dependent Pathway Can Regulate Net Hepatic Glucose Uptake in Vivo

Diabetes ◽  
2012 ◽  
Vol 61 (10) ◽  
pp. 2433-2441 ◽  
Author(s):  
Z. An ◽  
J. J. Winnick ◽  
M. C. Moore ◽  
B. Farmer ◽  
M. Smith ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Dependent Pathway

Kupffer cells play a major role in insulin-mediated hepatic glucose uptake in vivo

1992 ◽  
Vol 186 (1) ◽  
pp. 455-460 ◽  
Author(s):  
Zoltán Spolarics ◽  
Aurél Ottlakán ◽  
Charles H. Lang ◽  
John J. Spitzer
Keyword(s):  
Glucose Uptake ◽  
Kupffer Cells ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

Hepatic glucose uptake rapidly decreases after removal of the portal signal in conscious dogs

1998 ◽  
Vol 275 (6) ◽  
pp. E987-E992 ◽  
Author(s):  
Po-Shiuan Hsieh ◽  
Mary Courtney Moore ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Conscious Dogs ◽  
Glucose Load ◽  
Peripheral Vein ◽  
Peripheral Tissues ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Arterial Insulin

The aim of this study was to assess the decay of the effect of the portal signal on net hepatic glucose uptake (NHGU). Experiments were performed on five 42-h-fasted conscious dogs. After the 40-min basal period, somatostatin was given peripherally along with insulin (1.8 pmol ⋅ kg−1 ⋅ min−1) and glucagon (0.65 ng ⋅ kg−1 ⋅ min−1) intraportally. In the first experimental period (Pe-GLU-1; 90 min), glucose was infused into a peripheral vein to double the glucose load to the liver (HGL). In the second experimental period (Po-GLU; 90 min), glucose (20.1 μmol ⋅ kg−1 ⋅ min−1) was infused intraportally and the peripheral glucose infusion was reduced to maintain the same HGL. In the third period (Pe-GLU-2; 120 min), the portal glucose infusion was stopped and the peripheral glucose infusion was increased to again sustain HGL. Arterial insulin levels (42 ± 3, 47 ± 3, 43 ± 3 pmol/l) were basal and similar in the Pe-GLU-1, Po-GLU, and Pe-GLU-2 periods, respectively. Arterial glucagon levels were also basal and similar (51 ± 3, 49 ± 2, 46 ± 2 ng/l) in the three experimental periods. The glucose loads to the liver were 251 ± 11, 274 ± 14, and 276 ± 12 μmol ⋅ kg−1 ⋅ min−1, respectively. NHGU was 6.3 ± 2.4, 19.1 ± 2.8, and 9.2 ± 1.2 μmol ⋅ kg−1 ⋅ min−1, and nonhepatic glucose uptake (non-HGU) was 23.6 ± 3.0, 5.3 ± 1.8, and 25.5 ± 3.7 μmol ⋅ kg−1 ⋅ min−1in the three periods, respectively. Cessation of the portal signal for only 10 min shifted NHGU and non-HGU to 9.4 ± 2.2 and 25.0 ± 2.8 μmol ⋅ kg−1 ⋅ min−1, respectively; thus the effect of the portal signal was rapidly reversed both at the liver and peripheral tissues.

Sign in / Sign up

Export Citation Format

Share Document