Impact of continuous and pulsatile insulin delivery on net hepatic glucose uptake

2005 ◽  
Vol 289 (2) ◽  
pp. E232-E240 ◽  
Author(s):  
Jaime M. Grubert ◽  
Margaret Lautz ◽  
D. Brooks Lacy ◽  
Mary C. Moore ◽  
Ben Farmer ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Hepatic Metabolism ◽  
Insulin Delivery ◽  
Experimental Period ◽  
Constant Infusion ◽  
Glucose Levels ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Arterial Plasma ◽  
Hepatic Glucose Uptake

The pancreas releases insulin in a pulsatile manner; however, studies assessing the liver’s response to insulin have used constant infusion rates. Our aims were to determine whether the secretion pattern of insulin [continuous (CON) vs. pulsatile] in the presence of hyperglycemia 1) influences net hepatic glucose uptake (NHGU) and 2) entrains NHGU. Chronically catheterized conscious dogs fasted for 42 h received infusions including peripheral somatostatin, portal insulin (0.25 mU·kg−1·min−1), peripheral glucagon (0.9 ng·kg−1·min−1), and peripheral glucose at a rate double the glucose load to the liver. After the basal period, insulin was infused for 210 min at either four times the basal rate (1 mU·kg−1·min−1) or an identical amount in pulses of 1 and 4 min duration, followed by intervals of 11 and 8 min (CON, 1/11, and 4/8, respectively) in which insulin was not infused. A variable peripheral glucose infusion containing [3H]glucose clamped glucose levels at twice the basal level (∼200 mg/dl) throughout each study. Hepatic metabolism was assessed by combining tracer and arteriovenous difference techniques. Arterial plasma insulin (μU/ml) either increased from basal levels of 6 ± 1 to a constant level of 22 ± 4 in CON or oscillated from 5 ± 1 to 416 ± 79 and from 6 ± 1 to 123 ± 43 in 1/11 and 4/8, respectively. NHGU (−0.8 ± 0.3, 0.4 ± 0.2, and −0.9 ± 0.4 mg·kg−1·min−1) and net hepatic fractional extraction of glucose (0.04 ± 0.01, 0.04 ± 0.01, and 0.05 ± 0.01 mg·kg−1·min−1) were similar during the experimental period. Spectral analysis was performed to assess whether a correlation existed between the insulin secretion pattern and NHGU. NHGU was not augmented by pulsatile insulin delivery, and there is no evidence of entrainment in hepatic glucose metabolism. Thus the loss of insulin pulsatility per se likely has little or no impact on the effectiveness of insulin in regulating liver glucose uptake.

Route-dependent effect of nutritional support on liver glucose uptake

2005 ◽  
Vol 289 (5) ◽  
pp. R1319-R1327 ◽  
Author(s):  
Sheng-Song Chen ◽  
Carlos J Torres-Sanchez ◽  
Nadeen Hosein ◽  
Yiqun Zhang ◽  
D. Brooks Lacy ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Hepatic Metabolism ◽  
Insulin Requirement ◽  
Glucose Disposal ◽  
Nutrient Delivery ◽  
Lactate Release ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Arterial Plasma ◽  
Hepatic Glucose Uptake

The liver is a major site of glucose disposal during chronic (5 day) total parenteral (TPN) and enteral (TEN) nutrition. Net hepatic glucose uptake (NHGU) is dependent on the route of delivery when only glucose is delivered acutely; however, the hepatic response to chronic TPN and TEN is very similar. We aimed to determine whether the route of nutrient delivery altered the acute (first 8 h) response of the liver and whether chronic enteral delivery of glucose alone could augment the adaptive response to TPN. Chronically catheterized conscious dogs received either TPN or TEN containing glucose, Intralipid, and Travasol for either 8 h or 5 days. Another group received TPN for 5 days, but ∼50% of the glucose in the nutrition was given via the enteral route (TPN+EG). Hepatic metabolism was assessed with tracer and arteriovenous difference techniques. In the presence of similar arterial plasma glucose levels (∼6 mM), NHGU and net hepatic lactate release increased approximately twofold between 8 h and 5 days in TPN and TEN. NHGU (26 ± 1 vs. 23 ± 3 μmol·kg−1·min−1) and net hepatic lactate release (44 ± 1 vs. 34 ± 6 μmol·kg−1·min−1) in TPN+EG were similar to results for TPN, despite lower insulin levels (96 ± 6 vs. 58 ± 16 pM, TPN vs. TPN+EG). TEN does not acutely enhance NHGU or disposition above that seen with TPN. However, partial delivery of enteral glucose is effective in decreasing the insulin requirement during chronic TPN.

Impact of chronic fructose infusion on hepatic metabolism during TPN administration

2002 ◽  
Vol 283 (6) ◽  
pp. E1151-E1158 ◽  
Author(s):  
Christine M. Donmoyer ◽  
D. Brooks Lacy ◽  
Yiqun Zhang ◽  
Sheng-Song Chen ◽  
Owen P. McGuinness
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Inferior Vena ◽  
Vena Cava ◽  
Hepatic Metabolism ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Tracer Methods ◽  
Arterial Plasma ◽  
Hepatic Glucose Uptake

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) is markedly elevated. However, NHGU is reduced by the presence of an infection. We recently demonstrated that a small, acute (3-h) intraportal fructose infusion can correct the infection-induced impairment in NHGU. The aim of this study was to determine whether the addition of fructose to the TPN persistently enhances NHGU in the presence of an infection. TPN was infused continuously into the inferior vena cava of chronically catheterized dogs for 5 days. On day 3, a bacterial clot was implanted in the peritoneal cavity, and either saline (CON, n = 5) or fructose (+FRUC, 1.0 mg · kg−1· min−1, n = 6) infusion was included with the TPN. Forty-two hours after the infection was induced, hepatic glucose metabolism was assessed in conscious dogs with arteriovenous and tracer methods. Arterial plasma glucose concentration was lower with chronic fructose infusion (120 ± 4 vs. 131 ± 3 mg/dl, +FRUC vs. CON, P < 0.05); however, NHGU was not enhanced (2.2 ± 0.5 vs. 2.8 ± 0.4 mg · kg−1· min−1). Acute removal of the fructose infusion dramatically decreased NHGU (2.2 ± 0.5 to −0.2 ± 0.5 mg · kg−1· min−1), and net hepatic lactate release also fell (1.6 ± 0.3 to 0.5 ± 0.3 mg · kg−1· min−1). This led to an increase in the arterial plasma glucose (Δ13 ± 3 mg/dl, P < 0.05) and insulin (Δ5 ± 2 μU/ml) concentrations and to a decrease in glucagon (Δ−11 ± 3 pg/ml) concentration. In conclusion, the addition of chronic fructose infusion to TPN during infection does not lead to a persistent augmentation of NHGU.

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.

Hepatic glucose metabolism during intraduodenal glucose infusion: impact of infection

2000 ◽  
Vol 279 (1) ◽  
pp. E108-E115
Author(s):  
Owen P. McGuinness ◽  
Joseph Ejiofor ◽  
D. Brooks Lacy ◽  
Nancy Schrom
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glycogen Synthesis ◽  
Fibrin Clot ◽  
Glucose Absorption ◽  
Glucose Infusion ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Hepatic Glucose Uptake

We previously reported that infection decreases hepatic glucose uptake when glucose is given as a constant peripheral glucose infusion (8 mg · kg−1· min−1). This impairment persisted despite greater hyperinsulinemia in the infected group. In a normal setting, hepatic glucose uptake can be further enhanced if glucose is given gastrointestinally. Thus the aim of this study was to determine whether hepatic glucose uptake is impaired during an infection when glucose is given gastrointestinally. Thirty-six hours before study, a sham (SH, n = 7) or Escherichia coli-containing (2 × 109organisms/kg; INF; n = 7) fibrin clot was placed in the peritoneal cavity of chronically catheterized dogs. After the 36 h, a glucose bolus (150 mg/kg) followed by a continuous infusion (8 mg · kg−1· min−1) of glucose was given intraduodenally to conscious dogs for 240 min. Tracer ([3-3H]glucose and [U-14C]glucose) and arterial-venous difference techniques were used to assess hepatic and intestinal glucose metabolism. Infection increased hepatic blood flow (35 ± 5 vs. 47 ± 3 ml · kg−1· min−1; SH vs. INF) and basal glucose rate of appearance (2.1 ± 0.2 vs. 3.3 ± 0.1 mg · kg−1· min−1). Arterial insulin concentrations increased similarly in SH and INF during the last hour of glucose infusion (38 ± 8 vs. 46 ± 20 μU/ml), and arterial glucagon concentrations fell (62 ± 14 to 30 ± 3 vs. 624 ± 191 to 208 ± 97 pg/ml). Net intestinal glucose absorption was decreased in INF, attenuating the increase in blood glucose caused by the glucose load. Despite this, net hepatic glucose uptake (1.6 ± 0.8 vs. 2.4 ± 0.9 mg · kg−1· min−1; SH vs. INF) and consequently tracer-determined glycogen synthesis (1.3 ± 0.3 vs. 1.0 ± 0.3 mg · kg−1· min−1) were similar between groups. In summary, infection impairs net glucose absorption, but not net hepatic glucose uptake or glycogen deposition, when glucose is given intraduodenally.

Impact of infection on glucose-dependent liver glucose uptake during TPN: interaction with insulin

2004 ◽  
Vol 286 (2) ◽  
pp. E286-E295 ◽  
Author(s):  
Sheng-Song Chen ◽  
Christine M. Donmoyer ◽  
David A. Pearson ◽  
Adrian Poole ◽  
Yiqun Zhang ◽  
...  
Keyword(s):  
Parenteral Nutrition ◽  
Glucose Uptake ◽  
Total Parenteral Nutrition ◽  
Fibrin Clot ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
The Relationship ◽  
Glucose Dependence

Chronic total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU). This adaptive increase is impaired by an infection despite accompanying hyperinsulinemia. In the nonadapted state, NHGU is dependent on the prevailing glucose levels. Our aims were to determine whether the adaptation to TPN alters the glucose dependence of NHGU, whether infection impairs this dependence, and whether insulin modulates the glucose dependence of NHGU during infection. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, dogs received either a bacterial fibrin clot to induce a nonlethal infection (INF, n = 9) or a sterile fibrin clot (Sham, n = 6). Forty-two hours after clot implantation, somatostatin was infused. In Sham, insulin and glucagon were infused to match the level seen in Sham (9 ± 1 μU/ml and 23 ± 4 pg/ml, respectively). In infected animals, either insulin and glucagon were infused to match the levels seen in infection (25 ± 2 μU/ml and 101 ± 15 pg/ml; INF-HI; n = 5) or insulin was replaced to match the lower levels seen in Sham (13 ± 2 μU/ml), whereas glucagon was kept elevated (97 ± 9 pg/ml; INF-LO; n = 4). Then a four-step (90 min each) hyperglycemic (120, 150, 200, or 250 mg/dl) clamp was performed. NHGU increased at each glucose step in Sham (from 3.6 ± 0.6 to 5.4 ± 0.7 to 8.9 ± 0.9 to 12.1 ± 1.1 mg·kg–1·min–1); the slope of the relationship between glucose levels and NHGU (i.e., glucose dependence) was higher than that seen in nonadapted animals. Infection impaired glucose-dependent NHGU in both INF-HI (1.3 ± 0.4 to 2.9 ± 0.5 to 5.5 ± 1.0 to 7.7 ± 1.6 mg·kg–1·min–1) and INF-LO (0.5 ± 0.7 to 2.2 ± 0.6 to 4.2 ± 1.0 to 5.8 ± 0.8 mg·kg–1·min–1). In summary, TPN augments glucose-dependent NHGU, the presence of infection decreases glucose-dependent NHGU, and the accompanying hyperinsulinemia associated with infection does not sustain the glucose dependence of NHGU.

Fructose augments infection-impaired net hepatic glucose uptake during TPN administration

2001 ◽  
Vol 280 (5) ◽  
pp. E703-E711 ◽  
Author(s):  
Christine M. Donmoyer ◽  
Joseph Ejiofor ◽  
D. Brooks Lacy ◽  
Sheng-Song Chen ◽  
Owen P. McGuinness
Keyword(s):  
Glucose Uptake ◽  
Vena Cava ◽  
Fibrin Clot ◽  
Glycogen Storage ◽  
Glucose Disposal ◽  
Lactate Release ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Arteriovenous Difference

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) and net hepatic lactate release (NHLR) are markedly reduced (↓∼45 and ∼65%, respectively) with infection. Because small quantities of fructose are known to augment hepatic glucose uptake and lactate release in normal fasted animals, the aim of this work was to determine whether acute fructose infusion with TPN could correct the impairments in NHGU and NHLR during infection. Chronically catheterized conscious dogs received TPN for 5 days via the inferior vena cava at a rate designed to match daily basal energy requirements. On the third day of TPN administration, a sterile (SHAM, n = 12) or Escherichia coli-containing (INF, n = 11) fibrin clot was implanted in the peritoneal cavity. Forty-two hours later, somatostatin was infused with intraportal replacement of insulin (12 ± 2 vs. 24 ± 2 μU/ml, SHAM vs. INF, respectively) and glucagon (24 ± 4 vs. 92 ± 5 pg/ml) to match concentrations previously observed in sham and infected animals. After a 120-min basal period, animals received either saline (Sham+S, n = 6; Inf+S, n = 6) or intraportal fructose (0.7 mg · kg−1· min−1; Sham+F, n = 6; Inf+F, n = 5) infusion for 180 min. Isoglycemia of 120 mg/dl was maintained with a variable glucose infusion. Combined tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism. Acute fructose infusion with TPN augmented NHGU by 2.9 ± 0.4 and 2.5 ± 0.3 mg · kg−1· min−1in Sham+F and Inf+F, respectively. The majority of liver glucose uptake was stored as glycogen, and NHLR did not increase substantially. Therefore, despite an infection-induced impairment in NHGU and different hormonal environments, small amounts of fructose enhanced NHGU similarly in sham and infected animals. Glycogen storage, not lactate release, was the preferential fate of the fructose-induced increase in hepatic glucose disposal in animals adapted to TPN.

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.

Combined intraportal infusion of acetylcholine and adrenergic blockers augments net hepatic glucose uptake

2000 ◽  
Vol 278 (3) ◽  
pp. E544-E552 ◽  
Author(s):  
Masakazu Shiota ◽  
Patricia Jackson ◽  
Pietro Galassetti ◽  
Melanie Scott ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Nervous Activity ◽  
Adrenergic Blockade ◽  
Test Protocol ◽  
Control Protocol ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Adrenergic Blockers ◽  
Hepatic Glucose Uptake

Portal glucose delivery in the conscious dog augments net hepatic glucose uptake (NHGU). To investigate the possible role of altered autonomic nervous activity in the effect of portal glucose delivery, the effects of adrenergic blockade and acetylcholine (ACh) on hepatic glucose metabolism were examined in 42-h-fasted conscious dogs. Each study consisted of an equilibration (−120 to −20 min), a control (−20 to 0 min), and a hyperglycemic-hyperinsulinemic period (0 to 300 min). During the last period, somatostatin (0.8 μg ⋅ kg−1⋅ min−1) was infused along with intraportal insulin (1.2 mU ⋅ kg−1⋅ min−1) and glucagon (0.5 ng ⋅ kg−1⋅ min−1). Hepatic sinusoidal insulin was four times basal (73 ± 7 μU/ml) and glucagon was basal (55 ± 7 pg/ml). Glucose was infused peripherally (0–300 min) to create hyperglycemia (220 mg/dl). In test protocol, phentolamine and propranolol were infused intraportally at 0.2 μg and 0.1 μg ⋅ kg−1⋅ min−1from 120 min on. ACh was infused intraportally at 3 μg ⋅ kg−1⋅ min−1from 210 min on. In control protocol, saline was given in place of the blockers and ACh. Hyperglycemia-hyperinsulinemia switched the net hepatic glucose balance (mg ⋅ kg−1⋅ min−1) from output (2.1 ± 0.3 and 1.1 ± 0.2) to uptake (2.8 ± 0.9 and 2.6 ± 0.6) and lactate balance (μmol ⋅ kg−1⋅ min−1) from uptake (7.5 ± 2.2 and 6.7 ± 1.6) to output (3.7 ± 2.6 and 3.9 ± 1.6) by 120 min in the control and test protocols, respectively. Therefter, in the control protocol, NHGU tended to increase slightly (3.0 ± 0.6 mg ⋅ kg−1⋅ min−1by 300 min). In the test protocol, adrenergic blockade did not alter NHGU, but ACh infusion increased it to 4.4 ± 0.6 and 4.6 ± 0.6 mg ⋅ kg−1⋅ min−1by 220 and 300 min, respectively. These data are consistent with the hypothesis that alterations in nerve activity contribute to the increase in NHGU seen after portal glucose delivery.

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.

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