scholarly journals Increases in intestinal glucose absorption and hepatic glucose uptake elicited by luminal but not vascular glutamine in the jointly perfused small intestine and liver of the rat

1992 ◽  
Vol 283 (3) ◽  
pp. 759-765 ◽  
Author(s):  
A Gardemann ◽  
Y Watanabe ◽  
V Große ◽  
S Hesse ◽  
K Jungermann
Keyword(s):  
Small Intestine ◽  
Portal Vein ◽  
Superior Mesenteric Artery ◽  
Glucose Uptake ◽  
Mesenteric Artery ◽  
Hepatic Uptake ◽  
Glucose Absorption ◽  
Hepatic Glucose ◽  
Intestinal Glucose Absorption ◽  
Hepatic Glucose Uptake

1. Previous studies have shown that an arterial-to-portal glucose concentration gradient may be an important signal for insulin-dependent net hepatic glucose uptake. It is not known whether intestinal factors also contribute to the regulation of hepatic glucose utilization. This problem was studied in a newly developed model which allows luminal perfusion of the small intestine via the pyloric sphincter and a combined vascular perfusion of the small intestine via the gastroduodenal artery and superior mesenteric artery, and of the liver via the hepatic artery and portal vein. 2. In both the presence and the absence of 1 mM-glutamine in the vascular perfusate, only about 7% of a luminal bolus of 5500 mumol (1 g) of glucose was absorbed by the small intestine, and nothing was taken up by the liver. 3. With small doses of 75-380 mumol (11-55 mg) of luminal glutamine, but not with 300 mumol of alanine, the intestinal absorption of the luminal glucose bolus was increased almost linearly from 7% to a maximum of 40% and the hepatic uptake from 0% to a maximum of 22%. 4. The increase of hepatic glucose uptake caused by luminal glutamine was only observed when the glucose load was applied into the intestinal lumen, rather than into the superior mesenteric artery. 5. The relative hepatic glucose uptake (uptake/portal supply) was enhanced from 0% to 55% with an increase in portal supply by luminal glutamine, whereas with a similar range of portal glucose supply the relative hepatic uptake by the isolated liver, perfused simultaneously via the hepatic artery and portal vein, was slightly decreased, from 20% to 15%. 6. Addition of various amounts of portal glutamine and/or alterations in the Na+ content of the portal perfusate failed to mimic the luminal glutamine-dependent activation of hepatic glucose uptake. Therefore the luminal-glutamine-elicited activation of hepatic glucose uptake was apparently not caused by a simple increase in the portal-arterial glucose gradient, by glutamine itself or by Na(+)-dependent alterations in hepatic cell volume. The results suggest that luminal glutamine caused not only an increase in intestinal glucose absorption by unknown mechanisms but also the generation of one or more humoral or nervous ‘hepatotropic’ signals in the small intestine which enhanced the hepatic uptake of absorbed glucose.

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.

scholarly journals The Importance of the Mechanisms by which Insulin Regulates Meal-Associated Liver Glucose Uptake in the Dog

2021 ◽  
Author(s):  
Guillaume Kraft ◽  
Katie C. Coate ◽  
Marta Smith ◽  
Ben Farmer ◽  
Melanie Scott ◽  
...  
Keyword(s):  
Portal Vein ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Insulin Infusion ◽  
Insulin Receptors ◽  
Postprandial Glucose ◽  
Maximal Stimulation ◽  
Hepatic Glucose ◽  
Healthy Dogs ◽  
Hepatic Glucose Uptake

Hepatic glucose uptake (HGU) is critical for maintaining normal postprandial glucose metabolism. Insulin is clearly a key regulator of HGU, but the physiologic mechanisms by which it acts have yet to be established. This study sought to determine the mechanisms by which insulin regulates liver glucose uptake under postprandial-like conditions (hyperinsulinemia, hyperglycemia, and a positive portal vein to arterial glucose gradient). Portal vein insulin infusion increased hepatic insulin levels 5-fold in healthy dogs. In one group (n=7), the physiologic response was allowed to fully occur, while in another (n=7), insulin’s indirect hepatic effects, occurring secondary to its actions on adipose tissue, pancreas, and brain, were blocked. This was accomplished by infusing triglyceride (intravenous), glucagon (portal vein), and inhibitors of brain insulin action (intracerebroventricular) to prevent decreases in plasma free fatty acids or glucagon, while blocking increased hypothalamic insulin signaling for 4h. In contrast to the indirect hepatic effects of insulin, which were previously shown capable of independently generating a half-maximal stimulation of HGU, direct hepatic insulin action was by itself able to fully stimulate HGU. This suggests that under hyperinsulinemic/hyperglycemic conditions insulin’s indirect effects are redundant to direct engagement of hepatocyte insulin receptors.

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.

Impact of infection on hepatic disposal of a peripheral glucose infusion in the conscious dog

1995 ◽  
Vol 269 (2) ◽  
pp. E199-E207 ◽  
Author(s):  
O. P. McGuinness ◽  
J. Jacobs ◽  
C. Moran ◽  
B. Lacy
Keyword(s):  
Glucose Uptake ◽  
Hepatic Uptake ◽  
Glucose Infusion ◽  
Hepatic Glycogen ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Hepatic Glucose Uptake

The effect of infection on hepatic uptake and disposal of a continuous (180-min) intravenous glucose infusion (8 mg.kg-1.min-1) was examined in conscious, 54-h-fasted, chronically catheterized dogs. Thirty-six hours before a study, either infection was induced by implantation of an Escherichia coli-containing (INF; 2 x 10(9) organisms/kg body wt; n = 6) fibrinogen clot, or a sterile (SH; n = 6) clot was implanted into the peritoneal cavity. Hepatic glucose metabolism was assessed using tracer ([3-3H]glucose and [U-14C]glucose) and arteriovenous difference techniques. Infection increased the basal rate of glucose appearance (45%); glucose levels were not altered. In response to glucose infusion, average blood glucose levels increased to similar levels (140 +/- 9 vs. 147 +/- 11 mg/dl in INF and SH, respectively), whereas arterial insulin levels were higher in the infected group during the last hour of the glucose infusion (77 +/- 10 vs. 41 +/- 5 microU/ml in INF vs. SH). Infection impaired net hepatic glucose uptake (0.6 +/- 0.5 and 2.7 +/- 0.7 mg.kg-1.min-1 in INF and SH; P < 0.05). The liver remained a persistent lactate consumer (4.1 +/- 1.8 mumol.kg-1.min-1), whereas the sham group became a net producer of lactate (-3.8 +/- 1.3 mumol.kg-1.min-1). Infection decreased net hepatic glycogen deposition by 53%. In conclusion, infection impairs net hepatic glucose uptake and glycogen deposition despite an exaggerated increase in insulin levels.

scholarly journals The Importance of the Mechanisms by which Insulin Regulates Meal-Associated Liver Glucose Uptake in the Dog

2021 ◽  
Author(s):  
Guillaume Kraft ◽  
Katie C. Coate ◽  
Marta Smith ◽  
Ben Farmer ◽  
Melanie Scott ◽  
...  
Keyword(s):  
Portal Vein ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Insulin Infusion ◽  
Insulin Receptors ◽  
Postprandial Glucose ◽  
Maximal Stimulation ◽  
Hepatic Glucose ◽  
Healthy Dogs ◽  
Hepatic Glucose Uptake

Hepatic glucose uptake (HGU) is critical for maintaining normal postprandial glucose metabolism. Insulin is clearly a key regulator of HGU, but the physiologic mechanisms by which it acts have yet to be established. This study sought to determine the mechanisms by which insulin regulates liver glucose uptake under postprandial-like conditions (hyperinsulinemia, hyperglycemia, and a positive portal vein to arterial glucose gradient). Portal vein insulin infusion increased hepatic insulin levels 5-fold in healthy dogs. In one group (n=7), the physiologic response was allowed to fully occur, while in another (n=7), insulin’s indirect hepatic effects, occurring secondary to its actions on adipose tissue, pancreas, and brain, were blocked. This was accomplished by infusing triglyceride (intravenous), glucagon (portal vein), and inhibitors of brain insulin action (intracerebroventricular) to prevent decreases in plasma free fatty acids or glucagon, while blocking increased hypothalamic insulin signaling for 4h. In contrast to the indirect hepatic effects of insulin, which were previously shown capable of independently generating a half-maximal stimulation of HGU, direct hepatic insulin action was by itself able to fully stimulate HGU. This suggests that under hyperinsulinemic/hyperglycemic conditions insulin’s indirect effects are redundant to direct engagement of hepatocyte insulin receptors.

Simulated first-phase insulin release using Humulin or insulin analog HIM2 is associated with prolonged improvement in postprandial glycemia

2005 ◽  
Vol 289 (1) ◽  
pp. E46-E52 ◽  
Author(s):  
Catherine A. DiCostanzo ◽  
Mary Courtney Moore ◽  
Margaret Lautz ◽  
Melanie Scott ◽  
Ben Farmer ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Saline Group ◽  
Glucose Absorption ◽  
Insulin Analog ◽  
Postprandial Glycemia ◽  
Hepatic Glucose ◽  
Glucose Clearance ◽  
Group 2 ◽  
Arterial Plasma ◽  
Hepatic Glucose Uptake

We examined the extent to which priming the liver with a pulse of Humulin or the insulin analog hexyl-insulin monoconjugate 2 (HIM2) reduces postprandial hyperglycemia. Somatostatin (0.5 μg·kg−1·min−1) was given with basal intraportal insulin and glucagon for 4.5 h into three groups of 42-h-fasted conscious dogs. From 0–5 min, group 1 (BI, n = 6) received saline, group 2 (HI, n = 6) received a Humulin pulse (10 mU·kg−1·min−1), and group 3 (HIM2, n = 6) received a HIM2 pulse (10 mU·kg−1·min−1). Duodenal glucose was infused (5.0 mg·kg−1·min−1) from 15 to 270 min. Arterial insulin in BI remained basal (6 ± 1 μU/ml) and peaked at 52 ± 15 (HI) and 164 ± 44 μU/ml (HIM2) and returned to baseline by 30 and 60 min, respectively. Arterial plasma glucose plateaued at 265 ± 20, 214 ± 15, and 193 ± 14 mg/dl in BI, HI, and HIM2. Glucose absorption was similar in all groups. Significant net hepatic glucose uptake occurred at 85, 55, and 25 min in BI, HI, and HIM2, respectively. Nonhepatic glucose clearance at 270 min differed among groups (BI, HI, HIM2): 0.62 ± 0.11, 0.76 ± 0.26, and 1.61 ± 0.29 ml·kg−1·min−1( P < 0.05). A brief (5-min) insulin pulse improved postprandial glycemia, stimulating hepatic glucose uptake and prolonging enhancement of nonhepatic glucose clearance. HIM2 was more effective than Humulin, perhaps because its lowered clearance caused higher levels at the liver and periphery and its biological activity was not reduced proportionally to its decreased clearance.

scholarly journals Portal Vein Caffeine Infusion Enhances Net Hepatic Glucose Uptake during a Glucose Load in Conscious Dogs

2004 ◽  
Vol 134 (11) ◽  
pp. 3042-3046 ◽  
Author(s):  
R. Richard Pencek ◽  
Danielle Battram ◽  
Jane Shearer ◽  
Freyja D. James ◽  
D. Brooks Lacy ◽  
...  
Keyword(s):  
Portal Vein ◽  
Glucose Uptake ◽  
Conscious Dogs ◽  
Glucose Load ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

Synchronous celiac axis and superior mesenteric artery embolism

VASA ◽  
2011 ◽  
Vol 40 (6) ◽  
pp. 495-498 ◽  
Author(s):  
Rajkovic ◽  
Zelic ◽  
Papes ◽  
Cizmek ◽  
Arslani
Keyword(s):  
Atrial Fibrillation ◽  
Small Intestine ◽  
Abdominal Pain ◽  
Ct Scan ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Abdominal Cavity ◽  
Celiac Axis ◽  
Contrast Administration ◽  
Artery Embolism

We present a case of combined celiac axis and superior mesenteric artery embolism in a 70-year-old patient that was examined in emergency department for atrial fibrillation and diffuse abdominal pain. Standard abdominal x-ray showed air in the portal vein. CT scan with contrast showed air in the lumen of the stomach and small intestine, bowel distension with wall thickening, and a free gallstone in the abdominal cavity. Massive embolism of both celiac axis and superior mesenteric artery was seen after contrast administration. On laparotomy, complete necrosis of the liver, spleen, stomach and small intestine was found. Gallbladder was gangrenous and perforated, and the gallstone had migrated into the abdominal cavity. We found free air that crackled on palpation of the veins of the gastric surface. The patient’s condition was incurable and she died of multiple organ failure a few hours after surgery. Acute visceral thromboembolism should always be excluded first if a combination of atrial fibrillation and abdominal pain exists. Determining the serum levels of d-dimers and lactate, combined with CT scan with contrast administration can, in most cases, confirm the diagnosis and lead to faster surgical intervention. It is crucial to act early on clinical suspicion and not to wait for the development of hard evidence.

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