The effects of 2-deoxy-D-glucose given via the jugular or hepatic-portal vein on food intake and plasma glucose levels in pigs

1980 ◽  
Vol 25 (5) ◽  
pp. 691-697 ◽  
Author(s):  
D STEPHENS
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Plasma Glucose ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Hepatic Portal

Effect of hepatic portal glucose concentration on food intake and metabolism

1989 ◽  
Vol 257 (6) ◽  
pp. R1474-R1480 ◽  
Author(s):  
M. G. Tordoff ◽  
J. P. Tluczek ◽  
M. I. Friedman
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Jugular Vein ◽  
Hepatic Glycogen ◽  
Glucose Levels ◽  
Metabolic Event ◽  
Mock Control ◽  
Plasma Insulin Levels ◽  
Hepatic Portal Vein ◽  
Hepatic Portal

To examine the effect of different hepatic portal glucose concentrations on food intake and metabolism, rats were given hepatic portal or jugular infusions (83 microliters/min for 2 h) of 0.3, 0.6, and 1.2 M glucose, equiosmotic NaCl, or a mock control infusion. Food intake was decreased to the same extent by the three concentrations of glucose infused into the hepatic portal vein and unaffected by any concentration of glucose infused into the jugular vein. Parallel to the changes in food intake, hepatic glycogen content was increased by glucose infused into the hepatic portal vein but not jugular vein. Conversely, systemic plasma glucose levels were increased by glucose infused into the jugular vein but not hepatic portal vein. Plasma insulin levels increased to the same extent irrespective of the route of infusion. Food intake was unaffected by the osmolarity of glucose infused into the hepatic portal vein, but was decreased by hyperosmotic NaCl control infusions. Hyperosmotic NaCl infusions also elevated levels of circulating fat fuels, indicating a stress response. The results show that the critical metabolic event in the liver that influences food intake is only indirectly coupled to the concentration of glucose in the hepatic portal vein.

Infusion of CCK-8 into hepatic-portal vein fails to reduce food intake in rats

1987 ◽  
Vol 252 (5) ◽  
pp. R1015-R1018 ◽  
Author(s):  
D. Greenberg ◽  
G. P. Smith ◽  
J. Gibbs
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Test Meal ◽  
Intraperitoneal Administration ◽  
Meal Size ◽  
Reduce Food Intake ◽  
Hormonal Mechanism ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Intraportal Infusion

If the putative satiating effect of endogenous cholecystokinin (CCK) is produced through a circulating hormonal mechanism, then administration of exogenous CCK into the hepatic-portal vein should decrease meal size. To test this, one form of endogenous CCK, the C-terminal octapeptide CCK-8, was infused intraportally in doses of 4 and 8 micrograms/kg just prior to a test meal. Neither dose decreased food intake after intraportal infusion even though intraperitoneal administration of 4 micrograms/kg CCK-8 decreased meal size approximately 50% in the same rats. The results suggest that if endogenous CCK-8 has a satiating effect, it acts primarily through a paracrine mechanism.

scholarly journals Effects of infusions of lysine, leucine and ammonium chloride into the hepatic portal vein of chickens on voluntary food intake

1987 ◽  
Vol 58 (2) ◽  
pp. 325-331 ◽  
Author(s):  
Audrey A. Rusby ◽  
J. M. Forbes
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Ammonium Chloride ◽  
Jugular Vein ◽  
Free Access ◽  
Delayed Effect ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Access To Food ◽  
Portal Infusion

1. Adolescent cockerels of a laying strain were prepared with catheters whose tip lay in the hepatic portal vein, to study the effect of 3-h infusions of nutrients on food intake.2. Lysine, infused into the hepatic portal vein at rates of 150–450 mg/3 h reduced 3-h food intake by up to 58%, for a period of 6 h in previously starved birds, but had no effect on birds allowed free access to food. Infusions made into the jugular vein had no effect, suggesting a role for the liver in monitoring lysine levels.3. Portal infusion of leucine had a delayed effect while ammonium chloride, infused at isomolar rates to those of the lysine infusions, had very little effect on intake.4. The results support the concept of liver sensitivity to amino acids, but the mode of action is not clear; it appears not to be via the effects of ammonia.

Reduced feeding during water deprivation depends on hydration of the gut

2002 ◽  
Vol 283 (5) ◽  
pp. R1061-R1069 ◽  
Author(s):  
Guus H. M. Schoorlemmer ◽  
Mark D. Evered
Keyword(s):  
Drinking Water ◽  
Food Intake ◽  
Portal Vein ◽  
Water Deprivation ◽  
Dark Period ◽  
Vena Cava ◽  
Meal Frequency ◽  
Electrolyte Excretion ◽  
Hepatic Portal Vein ◽  
Hepatic Portal

Removal of drinking water at the start of the dark period reduced food intake in freely feeding rats within 45 min. Both first and later meals were smaller during 7.5 h of water deprivation, but meal frequency did not change. Ingestion of a normal-sized meal (3 g) rapidly increased plasma tonicity when drinking water was withheld, but intravenous infusions of hypertonic NaCl causing similar increases in plasma tonicity did not reduce feeding. Feeding during 6 h of water deprivation was restored by slowly infusing the volume of water normally drunk into the stomach, jejunum, or cecum, but not in the vena cava or hepatic portal vein. The infusions did not alter water or electrolyte excretion or affect food intake in rats allowed to drink. We conclude that the inhibition of feeding seen during water deprivation is mediated by a sensor that is located in the gastrointestinal tract or perhaps in the mesenteric veins draining the gut, but not the hepatic portal vein or the liver. In the absence of drinking water, signals from this sensor provoke the early termination of a meal.

Intraportally delivered GLP-1, in the presence of hyperglycemia induced via peripheral glucose infusion, does not change whole body glucose utilization

2008 ◽  
Vol 294 (2) ◽  
pp. E380-E384 ◽  
Author(s):  
Kathryn M. S. Johnson ◽  
Dale S. Edgerton ◽  
Tiffany Rodewald ◽  
Melanie Scott ◽  
Ben Farmer ◽  
...  
Keyword(s):  
Portal Vein ◽  
Glucose Uptake ◽  
Glucose Utilization ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Whole Body ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Pancreatic Hormone

After a meal, glucagon-like peptide-1 (GLP-1) and glucose levels are significantly greater in the hepatic portal vein than in the artery. We have previously reported that, in the presence of intraportal glucose delivery, a physiological increase of GLP-1 in the hepatic portal vein increases nonhepatic glucose uptake via a mechanism independent of changes in pancreatic hormone secretion. The aim of the present study was to determine whether intraportal glucose delivery is required to observe this effect. Experiments consisted of a 40-min basal period, followed by a 240-min experimental period, during which conscious 42-h fasted dogs received glucose peripherally to maintain arterial plasma glucose levels at ∼160 mg/dl. In addition, either saline ( n = 6) or GLP-1 (1 pmol·kg−1·min−1; GLP-1, n = 6) was administered intraportally during the experimental period. As in the previous study, the presence of GLP-1 did not alter pancreatic hormone levels; however, in the present study, intraportal GLP-1 infusion did not result in an increase in whole body glucose utilization. This is despite the fact that arterial and hepatic portal vein GLP-1 levels were maintained at the same level as the previous study. Therefore, a physiological elevation of GLP-1 in the hepatic portal vein does not increase whole body glucose uptake when hyperglycemia is induced by peripheral glucose infusion. This indicates that a physiological increase in GLP-1 augments glucose utilization only when GLP-1 and glucose gradients conditions mimic the postprandial state.

Hindbrain glucagon-like peptide-1 receptors (GLP-1R) mediate the eating-inhibitory effect of hepatic portal vein (HPV) GLP-1 infusions

Appetite ◽  
2010 ◽  
Vol 54 (3) ◽  
pp. 668 ◽  
Author(s):  
G. Pacheco-López ◽  
M. Punjabi ◽  
M. Graber ◽  
N. Geary ◽  
M. Arnold ◽  
...  
Keyword(s):  
Portal Vein ◽  
Inhibitory Effect ◽  
Hepatic Portal Vein ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Hepatic Portal

Complete pancreatic encasement of the proximal hepatic portal vein: A previously undescribed congenital anomaly

1997 ◽  
Vol 84 (6) ◽  
pp. 785-785 ◽  
Author(s):  
Y. Hamanaka ◽  
J. Evans ◽  
G. Sagar ◽  
J. P. Neoptolemos
Keyword(s):  
Congenital Anomaly ◽  
Portal Vein ◽  
Hepatic Portal Vein ◽  
Hepatic Portal

Rapid translocation of hepatic glucokinase in response to intraduodenal glucose infusion and changes in plasma glucose and insulin in conscious rats

2004 ◽  
Vol 286 (4) ◽  
pp. G627-G634 ◽  
Author(s):  
Chang An Chu ◽  
Yuka Fujimoto ◽  
Kayano Igawa ◽  
Joseph Grimsby ◽  
Joseph F. Grippo ◽  
...  
Keyword(s):  
Portal Vein ◽  
Plasma Glucose ◽  
Regulatory Protein ◽  
Glucose Infusion ◽  
Insulin Levels ◽  
Conscious Rats ◽  
Glucose Levels ◽  
Glucose Ingestion ◽  
Plasma Insulin Levels

The rate of liver glucokinase (GK) translocation from the nucleus to the cytoplasm in response to intraduodenal glucose infusion and the effect of physiological rises of plasma glucose and/or insulin on GK translocation were examined in 6-h-fasted conscious rats. Intraduodenal glucose infusion (28 mg·kg-1·min-1 after a priming dose at 500 mg/kg) elevated blood glucose levels (mg/dl) in the artery and portal vein from 90 ± 3 and 87 ± 3 to 154 ± 4 and 185 ± 4, respectively, at 10 min. At 120 min, the levels had decreased to 133 ± 6 and 156 ± 5, respectively. Plasma insulin levels (ng/ml) in the artery and the portal vein rose from 0.7 ± 0.1 and 1.8 ± 0.3 to 11.8 ± 1.5 and 20.2 ± 2.0 at 10 min, respectively, and 12.4 ± 3.1 and 18.0 ± 4.8 at 30 min, respectively. GK was rapidly exported from the nucleus as determined by measuring the ratio of the nuclear to the cytoplasmic immunofluorescence (N/C) of GK (2.9 ± 0.3 at 0 min to 1.7 ± 0.2 at 10 min, 1.5 ± 0.1 at 20 min, 1.3 ± 0.1 at 30 min, and 1.3 ± 0.1 at 120 min). When plasma glucose (arterial; mg/dl) and insulin (arterial; ng/ml) levels were clamped for 30 min at 93 ± 7 and 0.7 ± 0.1, 81 ± 5 and 8.9 ± 1.3, 175 ± 5 and 0.7 ± 0.1, or 162 ± 5 and 9.2 ± 1.5, the N/C of GK was 3.0 ± 0.5, 1.8 ± 0.1, 1.5 ± 0.1, and 1.2 ± 0.1, respectively. The N/C of GK regulatory protein (GKRP) did not change in response to the intraduodenal glucose infusion or the rise in plasma glucose and/or insulin levels. The results suggest that GK but not GKRP translocates rapidly in a manner that corresponds with changes in the hepatic glucose balance in response to glucose ingestion in vivo. Additionally, the translocation of GK is induced by the postprandial rise in plasma glucose and insulin.

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