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.

scholarly journals Intrameal Hepatic Portal and Intraperitoneal Infusions of Glucagon-Like Peptide-1 Reduce Spontaneous Meal Size in the Rat via Different Mechanisms

Endocrinology ◽  
2008 ◽  
Vol 150 (3) ◽  
pp. 1174-1181 ◽  
Author(s):  
Elisabeth B. Rüttimann ◽  
Myrtha Arnold ◽  
Jacquelien J. Hillebrand ◽  
Nori Geary ◽  
Wolfgang Langhans
Keyword(s):  
Food Intake ◽  
Vena Cava ◽  
Meal Size ◽  
Dark Phase ◽  
Hepatic Portal Vein ◽  
Vagal Afferent ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Hepatic Portal ◽  
Afferent Signaling

Peripheral administration of glucagon-like peptide (GLP)-1 reduces food intake in animals and humans, but the sites and mechanism of this effect and its physiological significance are not yet clear. To investigate these issues, we prepared rats with chronic catheters and infused GLP-1 (0.2 ml/min; 2.5 or 5.0 min) during the first spontaneous dark-phase meals. Infusions were remotely triggered 2–3 min after meal onset. Hepatic portal vein (HPV) infusion of 1.0 or 3.0 (but not 0.33) nmol/kg GLP-1 reduced the size of the ongoing meal compared with vehicle without affecting the subsequent intermeal interval, the size of subsequent meals, or cumulative food intake. In double-cannulated rats, HPV and vena cava infusions of 1.0 nmol/kg GLP-1 reduced meal size similarly. HPV GLP-1 infusions of 1.0 nmol/kg GLP-1 also reduced meal size similarly in rats with subdiaphragmatic vagal deafferentations and in sham-operated rats. Finally, HPV and ip infusions of 10 nmol/kg GLP-1 reduced meal size similarly in sham-operated rats, but only HPV GLP-1 reduced meal size in subdiaphragmatic vagal deafferentation rats. These data indicate that peripherally infused GLP-1 acutely and specifically reduces the size of ongoing meals in rats and that the satiating effect of ip, but not iv, GLP-1 requires vagal afferent signaling. The findings suggest that iv GLP-1 infusions do not inhibit eating via hepatic portal or hepatic GLP-1 receptors but may act directly on the brain. Intrameal hepatic portal and intraperitoneal (IP) infusions of GLP-1 reduce meal size in rats, but only IP GLP-1 requires vagal afferent signaling for this effect.

Evidence for gut factor in K+ homeostasis

2007 ◽  
Vol 293 (2) ◽  
pp. F541-F547 ◽  
Author(s):  
Felix N. Lee ◽  
Gisuk Oh ◽  
Alicia A. McDonough ◽  
Jang H. Youn
Keyword(s):  
Portal Vein ◽  
Jugular Vein ◽  
Deficient Diet ◽  
Apparent Increase ◽  
Marked Enhancement ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Fasted Rats ◽  
Intraportal Infusion

We tested the hypothesis that K+ intake is sensed by putative K+ sensors in the splanchnic areas, and renal K+ handling is regulated by this signal. K+ was infused for 2 h into overnight-fasted rats via the jugular vein (systemic infusion), hepatic portal vein (intraportal infusion), or stomach (intragastric infusion) ( n = 5 each), and plasma K+ concentration ([K+]) and renal K+ excretion were measured during the 2-h preinfusion, 2-h K+ infusion, and 3-h washout periods. During systemic K+ infusion, plasma [K+] increased by ∼1.3 mM ( P < 0.05), and, on cessation of the K+ infusion, plasma [K+] fell to the preinfusion level within 1–2 h. Renal K+ excretion changed in proportion to the changes in plasma [K+]. During intraportal or intragastric K+ infusion, plasma [K+] and renal K+ excretion profiles were similar to those with systemic infusion. The effects of K+ infusions via the different routes ( n = 5 or 6 each) were also studied during simultaneous feeding of overnight-fasted rats with a K+-deficient diet. During the meal, intraportal infusion resulted in increases in plasma [K+] similar to those with the systemic K+ infusion, while intragastric K+ infusion did not significantly increase plasma [K+]. Thus, when the intragastric K+ infusion was combined with a meal, there was marked enhancement of clearance of the K+ infused, which was associated with an apparent increase in renal efficiency of K+ excretion. These data suggest that there may be a gut factor that enhances renal efficiency of K+ excretion during meal (or dietary K+) intake.

Gastric emptying changes are neither necessary nor sufficient for CCK-induced satiety

1989 ◽  
Vol 256 (1) ◽  
pp. R56-R62
Author(s):  
K. L. Conover ◽  
S. M. Collins ◽  
H. P. Weingarten
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Significant Role ◽  
Test Meal ◽  
Meal Size ◽  
High Dose ◽  
Reduce Food Intake ◽  
Cholecystokinin Octapeptide ◽  
No Inhibition

If gastric emptying plays a significant role in the satiety produced by exogenous cholecystokinin octapeptide (CCK-8) then 1) the effects on emptying and feeding should share similar kinetics and 2) peptides that inhibit emptying should also inhibit feeding. In the first experiment, CCK-8 (5.6 micrograms/kg) injected immediately before the introduction of an intragastric load (10 ml saline) or presentation of a test meal (15% sucrose) produced a rapid inhibition of both emptying and feeding. In contrast, the same dose administered 15 min before testing caused no inhibition of emptying, even though it retained the ability to reduce meal size. In experiment 2, the abilities of the peptides pentagastrin (100 micrograms/kg), bombesin (8 and 16 micrograms/kg), and secretin (2.86, 14.3, and 28.6 micrograms/kg) to reduce food intake and inhibit emptying were tested. Pentagastrin influenced neither food intake nor gastric emptying. Bombesin caused a small transient delay in emptying but a large and sustained eating suppression. However, a high dose of secretin caused no significant reduction of food intake, in spite of the fact that it inhibited emptying to the same degree as 1.4 micrograms/kg CCK-8, which does reduce intake. These results suggest that the inhibition of emptying by CCK is not sufficient to explain the satiety effect of CCK-8.

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.

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.

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