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Effect of increasing oral glucose loads on the release of GIP and insulin during recovery after exhaustive exercise
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We conclude that i. NT mimics the pancreatic exccrine and endocrine pancreatic secretory effects of intestinal fat, 2. NT may contribute to fat-induced sti-mulation of tb~ pancreatic secretion and 3. the secretory effects of NT could be explained, at least in Dart, by increased pancreatic circulation and metabolism.
C H A R A C T E R I C S OF S T I M U L A T I O N OF P A N C R E A T I C S E C R E T I O N BY VIP IN DOGS E.~-F.Coelle, A . S c h a f m a y e r , W . Z i t z m a n n , H.-D.Becker. U n i v e r s i t y of Goettingen, Dept. of Surgery, Goettingen, W . - G e r m a n y It is reported that VIP has a secretion like effect on p a n c r e a t i c secretion by s t i m u l a t i n g the b i c a r b o n a t e secretion from the pancreas. F a h r e n k r u g et al s u g g e s t e d that VIP may act as a n e u r o t r a n s r mitter for p a n c r e a t i c secretion. In the present study we have tested the c o r r e l a t i o n b e t w e e n VIP plasma levels and p a n c r e a t i c secretion and c o m p a r e d with the secretin induced secretion. Methods: In 5 mongrel dogs ( w e i g h t 25-30 kg) a chronic pancreatic p o u c h was constructed. Four weeks p o s t o p @ r a t i v e l y the animals were p e r f u s e d with 0.5, I, 2 or 4 ~g k g - ] h r - l i n t r a v e n o u s l y . I n another set of e x p e r i m e n t s the dogs received O . 1 E Secretin for 4 hours and in a third set they were treated with VIP (0.5, I, 2, 4 ~g kg -I) olus O . 1 E Secretin. VIP was e s t i m a t e d by a sensitiv and specific RIA using antisera at a dilution of 1/400 O00 in the assay-system. P a n c r e a t i c juice was c o l l e c t e d in 15 min. portions and b i c a r b o n a t e - a n d p r o t e i n c o n c e n t r a t i o n was measured. Blood samples were c o l l e c t e d every 15 min. Results: The c o r r e l a t i o n between p a n c r e a t i c secretion and VIP nlasma levels is shown in the f o l l o w i n g table: I V I P ( ~g k g - l h r - ) basal 0.5 I 2 4 B i c a r b o n a t m m o l / 1 5 m i n -I 0.07 O.12 O.18 0.25 0.37 Protein m g / ~ 5 m i n 30 29.9 27.8 36.5 32.1 VIP pmol l - I / 1 5 m i n 3.0 12.4 31.4 58.8 116.O VIP had n o c o m p e t i t i v e e f f e c t on s e c r e t i n - i n d u c e d b i c a r b o n a t e - p r o tein-secretion. Summery: E x o g e n e o u s intravenous VIP stimulates dose d e p e n d e n t the b i c a r b o n a t e n a n c r e a t i c secretion in d~gs. VIP has no effect on p r o t e i n secretion. Infusion of 0.5 ~g- hr-lvIP causes p h y s i o l o g i c a l levels of VIP in plasma, indicating a possible ~ h y s i o l o g i c a l role of VIP in p a n c r e a t i c secretion.
INTERACTION OF PANCREATIC POLYPEPTIDE WITH .HOLECYSTOKININ AND GASTRIN ON PANCREATIC AND GASTRIC SECRETIONS. T.-M Lin, 0. C. Evans and R. E. Chance, L i l l y Research Laboratories, Eli L i l l y and Company, Indianapolis, IN 46285 USA Pancreatic polypeptide (PP) is released by food, sham-feeding, vagal stimulation, and some GI hormones. Submaximal gastric HCl secretion induced by gastrin was inhibited by pharmacological (10-40 ug/kg/hr) doses of BPP. The e f f e c t of PP on gastric acid and pancreatic secretions induced by endogenously released cholecystokinin (CCK) and a low dose of gastrin is the subject of t h i s study: ( I ) Pancreatic volume, BHC03, and protein secretion induced by intraduodenal perfusion (IDP) of an ~so-osmolar solution containing PHE and mannitol was s i g n i f i c a n t l y inhibited by BPP 2 ~g (472 p mole)/kg/hr given for 1 hr i . v . Gastric acid gradually decreased from control levels of secretion and remained inhibited for 1 hr. Percentage decreases of HCl outputs following BPP were s i g n i f i c a n t ; (2) Gastric and pancreatic secretions induced by IDP of an iso-osmolar solution containing PHE and TRP and i . v . t e t r a g a s t r i n (0.2 ug/kg/hr) were followed f o r 7 hr with
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or without BPP 1 ug (237 p mole)/kg/hr, i . v . Pancreatic volume, BHC03, and protein secretion was s i g n i f i c a n t l y inhibited after steady response to induction was established, but gastric HCI was inhibited only during the i n i t i a l periods of IDP; (3) Gastric acid secretion of pylorus-ligated rats was not significantly affected by 2-6 ug/kg of BPP, i . p . ; (4) Inhibition of pancreatic protein secretion induced by exogenous CCK and secretin was significantly greater than that of BHCO3 output; and (5) Plasmaconcentrations of PP induced by I-2 ug/kg/hr of BPP infusion were lower than those released by a meal. Results suggest that PP selectively inhibits the gastric and pancreatic stimulating actions of CCK. PP is unlikely to inhibit gastric acid secretion induced by histamine or high doses of gastrin under physiological conditions.
EFFECT OF INCREASING ORAL GLUCOSE LOADS ON THE RELEASE OF GIP AND INSULIN DURING RECOVERY AFTER EXHAUSTIVE EXERCISE. P. Blom, O.Flaten, O.Vaage, S.M~hlum, T.Sand, L.Hermansen. Institute of Muscle Physiology, Oslo, Norway. We have reported an increasing rate of muscle glycogen resynthesis after exhaustive exercise,with increasing oral glucose loads up to a certain level.A glucose load above this level,gave no further increase#in resynthesis rate.ln order to obtain additional information about glucose metabolism after exhaustive exercise, we measured GIP and Insulin. Three groups of five subjects (Group A,B and C)were given 0.7, 1.4 and 2.0 grams of glucose in water per kg body weight respectively, every second hour after prolonged exercise to exhaustion. Blood samples were obtained every hour of the first 8 hours of the recovery period. GIP and Insulin were measured by RIA in extrcted plasma. Blood glucose was measured by an enzymatic method. Results:Blood glucose increased during the first hour after glucose intake,and decreased prior to the next glucose intake. Peak values were 8.9±1.0, 8.5±0.6, 7.2±0.9, 7.1±0.7 and 9.1± 0.3, 8.1±0.7, 6.4±0.3, 5.8±0.4 and 9.7±1.0, 7.3±0.8, 5.3±0.7, 4.6±0.6 mM for group A,B and C respectively.ln group A GIP increased to peak values 66.3±6.6 63.0±8.6, 59.6±4.4 56.6~4.9 after each glucose intake.ln group B and C GIP increased continously from 36.0±2.6 and 34.0±2.1 to 187.6±39.9 and 229±6.5pM respectively. Insulin increased during the first hour after glucose intake, and decreased prior to the next glucose intake. Peak values were 35±5, 35~2, 33±6, 30±7 and 35+4, 49~3, 50±4, 51±10 and 44~8, 83±21, 79±20~ mU for group A,B and C respectively. Conclusion: When increasing oral glucose loads are given during recovery after exhaustive exercise, the rate of muscle glycogen resynthesis levels off without a concomitant levelling off in GIP and Insulin release.
We conclude that i. NT mimics the pancreatic exccrine and endocrine pancreatic secretory effects of intestinal fat, 2. NT may contribute to fat-induced sti-mulation of tb~ pancreatic secretion and 3. the secretory effects of NT could be explained, at least in Dart, by increased pancreatic circulation and metabolism.
C H A R A C T E R I C S OF S T I M U L A T I O N OF P A N C R E A T I C S E C R E T I O N BY VIP IN DOGS E.~-F.Coelle, A . S c h a f m a y e r , W . Z i t z m a n n , H.-D.Becker. U n i v e r s i t y of Goettingen, Dept. of Surgery, Goettingen, W . - G e r m a n y It is reported that VIP has a secretion like effect on p a n c r e a t i c secretion by s t i m u l a t i n g the b i c a r b o n a t e secretion from the pancreas. F a h r e n k r u g et al s u g g e s t e d that VIP may act as a n e u r o t r a n s r mitter for p a n c r e a t i c secretion. In the present study we have tested the c o r r e l a t i o n b e t w e e n VIP plasma levels and p a n c r e a t i c secretion and c o m p a r e d with the secretin induced secretion. Methods: In 5 mongrel dogs ( w e i g h t 25-30 kg) a chronic pancreatic p o u c h was constructed. Four weeks p o s t o p @ r a t i v e l y the animals were p e r f u s e d with 0.5, I, 2 or 4 ~g k g - ] h r - l i n t r a v e n o u s l y . I n another set of e x p e r i m e n t s the dogs received O . 1 E Secretin for 4 hours and in a third set they were treated with VIP (0.5, I, 2, 4 ~g kg -I) olus O . 1 E Secretin. VIP was e s t i m a t e d by a sensitiv and specific RIA using antisera at a dilution of 1/400 O00 in the assay-system. P a n c r e a t i c juice was c o l l e c t e d in 15 min. portions and b i c a r b o n a t e - a n d p r o t e i n c o n c e n t r a t i o n was measured. Blood samples were c o l l e c t e d every 15 min. Results: The c o r r e l a t i o n between p a n c r e a t i c secretion and VIP nlasma levels is shown in the f o l l o w i n g table: I V I P ( ~g k g - l h r - ) basal 0.5 I 2 4 B i c a r b o n a t m m o l / 1 5 m i n -I 0.07 O.12 O.18 0.25 0.37 Protein m g / ~ 5 m i n 30 29.9 27.8 36.5 32.1 VIP pmol l - I / 1 5 m i n 3.0 12.4 31.4 58.8 116.O VIP had n o c o m p e t i t i v e e f f e c t on s e c r e t i n - i n d u c e d b i c a r b o n a t e - p r o tein-secretion. Summery: E x o g e n e o u s intravenous VIP stimulates dose d e p e n d e n t the b i c a r b o n a t e n a n c r e a t i c secretion in d~gs. VIP has no effect on p r o t e i n secretion. Infusion of 0.5 ~g- hr-lvIP causes p h y s i o l o g i c a l levels of VIP in plasma, indicating a possible ~ h y s i o l o g i c a l role of VIP in p a n c r e a t i c secretion.
INTERACTION OF PANCREATIC POLYPEPTIDE WITH .HOLECYSTOKININ AND GASTRIN ON PANCREATIC AND GASTRIC SECRETIONS. T.-M Lin, 0. C. Evans and R. E. Chance, L i l l y Research Laboratories, Eli L i l l y and Company, Indianapolis, IN 46285 USA Pancreatic polypeptide (PP) is released by food, sham-feeding, vagal stimulation, and some GI hormones. Submaximal gastric HCl secretion induced by gastrin was inhibited by pharmacological (10-40 ug/kg/hr) doses of BPP. The e f f e c t of PP on gastric acid and pancreatic secretions induced by endogenously released cholecystokinin (CCK) and a low dose of gastrin is the subject of t h i s study: ( I ) Pancreatic volume, BHC03, and protein secretion induced by intraduodenal perfusion (IDP) of an ~so-osmolar solution containing PHE and mannitol was s i g n i f i c a n t l y inhibited by BPP 2 ~g (472 p mole)/kg/hr given for 1 hr i . v . Gastric acid gradually decreased from control levels of secretion and remained inhibited for 1 hr. Percentage decreases of HCl outputs following BPP were s i g n i f i c a n t ; (2) Gastric and pancreatic secretions induced by IDP of an iso-osmolar solution containing PHE and TRP and i . v . t e t r a g a s t r i n (0.2 ug/kg/hr) were followed f o r 7 hr with
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or without BPP 1 ug (237 p mole)/kg/hr, i . v . Pancreatic volume, BHC03, and protein secretion was s i g n i f i c a n t l y inhibited after steady response to induction was established, but gastric HCI was inhibited only during the i n i t i a l periods of IDP; (3) Gastric acid secretion of pylorus-ligated rats was not significantly affected by 2-6 ug/kg of BPP, i . p . ; (4) Inhibition of pancreatic protein secretion induced by exogenous CCK and secretin was significantly greater than that of BHCO3 output; and (5) Plasmaconcentrations of PP induced by I-2 ug/kg/hr of BPP infusion were lower than those released by a meal. Results suggest that PP selectively inhibits the gastric and pancreatic stimulating actions of CCK. PP is unlikely to inhibit gastric acid secretion induced by histamine or high doses of gastrin under physiological conditions.
EFFECT OF INCREASING ORAL GLUCOSE LOADS ON THE RELEASE OF GIP AND INSULIN DURING RECOVERY AFTER EXHAUSTIVE EXERCISE. P. Blom, O.Flaten, O.Vaage, S.M~hlum, T.Sand, L.Hermansen. Institute of Muscle Physiology, Oslo, Norway. We have reported an increasing rate of muscle glycogen resynthesis after exhaustive exercise,with increasing oral glucose loads up to a certain level.A glucose load above this level,gave no further increase#in resynthesis rate.ln order to obtain additional information about glucose metabolism after exhaustive exercise, we measured GIP and Insulin. Three groups of five subjects (Group A,B and C)were given 0.7, 1.4 and 2.0 grams of glucose in water per kg body weight respectively, every second hour after prolonged exercise to exhaustion. Blood samples were obtained every hour of the first 8 hours of the recovery period. GIP and Insulin were measured by RIA in extrcted plasma. Blood glucose was measured by an enzymatic method. Results:Blood glucose increased during the first hour after glucose intake,and decreased prior to the next glucose intake. Peak values were 8.9±1.0, 8.5±0.6, 7.2±0.9, 7.1±0.7 and 9.1± 0.3, 8.1±0.7, 6.4±0.3, 5.8±0.4 and 9.7±1.0, 7.3±0.8, 5.3±0.7, 4.6±0.6 mM for group A,B and C respectively.ln group A GIP increased to peak values 66.3±6.6 63.0±8.6, 59.6±4.4 56.6~4.9 after each glucose intake.ln group B and C GIP increased continously from 36.0±2.6 and 34.0±2.1 to 187.6±39.9 and 229±6.5pM respectively. Insulin increased during the first hour after glucose intake, and decreased prior to the next glucose intake. Peak values were 35±5, 35~2, 33±6, 30±7 and 35+4, 49~3, 50±4, 51±10 and 44~8, 83±21, 79±20~ mU for group A,B and C respectively. Conclusion: When increasing oral glucose loads are given during recovery after exhaustive exercise, the rate of muscle glycogen resynthesis levels off without a concomitant levelling off in GIP and Insulin release.