Insulin output via the pancreatic vein and plasma insulin response to glucose in dogs

Kanazawa, Yasunori; Kuzuya, T; Ide, Takehiko

doi:10.1152/ajplegacy.1968.215.3.620

Cited by 42 publications

(15 citation statements)

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“…Because a single-pass perfusion system is used, insulin released from the beta cells must be acting on the exocrine cells prior to entering the pancreatoduodenal and portal veins. This is, to our knowledge, the first functional demonstration of the islet-acinus portal vessel system previously postulated on morphological grounds (1,2,18,19) (20,21). In this case where the portal vein collects blood from a numilber of organs besides the pancreas, intrapanicreatic instulini concentrations would be expected to be mnuch higher than those in the portal vein.…”

Section: Discussionmentioning

confidence: 54%

Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.

Saito¹,

Williams²,

Kanno³

1980

J. Clin. Invest.

119

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A B S T R A C T Using an isolated perfused rat pancreas preparation, the interrelationship between the endocrine and exocrine portions of the pancreas were studied. Addition of exogenous rat insulin (1-20 mU/ml) to the perfusing solution potentiated the action of cholecystokinin (CCK) (1 mU/ml) to increase both pancreatic juice flow and the release of the enzyme, amnylase. Raising the glucose concentration in the perfusing solution from 2.5 to 17.5 mM both increased endogenous insulin release and potentiated the CCKinduced exocrine secretory response. Two lines of evidence indicated that this effect of glucose on the exocrine pancreas was mediated by endogenous insulin release. First, the addition ofcomparable amounts of xylose or galactose to the perfusion medium neither released insulin nor potentiated the CCK-induced response. Second, epinephrine blocked the effect of high glucose on both insulin release and potentiation of CCK action. Epinephrine alone did not affect the action of CCK. The magnitude of the exocrine response induced by high glucose was comparable to that of 2.5 mU/ml exogenous insulin. It seems possible that pancreatic acinar cells can be exposed to insulin levels of this magnitude in situ.

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Section: Discussionmentioning

confidence: 54%

Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.

Saito¹,

Williams²,

Kanno³

1980

J. Clin. Invest.

119

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“…An electric heating blanket was adjusted manually to maintain rectal temperature between 37.5-39.50C because we noticed in our initial experiments that body temperature rapidly drops in nonheated dogs under these experimental conditions. In order to be able to measure pancreatic insulin output, laparotomy was performed and an extracorporeal pancreatic blood circuit was made using a modification of the method of Kanazawa, Kuzuya, and Ide (16). First, the inferior pancreaticoduodenal vein was tied and cannulated by a small polyethylene cannula.…”

Section: Methodsmentioning

confidence: 99%

“…Received for publication 16 August 1972 and in revised form 9 October 1972. affect insulin output suggests that if they were to be released, they would be expected to alter insulin secretion directly and influence the islet cell response to other regulators of insulin secretion. Norepinephrine, the sympathetic neurotransmitter, has been found to inhibit insulin release by stimulation of the alpha adrenergic receptor (4,5).…”

Section: Introductionmentioning

confidence: 99%

Neural Regulation of Insulin Secretion in the Dog

Porte¹,

Girardier²,

Seydoux³

et al. 1973

J. Clin. Invest.

162

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A B S T R A C T The effects of stimulation of the mixed autonomic nerve to the dog pancreas has been studied under conditions in which both pancreaticoduodenal vein blood flow and insulin concentration were determined. Stimulation resulted in increased insulin output, which was blocked by prior administration of atropine. Blood flow was reduced by stimulation in proportion to the rate of stimulation. At 40 stimuli/s a maximum effect was found at 1 min with a gradual return toward base line despite continued application of the stimulus. Atropinization had no effect on blood flow changes. Insulin responses to 0.1 g/kg glucose were reduced on the average 40% by simultaneous stimulation of the pancreatic nerve at 40 cycles/s in atropinized animals. These studies establish this preparation as a reproducible model for the direct examination of autonomic influences on endocrine pancreatic function. From them it is concluded that the nerve supply to the endocrine pancreas of the dog is sufficient to inhibit insulin secretion by activation of the sympathetic nerves and to stimulate insulin secretion by activation of the parasympathetic nerves.

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“…Kanazawa et al [21], Lefebvre and Luyckx [24] and Porte et al [33] estimated the IRI secretion rate of anaesthetized dogs by sampling superior pancreaticoduodenal vein. In that experimental arrangement, however, the pancreatic blood stream could be altered and only a part of the pancreas is considered.…”

mentioning

confidence: 99%

Estimation of pancreatic IRI output rate and its relation to glucose tolerance in normal anaesthetized dogs

et al. 1975

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Summary. The pancreaticoduodenal and portal venous blood flows were recorded electromagnetically in anaesthetized dogs. Blood glucose and IRI were measured in the arterial, portal, and peripheral venous as well as in the intestinal venous blood. By a mathematical model the actual net IRI output of the whole pancreas was estimated. Under basal conditions it is 10.2 + 2.4 mU/min (n = 30; 26 kg mean body wt.). After i.v. glucose injection, IRI output is rapidly enhanced. The biphasic nature of this reaction was unequivocally demonstrated by consideration of the ratio IRI output : blood glucose. Pancreaticoduodenal blood flow increases transiently in relation to the increased blood glucose concentration. The IRI secretion rate is well correlated with the blood glucose concentration and to the amounts of glucose or of blood reaching the whole pancreas. It is also correlated with the portal IRI concentration. The overall peripheral venous or arterial IRI concentrations are correlated with the IRI secretion rate, but not in all individual experiments. The different phases of IRI output (basal rate, stimulated output 1-10 min and 10-60 min) show no influence on each other, nor are they correlated with the peripheral IRI concentration area. Basal IRI output is negatively correlated with the glucose assimilation constants. These constants or the peripheral BG areas, however, are independent of the stimulated IRI output rate. However, both the assimilation constants and the peripheral BG areas are related to the peripheral IRI concentration areas. Hepatic uptake of insulin and dynamics of pancreatic blood flow seem to contribute considerably to the estimated correlation pattern.

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Insulin output via the pancreatic vein and plasma insulin response to glucose in dogs

Cited by 42 publications

References 0 publications

Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.

Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.

Neural Regulation of Insulin Secretion in the Dog

Estimation of pancreatic IRI output rate and its relation to glucose tolerance in normal anaesthetized dogs

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