Comparison of Dose–Response Relations of Insulin and 2-Deoxy-D-Glucose for Biliary and Gastric Acid Secretion in Dogs

Jones, R. Scott; Geist, Richard E.; Hall, Albert D.

doi:10.1016/s0016-5085(19)33672-8

Cited by 14 publications

(6 citation statements)

References 14 publications

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“…The effect of graded doses of insulin on bile flow is in accordance with the expts. of Jones, Geist and Hall (1970) on conscious dogs and an increase in flow rate of about 5 ,d/kg/min at an insulin dose of 1-2 U/kg is compatible with the results of these and other expts. (e.g.…”

Section: Discussionsupporting

confidence: 90%

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Insulin‐stimulated bile formation in cats

Larsen

Christensen

1978

Acta Physiologica Scandinavica

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The effects of insulin on bile flow and composition were examined in fasting, chloralose-anesthetized cats. Insulin in doses from 0.01 to 2.00 U/kg increased bile flow and biliary erythritol clearance without any detectable change in the difference between them; thus insulin presumably had no effect on ductular fluid transport. Continuous infusion of insulin (0.8 U/kg+0.05 U/kg/min or 0.05 U/kg+0.002 U/kg/min) increased biliary erythritol clearance by 22%. The increase was caused by a rise in the bile acid-independent fraction of bile production and accompanied by a parallel increase in the rates of biliary excretion of Na+ and Cl-. When ouabain, 80 micrograms/kg, was injected intraportally during insulin infusion the erythritol clearance, bile flow and the rates of biliary excretion of Na+ and Cl- were lowered towards but not to their preinsulin levels. The effects of insulin on these parameters were unchanged after atropin or gastrectomy and 2-Deoxy-D-Glucose was without effect on bile production. The results indicate that administration of insulin affects bile formation by stimulating the active transport of sodium across the canalicular membrane.

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Section: Discussionsupporting

confidence: 90%

“…However, in agreement with the expts. of Konturek, Kieta-Fyda and Moczurad (1967) in cats, but contrary to findings in dogs (Jones et a/. 1970, Geist, Jones and Hall 1970, and Gourlay and Jones 1972, the cytoglucopenic agent, 2 Deoxy-D-Glucose, did not effect bile flow, which seems to speak against a direct effect of hypoglycemia.…”

Section: Discussioncontrasting

confidence: 60%

Insulin‐stimulated bile formation in cats

Larsen

Christensen

1978

Acta Physiologica Scandinavica

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“…In the present study insulin and reserpine were used as t h e m a j o r stimulatory or inhibitory reagents because pentagastrin, histamine, secretin, atropine, and prostaglandin E~ did not produce changes in cell structure that were as consistent or extensive. Insulin stimulation of acid secretion is generally acknowledged (10,22,23,30). Reserpine is known to cause increased acid secretion in rats (23), but in mice reserpine injection in high doses does not stimulate acid secretion (2).…”

mentioning

confidence: 99%

Studies on the Depletion and Accumulation of Microvilli and Changes in the Tubulovesicular Compartment of Mouse Parietal Cells in Relation to Gastric Acid Secretion

Ito

Schofield

1974

The Journal of Cell Biology

166

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Gastric parietal cells in mice present a spectrum of microscopic appearances due mainly to variations in the abundance of the tubular and vesicular component of the cytoplasm and in the size and number of microvilli lining the intracellular canaliculi. Differences in the range of forms among parietal cells of fasting versus fed mice were not especially striking, but cells with very numerous tubules and vesicles were more common after fasting. However, in mice treated with drugs or hormones that induce acid secretion, parietal cells were more uniform in appearance. There was a marked reduction of these cytoplasmic membranes and a concomitant increase in both the number and size of microvilli. Measurements of acid secretion in control animals and in animals treated with acid secretagogues indicated hydrogen ion secretion contemporaneous with depletion of the cytoplasmic tubulovesicular membranes and with increase of the microvilli. In mice with inhibited acid secretion, parietal cells showed an accumulation of cytoplasmic tubules and vesicles and reduction in the numbers of microvilli. Stereological methods were used to quant~tate 10 different parietal cell compartments. Tracer studies with lanthanum did not reveal continuity between the tubules and the plasma membrane. However, there were regions of close apposition between the tubulovesicular membranes and the cell membrane of the canaliculus, and instances where cytoplasmic tubules extended from the cell into the core of enlarged microvilli.

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“…Glucagon had rather generalized actions on the electrolytes the body. Its stimulatory effect on intestinal (Barbezat and Grossman., 1971), renal (Staub et al, 1957) and bile (Jones et al, 1970;Jones et al, 1971) secretions was well documented. Given subcutaneously to conscious dogs, glucagon caused transient hyperkalemia and hyperglycemia that were accompanied by diuresis and renal electrolyte excretion (Lin et al, 1973b).…”

Section: Posssible Mechanism Of Actionmentioning

confidence: 93%

“…In cholecystectomized dog (Jones et al, 1970;Jones et al, 1971;Morris et al, 1967) and man (Dyck and Janowitz, 1971;Kuska, 1974) glucagon caused choleresis. Some found augmentation of bile flow without altering the composition of the hepatic bile (Dyck and Janowitz, 1971), and others found both increases of volume and electrolyte outputs (Morris et al, 1967) or increased bile flow and cl-concentration with no effect on bicarbonate and a decrease in bile salt content (Jones et al, 1970;Jones et al, 1971).…”

Section: Bile Secretion (A) Choleretic Actionmentioning

confidence: 99%