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The Secretion of Gastric Acid in Response to a Lack of Metabolizable Glucose

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Journal J Physiol
Specialty Physiology
Date 1969 May 1
PMID 5770922
Citations 7
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Abstract

1. The onset of the secretion of acid from the stomach of rats during insulin-induced hypoglycaemia has been found to correspond to a mean plasma glucose concentration of 72 mg/100 ml. (equivalent to a blood glucose concentration of 44 mg/100 ml.).2. Infusions of the non-metabolizable sugar, 3-O-methylglucose, into rats with denervated adrenal glands caused a large and sustained rise in the gastric acid output. This gastric acid secretion could be prevented by prior vagotomy or stopped, when previously established, by cutting the vagi or by the administration of glucose.3. A consistent relationship was demonstrated between the plasma concentration of glucose and the total concentration of glucoses (glucose plus 3-O-methylglucose) in the plasma at the onset of gastric acid secretion during the infusion of 3-O-methylglucose into these rats. The theoretical basis for this relationship is discussed.4. 3-O-methylglucose did not cause the release of gastric acid when infused into rats with intact sympathetic nervous systems owing to the effects of the secretion of adrenaline provoked by this agent.5. The qualitative and quantitative similarities between the factors governing both the secretion of gastric acid and the release of adrenaline in the absence of a sufficiency of metabolizable glucose are discussed. It is suggested that the reactions of both these systems under such circumstances are determined by chemoreceptors which possess identical characteristics.

Citing Articles

Metabolic mapping of neural pathways involved in gastrosecretory response to insulin hypoglycaemia in the rat.

Kadekaro M, Savaki H, Sokoloff L J Physiol. 1980; 300:393-407.

PMID: 6770083 PMC: 1279361. DOI: 10.1113/jphysiol.1980.sp013168.


Hypothalamic control of adrenaline secretion in response to insufficient glucose.

HIMSWORTH R J Physiol. 1970; 206(2):411-7.

PMID: 5498492 PMC: 1348654. DOI: 10.1113/jphysiol.1970.sp009021.


The location of the chemoreceptor controlling gastric acid secretion during hypoglycaemia.

Colin-Jones D, HIMSWORTH R J Physiol. 1970; 206(2):397-409.

PMID: 5498491 PMC: 1348653. DOI: 10.1113/jphysiol.1970.sp009020.


The assay of gastrin using the perfused rat stomach.

Smith G, Lawrence A, Colin-Jones D, SCHILD H Br J Pharmacol. 1970; 38(1):206-13.

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Factors which determine the gastric secretory response to 2-deoxy-D-glucose.

HIMSWORTH R, Colin-Jones D Gut. 1969; 10(12):1015-9.

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References
1.
Davis R, BROOKS F, ROBERT Jr C . GASTRIC SECRETORY RESPONSE TO GRADED INSULIN HYPOGLYCEMIA. Am J Physiol. 1965; 208:6-8. DOI: 10.1152/ajplegacy.1965.208.1.6. View

2.
BACHRACH W . On the question of a pituitary-adrenal component in the gastric secretory response to insulin hypoglycemia. Gastroenterology. 1963; 44:178-89. View

3.
Crone C . Facilitated transfer of glucose from blood into brain tissue. J Physiol. 1965; 181(1):103-13. PMC: 1357441. DOI: 10.1113/jphysiol.1965.sp007748. View

4.
GHOSH M, SCHILD H . Continuous recording of acid gastric secretion in the rat. Br J Pharmacol Chemother. 1958; 13(1):54-61. PMC: 1481706. DOI: 10.1111/j.1476-5381.1958.tb00190.x. View

5.
HIMSWORTH R . Compensatory reactions to a lack of metabolizable glucose. J Physiol. 1968; 198(2):451-65. PMC: 1365333. DOI: 10.1113/jphysiol.1968.sp008616. View