A hypothesis of couplet molecules and couplet cells in gastric function and an association with Helicobacter pylori

Abstract

Background: Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormones that regulate gastric activity.

Discussion: It is proposed that the G-cells and the ECL cells are coupled by the couplet molecules gastrin and histamine and by a prior asymmetrical cell division. The gastrin (from G-cells) stimulates the ECL cells to produce and secrete histamine while, in a reciprocal way, this histamine (from ECL cells), stimulates the G-cells to produce and secrete gastrin. These molecules would also stimulate cell division - the gastrin would stimulate cell division of ECL cells while histamine would stimulate that of G-cells. A chemical complex of gastrin and histamine is postulated as is also the asymmetric cell divisions of precursor cells to produce the coupled G-cells and ECL cells.

Conclusion: There is sufficient evidence to support the feasibility of the model in general, but more direct experimental evidence is required to validate the model as applied here to gastric function.

Fig. 1

The Simple Interaction of a G-Cell and an ECL Cell. The reciprocal interactions of a G-Cell and an ECL Cell (^GC and ^ECLC) are illustrated. The stimulatory effects of Gastrin (GAS) and Histamine (HTM) occur by acting via cell membrane receptors ^GASR and ^HTMR

Fig. 2

A Possible Complex Interaction of a G-Cell and an ECL Cell. The reciprocal interactions of a G-Cell and an ECL Cell (^GC and ^ECLC) are illustrated as in Fig. 1. In addition, this model incorporates a possible extracellular receptor for the Gastrin:Histamine complex (the CC in this particular case)