Published online Sep 21, 2018. doi: 10.3748/wjg.v24.i35.4028
Peer-review started: June 8, 2018
First decision: July 3, 2018
Revised: July 12, 2018
Accepted: July 22, 2018
Article in press: July 22, 2018
Published online: September 21, 2018
The adipose-tissue derived hormone adiponectin (ADPN) has been reported to have a role as a key neuromodulator of food intake. It is known that gastrointestinal motor phenomena represent a source of peripheral signals involved in the control of feeding behavior. However, no data are available concerning on the effects of ADPN on gastrointestinal motility. This novel information could highlight an additional mechanism engaged by the hormone in the control of food intake.
The finding that ADPN could influence gastric motility might represent an initial step to regard the peripheral effects of the hormone as possible signals involved in the control of food intake. This aspect, that certainly deserves to be deeper investigated, could lead to consider ADPN as a potential candidate for both novel therapeutic strategies in eating disorders and diagnostic tools.
The main objective of the present study was to investigate the influence of ADPN on the mechanical responses and the expression of its receptors in the mouse gastric fundus.
For the mechanical experiments, longitudinal muscle strips from the mouse gastric fundus were connected to force displacement transducers for continuous recording of isometric tension. The expression of ADPN receptors in gastric fundal tissue was revealed by touchdown- polymerase chain reaction (PCR) analysis.
The present results highlight that, in the mouse gastric strips, ADPN induces inhibitory effects by decreasing the amplitude of the neurally-induced contractile responses, enhancing that of the relaxant ones and causing a decay of the basal tension. Some of these actions appear to be mediated, at least in part, by nitric oxide although further studies are needed to better clarify the mechanism through which the hormone exerts its effects.
The results of the present study indicate for the first time that ADPN is able to exert inhibitory effects on the mechanical responses of the mouse gastric fundus in which we revealed the expression of ADPN receptors. It could be hypothesized that the hormone effects may be directed to facilitate muscle relaxation, so increasing the distension of the gastric wall that represents a peripheral satiety signal. In this view, the results of the present study may furnish the basis to better explore the link between peripheral and central effects of ADPN in the regulation of food intake.
The results of the present basic research might furnish a contribution to consider ADPN as a potential candidate for both novel therapeutic strategies in eating disorders and diagnostic tools.