Published online May 28, 2020. doi: 10.3748/wjg.v26.i20.2472
Peer-review started: December 23, 2019
First decision: March 27, 2020
Revised: April 13, 2020
Accepted: May 13, 2020
Article in press: May 13, 2020
Published online: May 28, 2020
The regulation of food intake is a complex mechanism, and the hypothalamus is the main central structure implicated. In particular, the arcuate nucleus appears to be the most critical area in the integration of multiple peripheral signals. Among these signals, those originating from the white adipose tissue and the gastrointestinal tract are known to be involved in the regulation of food intake. The present paper focuses on adiponectin, an adipokine secreted by white adipose tissue, which is reported to have a role in the control of feeding by acting centrally. The recent observation that adiponectin is also able to influence gastric motility raises the question of whether this action represents an additional peripheral mechanism that concurs with the central effects of the hormone on food intake. This possibility, which represents an emerging aspect correlating the central and peripheral effects of adiponectin in the hunger-satiety cycle, is discussed in the present paper.
Core tip: Central structures involved in the regulation of food intake receive and integrate signals from peripheral organs, including white adipose tissue. This paper summarizes the main findings on the influence of adiponectin, a pleiotropic hormone secreted by adipocytes, on food intake. In addition to its central actions, adiponectin has been recently reported to cause gastric motor changes known to be peripheral signals implicated in the hunger-satiety cycle. In this light, we discuss the potential role of adiponectin as a peripheral signal in the signaling network underlying hunger and satiety.