Could hop-derived bitter compounds improve glucose homeostasis by stimulating the secretion of GLP-1?

ABSTRACT

Hops (Humulus lupulus L.) is by far the greatest contributors to the bitter property of beer. Over the past years, a large body of evidence demonstrated the presence of taste receptors in different locations of the oral cavity. In addition to the taste buds of the tongue, cells expressing these receptors have been identified in olfactory bulbs, respiratory and gastrointestinal tract. In the gut, the attention was mainly directed to sweet Taste Receptor (T1R) and bitter Taste Receptor (T2R) receptors. In particular, T2R has shown to modulate secretion of different gut hormones, mainly Glucagon-like Peptide 1 (GLP-1), which are involved in the regulation of glucose homeostasis and the control of gut motility, thereby increasing the sense of satiety. Scientific interest in the activity of bitter taste receptors emerges because of their wide distribution in the human species and the large range of natural substances that interact with them. Beer, whose alcohol content is lower than in other common alcoholic beverages, contains a considerable amount of bitter compounds and current scientific evidence shows a direct effect of beer compounds on glucose homeostasis. The purpose of this paper is to review the available literature data in order to substantiate the novel hypothesis of a possible direct effect of hop-derived bitter compounds on secretion of GLP-1, through the activation of T2R, with consequent improvement of glucose homeostasis.

KEYWORDS:

• Hop-derived Bitter Compounds
• Glucose Homeostasis
• GLP-1

Disclosure statement

The Authors have nothing to disclose. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author contributions

The Authors' responsibilities were as follows: LB and GA: were responsible for the concept of this paper and drafted the manuscript; GM, AA, GCT, AC and SS: provided a critical review of the paper. All Authors contributed to and agreed on the final version of the manuscript.