Humans have 25 different taste receptors for bitter substances (mice, in comparison, have 35), while we have only one each for salty, sour, umami, and sweet flavors. Bitter taste receptors are present in numerous organs and immune cell populations, and the gastrointestinal tract variously expresses bitter receptor types throughout its length. Altered bitter signaling can impact energy metabolism, and intestinal bitter signaling is known to influence satiety, gastric emptying, and intestinal motility.
Altered production of digestive factors (like GLP-1 and ghrelin) that affect appetite and the glycemic response is implicated in obesity, diabetes, and metabolic syndrome, and changes in bile acid excretion may also contribute. Heightened GLP-1 activity is a well-known mechanism for improving glucose homeostasis, and it may partly explain the health benefits of bitter-tasting foods. In clinical studies, supplementation with bitter principles derived from hops has improved body mass index (BMI), fat mass, fasting blood glucose, and HbA1c levels, though the mechanisms underlying these effects were unknown.
In these studies, bitter substances derived from the hops plant were assayed for their ability to bind with human and mouse bitter receptors. Animals with diet-induced obesity were then given an isolate (called KDT501) prepared from hops-derived bitters and tested for a range of immunometabolic parameters, including GLP-1 secretion, energy expenditure, liver fat accumulation, and circulating levels of lipids, ketones, liver enzymes, and gut hormones. The experiments were designed to determine the degree to which GLP-1 secretion is responsible for the salutary metabolic effects of the KDT501 bitter compound.
Bitter Tastes Can Have Sweet Effects on Energy Metabolism
According to the authors, “beyond its role in nutrient absorption, the GI tract is emerging as a powerful regulator of systemic energy balance.”
This study illustrates many immunometabolic advantages offered by food-derived bitter molecules that enhance secretion of the gut peptide GLP-1.