Oenothein B in Eucalyptus Leaf Extract Suppresses Fructose Absorption in Caco-2 Cells.

Keiichiro Sugimoto,Tomoyuki Fujita,Hiroaki Takeuchi,Hiroshi Inui,Shigeo Takenaka,Kazuya Nakagawa,Yoshiaki Amakura,Morio Yoshimura,Midori Amako

doi:10.3390/molecules27010122

Abstract

Inhibition of fructose absorption may suppress adiposity and adiposity-related diseases caused by fructose ingestion. Eucalyptus leaf extract (ELE) inhibits intestinal fructose absorption (but not glucose absorption); however, its active compound has not yet been identified. Therefore, we evaluated the inhibitory activity of ELE obtained from Eucalyptus globulus using an intestinal fructose permeation assay with the human intestinal epithelial cell line Caco-2. The luminal sides of a cell monolayer model cultured on membrane filters were exposed to fructose with or without the ELE. Cellular fructose permeation was evaluated by measuring the fructose concentration in the medium on the basolateral side. ELE inhibited 65% of fructose absorption at a final concentration of 1 mg/mL. Oenothein B isolated from the ELE strongly inhibited fructose absorption; the inhibition rate was 63% at a final concentration of 5 μg/mL. Oenothein B did not affect glucose absorption. In contrast, the other major constituents (i.e., gallic acid and ellagic acid) showed little fructose-inhibitory activity. To our knowledge, this is the first report that oenothein B in ELE strongly inhibits fructose absorption in vitro. ELE containing oenothein B can prevent and ameliorate obesity and other diseases caused by dietary fructose consumption.

Highlights

Fructose consumption has increased in the past five decades because of the use of high-fructose corn syrups as sweeteners in beverages and processed foods [1,2]
We examined the effects of Eucalyptus leaf extract (ELE) and its constituents on fructose permeation across an intestinal epithelial cell monolayer model from the luminal side to the basolateral side using Caco-2 cells to identify the active constituent of the extract
Before evaluating the inhibitory effect of ELE on fructose absorption using Caco-2 cells, we confirmed that glucose transporter 5 (GLUT5) regulates fructose absorption in this model; we verified that cytochalasin B [33], a GLUT2 inhibitor, does not affect fructose absorption at a final concentration of 100 μmol/L

Summary

Introduction

Fructose consumption has increased in the past five decades because of the use of high-fructose corn syrups as sweeteners in beverages and processed foods [1,2]. Sucrose is ingested in large amounts, as it is traditionally used in many foods and beverages [3]. Fructose is more lipogenic than glucose in the liver because its metabolic pathway does not include the step catalyzed by 6-phosphofructokinase, the main rate-controlling enzyme in glycolysis; large amounts of ingested fructose can be rapidly metabolized without metabolic regulation [14]. Fructose serves as the carbon source for both the glycerol and acyl portions of triacylglycerol molecules, leading to de novo lipogenesis [2,5]

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