Similar to our findings, another study reported that a 30 day high-fructose diet resulted in the permanent presence of GLUT2 in the apical membrane. Furthermore, GLUT2 plays a key role in glucose and fructose detection, thus controlling feeding behavior in mice. GLUT2 is also proposed to regulate sugar intake in humans. For example, individuals with a GLUT2 allelic variant from two separate Canadian populations have a higher daily intake of sugars. In line with our findings, other studies verified that a highfructose diet increased intestinal GLUT5 or GLUT2 short term expression. Similar results were obtained when rodents were intestinally perfused with increasing fructose concentrations. We confirm and extend such data by showing enhanced GLUT2, but not GLUT5 expression feeding the liquid high-fructose diet, when compared to the solid high-fructose or the Org 12962 hydrochloride control diets. Sugars also stimulate the sweet taste receptor type 1 member 3 and gustducin followed by the up-regulation of SGLT1 expression. Since we measure an increase of T1R3 but not SGLT1 mRNA expression we assume that the here shown effects are due to a long term sugar stimulation. We postulate that SGLT1 elevation may occur within a very short time frame after sugar consumption, keeping in mind that the SGLT1 is saturated by a relatively small sugar concentration. Nevertheless, SGLT1 seems to play a role as a glucose sensor involved in the control of apical GLUT2 insertion. If the SGLT1 is involved in the here shown GLUT2 enhancement needs further investigation. Similar to the up-regulation of intestinal GLUT2 and GLUT5, the satiety hormone CCK is enhanced in the ileum of mice fed with liquid high-sugar diets, in contrast to mice fed with solid highsugar diets or control diets. CCK is known to suppress Pemetrexed carbohydrate intake via the CCK-A receptor. In both, preclinical and clinical studies, CCK decreased food intake by reducing meal size and duration. However, no reduction of 24-h food intake was seen due to compensatory increases of CCK. Similarly, in clinical trials after 24-h continuous CCK infusion, subjects developed tolerance. Hence, the here shown up-regulation of CCK after feeding liquid high-sugar diets to mice, might be compensated by not yet known mechanisms. As confirmed for CCK, ghrelin is known to influence feeding behavior in the periphery as well as centrally. According to our data, the different sugar diets have only minor effects on ghrelin and virtually no effects on nesfatin-1 and PYY expression. Consequently, a rather selective influence of sugars in liquid form on particular weight regulating hormones, such as CCK, is anticipated. Hepatic triglycerides show a similar enhancement when being compared to GLUT2 and CCK mRNA expression in the intestine after feeding liquid high-sugar diets compared to control mice.