Abstract
ObjectiveSugar consumption has increased dramatically over the last decades in Western societies. Especially the intake of sugar-sweetened beverages seems to be a major risk for the development of obesity. Thus, we compared liquid versus solid high-sugar diets with regard to dietary intake, intestinal uptake and metabolic parameters in mice and partly in humans.MethodsFive iso-caloric diets, enriched with liquid (in water 30% vol/vol) or solid (in diet 65% g/g) fructose or sucrose or a control diet were fed for eight weeks to C57bl/6 mice. Sugar, liquid and caloric intake, small intestinal sugar transporters (GLUT2/5) and weight regulating hormone mRNA expression, as well as hepatic fat accumulation were measured. In obese versus lean humans that underwent either bariatric surgery or small bowel resection, we analyzed small intestinal GLUT2, GLUT5, and cholecystokinin expression.ResultsIn mice, the liquid high-sucrose diet caused an enhancement of total caloric intake compared to the solid high-sucrose diet and the control diet. In addition, the liquid high-sucrose diet increased expression of GLUT2, GLUT5, and cholecystokinin expression in the ileum (P<0.001). Enhanced liver triglyceride accumulation was observed in mice being fed the liquid high-sucrose or -fructose, and the solid high-sucrose diet compared to controls. In obese, GLUT2 and GLUT5 mRNA expression was enhanced in comparison to lean individuals.ConclusionsWe show that the form of sugar intake (liquid versus solid) is presumably more important than the type of sugar, with regard to feeding behavior, intestinal sugar uptake and liver fat accumulation in mice. Interestingly, in obese individuals, an intestinal sugar transporter modulation also occurred when compared to lean individuals.
Highlights
Sugar consumption has increased dramatically over the last decades in Western societies and is regarded as a major risk for the development of obesity [1]
Short-term studies in mouse and man revealed that monosaccharide transport across epithelial membranes in the intestine is mediated by the family of sodium-driven sugar co-transporters (SGLTs) and glucose transporters (GLUTs), respectively [14]
Only mice fed the liquid high-sucrose diet had a significant elevated liquid intake and a reduced solid food intake compared to control mice and mice fed the solid high-sucrose diet (P,0.05; Figure 1A). It is of note, that the metabolisable energy absorbed by the mice was not significant different between the liquid or solid high-sugar diets, meaning that these diets are comparable (Table S1)
Summary
Sugar consumption has increased dramatically over the last decades in Western societies and is regarded as a major risk for the development of obesity [1]. Changes in dietary and eating behavior such as preferring sugar-sweetened beverages and sugar-rich processed food, in addition to a sedentary life style, are associated with the sharp rise in obesity [2,3,4]. Various studies have shown that altered sugar signaling pathways influence feeding behavior, modulate intestinal sweet taste receptors, sugar transporters, and alter weight-regulating gastrointestinal hormone expression [10,11,12,13]. Short-term studies in mouse and man revealed that monosaccharide transport across epithelial membranes in the intestine is mediated by the family of sodium-driven sugar co-transporters (SGLTs) and glucose transporters (GLUTs), respectively [14]. SGLT1, is a low-capacity, high-affinity transporter and the only transporter capable of moving glucose against a concentration gradient. GLUT2 is capable of recognizing galactose and has been involved in the control of food intake in the hypothalamus [16]
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