13 research outputs found

    A genetic variant in proximity to the gene <i>LYPLAL1</i> is associated with lower hunger feelings and increased weight loss following Roux-en-Y gastric bypass surgery

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    <p><b>Objective:</b> Bariatric surgery is the most efficient treatment of severe obesity. We investigated to what extent BMI- or waist-hip ratio (WHR)-related genetic variants are associated with excess BMI loss (EBMIL) two years after Roux-en-Y gastric bypass (RYGB) surgery, and elucidated the affected biological pathways.</p> <p><b>Methods:</b> Two-hundred fifty-one obese patients (age: 43 ± 10.7, preoperative BMI: 45.1 ± 6.1 kg/m<sup>2</sup>, 186 women) underwent RYGB surgery and were followed up after two years with regard to BMI. Patients were genotyped for 32 single-nucleotide polymorphisms (SNPs) that were investigated with regard to their impact on response to RYGB and preoperatively measured Three Factor Eating Questionnaire (TFEQ) scores.</p> <p><b>Results:</b> Homozygous T carriers of the SNP rs4846567 in proximity to the Lysophospholipase-like 1 (<i>LYPLAL1</i>) gene showed a 7% higher EBMIL compared to wild-type and heterozygous carriers (<i>p</i> = 0.031). TT-allele carriers showed furthermore lower scores for Hunger (74%, <i>p</i> < 0.001), lower Disinhibition (53%, <i>p</i> < 0.001), and higher Cognitive restraint (21%, <i>p</i> = 0.017) than GG/GT carriers in the TFEQ. Patients within the lowest quartile of Hunger scores had a 32% greater EBMIL compared to patients in the highest quartile (<i>p</i> < 0.001).</p> <p><b>Conclusion:</b> The <i>LYPLAL1</i> genotype is associated with differences in eating behavior and loss of extensive body weight following RYGB surgery. Genotyping and the use of eating behavior-related questionnaires may help to estimate the RYGB-associated therapy success.</p

    Effect of High Sugar Intake on Glucose Transporter and Weight Regulating Hormones in Mice and Humans

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    <div><p>Objective</p><p>Sugar 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.</p><p>Methods</p><p>Five 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.</p><p>Results</p><p>In 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.</p><p>Conclusions</p><p>We 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.</p></div

    Comparison of liquid and solid high-sugar diets as well as sugar type.

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    <p>Liquid compared to solid sugar form (*P<0.05; **P<0.01; ***P<0.001) or fructose compared to sucrose (<sup>§</sup>P<0.05; <sup>§§§</sup>P<0.001). Detailed feeding protocols of the four animal groups are described in material and methods. Data are means ± SEM (n = 9–10). P-values are calculated using the 2-way ANOVA. GLUT2/5, glucose transporter 2/5; CCK, cholecystokinin; TG, triglycerides; C, control diet; Fl, fructose liquid; Fs, fructose solid; Sl, sucrose liquid; Ss, sucrose solid.</p

    Elevated liquid sucrose intake increased caloric intake in mice.

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    <p>Sugar, liquid and food intake was analyzed (A). Total caloric, liquid and food caloric intake was determined (B). Data in panels A and B are shown as means ± SEM (n = 10). */**P<0.01, compared to control; <sup>§</sup>P<0.05, compared to sucrose solid. C, control; Fl, fructose liquid; Fs, fructose solid; Sl, sucrose liquid; Ss, sucrose solid.</p

    Primers used for mRNA detection.

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    <p>GLUT2/5, glucose transporter 2/5; h, human; SGLT1, sodium-driven sugar co-transporter 1; T1R3, taste receptor type 1 member 3; CCK, cholecystokinin; PYY, Peptide YY.</p

    Weight parameters and blood glucose.

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    <p>Data are means ± SEM (<i>n</i> = 10).</p><p>*P<0.05 and **P<0.01 compared to C;</p>§<p>P<0.05 compared to Sl.</p><p>C, control diet; Fl, fructose liquid; Fs, fructose solid; Sl, sucrose liquid; Ss, sucrose solid.</p

    Obese humans showed an increased small intestinal sugar transporter expression compared to normal weight humans.

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    <p>Small intestinal hGLUT2, hGLUT5 and hCCK mRNA expression was detected (A/B/C). Data are shown as means ± SEM (*P<0.05; **P<0.01; n = 12–20). hGLUT2/5, human glucose transporter 2/5; hCCK, human cholecystokinin; Ob, obese; Nw, normal weight.</p

    Liquid high-sugar diets increased intestinal sugar transporter and weight regulating hormone expression.

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    <p>Ileal GLUT2, GLUT5, CCK and ghrelin mRNA expression was detected (A/B/C/D). Data are shown as means ± SEM (*P<0.05, **P<0.01, ***P<0.001; n = 9–10). GLUT2/5, glucose transporter 2/5; CCK, cholecystokinin, for diet abbreviations see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101702#pone-0101702-g001" target="_blank">Figure 1</a>.</p

    Effect of high-sugar diets on hepatic lipid accumulation.

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    <p>Concentrations of triglycerides in the liver (A), and liver to body ratio (B) were detected. Portal endotoxin (C), and Oil Red O staining showing fat accumulation in the liver (D) are shown. Data is shown as means ± SEM (*P<0.05, **P<0.01, ***P<0.001; n = 6–10). For Abbreviations see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101702#pone-0101702-g001" target="_blank">Figure 1</a>.</p
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