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A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
Published on: April 28, 2016
Glucagon-like peptide-1 release and satiety after a nutrient challenge in normal-weight and obese subjects
Tanja C M Adam1, Margriet S Westerterp-Plantenga
1Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Department of Human Biology, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. T.Adam@hb.unimaas.nl
Abstract:
The present study was conducted to assess whether glucagon-like peptide-1 (GLP-1) release and appetite after a breakfast with or without an additional galactose/guar gum stimulation is different in normal-weight compared with overweight/obese subjects. Twenty-eight overweight/obese (BMI 30.3 (sd 2.7) kg/m2; age 44.3 (sd 9.7) years) and thirty normal-weight subjects (BMI 22.8 (sd 1.4), age 31.5 (sd12.8) years) participated in a crossover study. Fasting and postprandial plasma GLP-1, insulin, glucose and free fatty acid concentrations were measured in response to either a galactose (50 g)/guar gum (2.5 g) load (836 kJ) and a standard breakfast (1.9 MJ; GG), or water (250 ml) and the standard breakfast (W) every 30 min relative to the ingestion for 120 min. Appetite was assessed using 100 mm visual analogue scales. GLP-1 concentrations were significantly increased after GG at 30 and 60 min compared with W in both groups. Plasma GLP-1 concentrations in the W condition were higher in normal-weight than overweight/obese subjects (P=0.03). No difference was observed in the GG condition between groups. Satiety was increased in normal-weight compared with overweight/obese subjects in the GG condition at 30 (P=0.02) and 60 (P=0.04) min. We conclude that after a standard breakfast with water, GLP-1 release was lower in the overweight/obese than the normal-weight subjects. However, postprandial GLP-1 release in overweight/obese subjects was no different from that of normal-weight subjects when galactose/guar gum was added to the breakfast. The latter was not mirrored by subjective feelings of satiety. Disturbed perception of the physiological feedback of a satiety hormone rather than disturbed feedback itself might contribute to obesity.
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