Sweet tooth reconsidered: Taste responsiveness in human obesity

Taste responses of normal-weight, obese, and formerly obese individuals for sucrose and fat containing stimuli were examined using a mathematical modelling technique known as the Response Surface Method. The subjects accurately rated intensities of sweetness, fatness, and creaminess of 20 different mixtures of milk, cream, and sugar, and no mixture phenomena or inter-group differences were observed. In contrast, hedonic taste responses varied across subject groups, and were affected differentially by the sucrose and lipid content of the stimuli. Normal-weight subjects optimally preferred stimuli containing 20% lipid and less than 10% sucrose. Obese subjects preferred high-fat stimuli (>34% lipid) that contained less than 5% sucrose, while formerly obese subjects showed enhanced responsiveness to both sugar and fat. Hedonic responsiveness as measured by the optimal sugar/fat ratio was negatively correlated with the degree of overweight (body mass index: weight/height2). We hypothesize that sensory preferences for dietary sugars and fats are determined by body-weight status and may affect the patterns of food consumption.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25560/1/0000102.pd

Defective enzyme protein in lipoprotein lipase deficiency

A monoclonal antibody to lipoprotein lipase (LPL) has been used in an enzyme-linked immunosorbent assay (ELISA) for LPL protein mass. Measurement of LPL immunoreactive mass in pre- and postheparin plasma distinguished three classes of abnormalities in patients with classical deficiency of lipoprotein lipase activity. The class I defect consisted of the absence of LPL immunoreactive homodimer in pre- and postheparin plasma compatible with a potential 'null allele'. Patients with a class II defect had almost no LPL immunoreactive mass in preheparin plasma but showed an increase in their LPL mass of 68 +/- 23 ng ml-1 (mean +/- SD) after heparin. Patients with the class III defect had considerable amounts of LPL immunoreactive material in preheparin plasma (159 +/- 190 ng ml-1). Heparin administration, however, caused very little additional release of LPL into the plasma (16 +/- 51 ng ml-1). Thus although both class II and class III patients had an LPL protein with abnormal catalytic activity, class III patients also appeared to have a defect in heparin binding of LPL. To test this hypothesis, postheparin plasma of classes II and III patients was analysed by heparin-Sepharose chromatography. In contrast to class II patients, the LPL immunoreactive mass of class III patients did not show affinity for the heparin and eluted in the column void volume, suggesting the class III defect is also associated with a defect in heparin binding