Tomoshige Umeda

Basic studies for the practical use of bitterness inhibitors: selective inhibition of bitterness by phospholipids.

AbstractPurpose. We examined the effects of phospholipids such as phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol (PI), and phosphatidic acid (PA) on human taste sensation to various substances. Methods. The effects were evaluated psychophysically using paid volunteers. Results. PA inhibited the bitterness of various substances dissolved in water without affecting sweetness, saltiness, and sourness, although its inhibitory activity was less than that of PA-LG. PI also showed inhibitory activity on bitterness, although its activity was less than PA. A soybean lecithin fraction containing high contents of PA and PI also demonstrated inhibitory activity on the bitterness of various substances. Both the incorporation of either PA or the lecithin fraction into granules containing quinine and the coating of the granules with PA or the fraction effectively inhibited the bitterness of quinine. Conclusions. The lecithin fraction is permitted for use as an additive to drugs and food and can be produced on an industrial scale. It is expected that the lecithin fraction will be used safely as a bitterness inhibitor for practical applications.

Metabolic and Hormonal Alterations with Diacylglycerol and Low Glycemic Index Starch during Canine Weight Loss

Obesity increases insulin resistance and disregulation of glucose homeostasis. This study investigated low glycemic index starch (LGIS)/diacylglycerol (DAG) diet on plasma insulin and circulating incretin hormones during canine weight loss. Obese Beagle dogs were fed one of four starch/oil combination diets (LGIS/DAG; LGIS/triacylglycerol (TAG); high glycemic index starch (HGIS)/DAG; and HGIS/TAG) for 9 weeks during the weight loss period. At weeks 1 and 8, fasting plasma insulin, glucose, nonesterified fatty acid (NEFA), glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1) were determined. Weight loss did not affect fasting insulin, glucose, and NEFA, but fasting GIP increased and GLP-1 decreased. LGIS affected postprandial insulin at both times and glucose was similar to insulin, except 60 min postprandially with DAG at week 8. NEFA lowering was less with the LGIS diets initially but not thereafter. At 60 min postprandially on week 8, GIP was significantly elevated by DAG, while GLP-1 was increased only with the HD diet. LGIS suppressed insulin and glucose responses up to 180 min postprandially at both sample times. DAG increased incretin hormones as did the DAG/HGIS combination but only at week 8. This latter finding appeared to be related to the glucose response but not to insulin at 60 min.