Effect of α-linolenic acid-rich diacylglycerol oil on protein kinase C activation in the rat digestive tract and lingual mucosa.

1,2-Diacylglycerol with short chain fatty acids is an endogenous activator of protein kinase C (PKC), which involved in multiple cellular processes implicated in cancer. The aim of the present study was to assess the effects of dietary α-linolenic acid-rich diacylglycerol (ALA-DAG) oil on PKC activation in the rat digestive tract and lingual mucosa in comparison with the effects of α-linolenic acid-rich triacylglycerol (ALA-TAG) oil, and common dietary oil. Membranous PKC activity in the lingual mucosa of male Wistar rats was significantly activated by treatment of the tongue with 1,2-tetradecarnoylphorbol-13-acetate (100 µM) twice in 1 day. In contrast, animals consuming a diet containing either ALA-DAG oil (7.5% or 30%), ALA-TAG oil (7.5% or 30%), or rapeseed oil (30%) for 4 weeks exhibited no significant differences in the cytosolic and membrane PKC activity in the lingual, esophageal, gastric, small intestinal, and colonic mucosa. Dose-related increases in PKC activity were not observed in the ALA-DAG oil-fed groups. Thus, the effects of dietary ALA-DAG oil on PKC activation in the digestive tract and lingual mucosa was similar to those of the ALA-TAG and rapeseed oils. These findings suggest that replacement of common dietary oil with ALA-DAG oil would not increase the risk of carcinogenesis.

Triterpene alcohols and sterols from rice bran lower postprandial glucose-dependent insulinotropic polypeptide release and prevent diet-induced obesity in mice.

Obesity is now a worldwide health problem. Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone that is secreted following the ingestion of food and modulates energy metabolism. Previous studies reported that lowering diet-induced GIP secretion improved energy homeostasis in animals and humans, and attenuated diet-induced obesity in mice. Therefore, food-derived GIP regulators may be used in the development of foods that prevent obesity. Rice bran oil and its components are known to have beneficial effects on health. Therefore, the aim of the present study was to clarify the effects of the oil-soluble components of rice bran on postprandial GIP secretion and obesity in mice. Triterpene alcohols [cycloartenol (CA) and 24-methylene cycloartanol (24Me)], ß-sitosterol, and campesterol decreased the diet-induced secretion of GIP in C57BL/6J mice. Mice fed a high-fat diet supplemented with a triterpene alcohol and sterol preparation (TASP) from rice bran for 23 wk gained less weight than control mice. Indirect calorimetry revealed that fat utilization was higher in TASP-fed mice than in control mice. Fatty acid oxidation-related gene expression in the muscles of mice fed a TASP-supplemented diet was enhanced, whereas fatty acid synthesis-related gene expression in the liver was suppressed. The treatment of HepG2 cells with CA and 24Me decreased the gene expression of sterol regulatory element-binding protein (SREBP)-1c. In conclusion, we clarified for the first time that triterpene alcohols and sterols from rice bran prevented diet-induced obesity by increasing fatty acid oxidation in muscles and decreasing fatty acid synthesis in the liver through GIP-dependent and GIP-independent mechanisms.

Suppression of a phosphatidylinositol 3-kinase signal by a specific spliced variant of Drosophila PTEN.

Drosophila PTEN (dPTEN) plays indispensable roles in the development of Drosophila melanogaster by controlling cell size and number. Although three potential spliced forms of dPTEN have been isolated, functional distinction among these forms remains elusive. In this study, we demonstrate that all spliced forms of dPTEN dephosphorylate phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3)); however, PI(3,4,5)P(3)-dependent activation of Drosophila Akt is suppressed specifically by one of three spliced forms, dPTEN3. Further, dPTEN3 dramatically changes its expression during the Drosophila development, while the other forms are expressed throughout the development. Our results suggest that dPTEN3 is the predominant spliced form that participates in PI(3,4,5)P(3)-mediated signaling pathways.