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Aroma is an important quality factor for unrefined vegetable oils especially the condiment oils, whose application and acceptability largely depend on their aroma attributes. The ever-advanced techniques including extraction, separation, detection and identification in flavor science allow hundreds of volatile compounds and aroma-active compounds with high complexity to be identified, which enables us a deep and comprehensive understanding of the aroma in various type of vegetable oils. Studies show that several avenues, mainly including enzymatic reaction, Maillard reaction, Strecker degradation, caramelization, lipid oxidation and thermal degradation of other compounds, account for the formation of these aroma compounds, though some may dominate over others depending on the processing methods/conditions. Based on these findings, novel approaches such as mild-heat treatment, roasting, microwave processing, infrared radiation, enzymatic treatment and fermentation, among others, have been applied to pretreat oil seeds or fruits with the aim to modulate the flavor generation and sensory quality in oils, whereby promising and insightful results are obtained. This review summarizes and discusses the volatile composition and key aroma compounds in common unrefined vegetable oils, their generation pathways as well as the approaches used to modulate their formations. [ABSTRACT FROM AUTHOR]

Osteoporosis-related bone fracture and falls have a severe impact on patients’ daily lives. Osteoblasts are bone-building cells that play a vital role in bone formation and remodeling. Imbalanced osteoblast differentiation could lead to osteoporosis. GPR39 is an orphan G protein-coupled receptor that mediates metabolic pathways. In this study, we show that GPR39 is expressed in MC3T3-E1 cells. Osteoblast differentiation culture media induces GPR39, suggesting that GPR39 is a differentiation-responsive factor. Activation of GPR39 using its selective agonist TC-G 1008 induces alkaline phosphatase (ALP), osteocalcin (OCN), and type I collagen (Col-I) expression, and increases cellular ALP activity and calcium deposition, implying that GPR activation promotes cells toward osteoblast differentiation. Treatment with TC-G 1008 also increases Runx-2 expression and AMPK activation. However, the inhibition of AMPK by Compound C abolished TC-G 1008-mediated ALP, OCN, and Col-I induction, and reduces ALP activity and cellular calcium deposition as well as Runx-2 induction. These data indicate that TC-G 1008-mediated GPR39 activation involves AMPK-mediated Runx-2 induction. In summary, our study uncovers a new role of GPR39 activation in osteoblast differentiation, implying that GPR39 could be a promising therapeutic target for osteoporosis. [ABSTRACT FROM AUTHOR]