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Water‐in‐oil (W/O) emulsions can be used to encapsulate and control the release of bioactive compounds for nutrition fortification in fat‐based food products. However, long‐term stabilization of W/O emulsions remains a challenging task in food science and thereby limits their potential application in the food industry. To develop high‐quality emulsion‐based food products, it is essential to better understand the factors that affect the emulsions’ stability. In real food system, the stability situation of W/O emulsions is more complicated by the fact that various additives are contained in the products, such as NaCl, sugar, and other large molecular additives. The potential stability issues of W/O emulsions caused by these encapsulated additives are a current concern, and special attention should be given to the relevant theoretical knowledge. This article presents several commonly used methods for the preparation of W/O emulsions, and the roles of different additives (water‐ and oil‐soluble types) in stabilizing W/O emulsions are mainly discussed and illustrated to gain new insights into the stability mechanism of emulsion systems. In addition, the review provides a comprehensive and state‐of‐art overview of the potential applications of W/O emulsions in food systems, for example, as fat replacers, controlled‐release platforms of nutrients, and delivery carrier systems of water‐soluble bioactive compounds. The information may be useful for optimizing the formulation of W/O emulsions for utilization in commercial functional food products.

BackgroundMany cardioprotective pharmacological agents failed to exert their protective effects in diabetic hearts subjected to myocardial ischemia/reperfusion (MI/R). Identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic conditions. Importantly, recent studies indicated that Drp1-mediated mitochondrial fission is enhanced in the myocardium of diabetic mice. The above evidences suggested that Drp1 may be one critical molecule linking diabetes with MI/R injury. We hypothesized that inhibition of Drp1 may be effective to reduce MI/R injury in diabetic hearts.MethodsHigh-fat diet and streptozotocin-induced diabetic mice were subjected to MI/R or sham operation. Mdivi-1 (1.2 mg/kg), a small molecule inhibitor of Drp1 or vehicle was administrated 15 min before the onset of reperfusion. Outcome measures included mitochondrial morphology, mitochondrial function, myocardial injury, cardiac function and oxidative stress.ResultsMitochondrial fission was significantly increased following MI/R as evidenced by enhanced translocation of Drp1 to mitochondria and decreased mitochondrial size. Delivery of Mdivi-1 into diabetic mice markedly inhibited Drp1 translocation to the mitochondria and reduced mitochondrial fission following MI/R. Inhibition of Drp1 in diabetic hearts improved mitochondrial function and cardiac function following MI/R. Moreover, inhibition of Drp1 reduced myocardial infarct size and serum cardiac troponin I and lactate dehydrogenase activities. These cardioprotective effects were associated with decreased cardiomyocyte apoptosis and malondialdehyde production and increased activities of antioxidant enzyme manganese superoxide dismutase.ConclusionsPharmacological inhibition of Drp1 prevents mitochondrial fission and reduces MI/R injury in diabetic mice. The findings suggest Drp1 may be a potential novel therapeutic target for diabetic cardiac complications.