A versatile targeted metabolomics method for rapid quantification of multiple classes of phenolics in fruit and beverages

Compelling evidence of the health benefits of phenolic compounds and their impact on food quality have stimulated the development of analytical methods for the identification and quantification of these compounds in different matrices in recent years. We have developed a targeted metabolomics method for the quantification of 140 phenolics,such as benzoates, phenylpropanoids, coumarins, stilbenes, dihydrochalcones and flavonoids in fruit and tea extracts and wine using UPLC-MS/MS. Chromatography was optimised to achieve separation of the compounds over a period of 15 minutes and MRM transitions were selected for accurate quantification. The effectiveness of the method was validated by studying the detection and quantification limits, the linearity ranges of instrumental response and the repeatability of the analysis. The method was validated for the analysis of apples, berries, green tea and red wine and represents a valuable tool for food quality evaluation and breeding studies

Recurrent Hypoglycemia Exacerbates Cerebral Ischemic Damage in Diabetic Rats via Enhanced Post-Ischemic Mitochondrial Dysfunction

Diabetes significantly increases the risk of stroke and post-stroke mortality. Recurrent hypoglycemia (RH) is common among diabetes patients owing to glucose-lowering therapies. Earlier, we showed that RH in a rat model of insulin-dependent diabetes exacerbates cerebral ischemic damage. Impaired mitochondrial function has been implicated as a central player in the development of cerebral ischemic damage. Hypoglycemia is also known to affect mitochondrial functioning. The present study tested the hypothesis that prior exposure of insulin-treated diabetic (ITD) rats to RH exacerbates brain damage via enhanced post-ischemic mitochondrial dysfunction. In a rat model of streptozotocin-induced diabetes, we evaluated post-ischemic mitochondrial function in RH-exposed ITD rats. Rats were exposed to five episodes of moderate hypoglycemia prior to the induction of cerebral ischemia. We also evaluated the impact of RH, both alone and in combination with cerebral ischemia, on cognitive function using the Barnes circular platform maze test. We observed that RH exposure to ITD rats leads to increased cerebral ischemic damage and decreased mitochondrial complex I activity. Exposure of ITD rats to RH impaired spatial learning and memory. Our results demonstrate that RH exposure to ITD rats potentially increases post-ischemic damage via enhanced post-ischemic mitochondrial dysfunction