Aim: To enhance the bioavailability and brain uptake of probucol and examine whether it attenuates neuroinflammation and neurodegeneration by utilizing a sodium alginate nanoencapsulation technique. Materials & methods: Wild-type mice were given either low-fat standard chow, high-fat (HF) diet to induce neuroinflammation and neurodegeneration, HF diet supplemented with nanocapsuled probucol at a concentration of 0.1% (w/w), HF diet supplemented with noncapsulated probucol at the same concentration of 0.1%, or HF diet supplemented with noncapsulated probucol at higher concentration (1%) for 24 weeks. Results & conclusion: The nanoencapsulation increased the plasma and brain concentration of probucol significantly compared with the mice that was given the same dosage of probucol without capsulation, and significantly suppressed the neuroinflammation and neurodegeneration.

Energy drinks containing significant quantities of caffeine, taurine and sugar are increasingly consumed, particularly by adolescents and young adults. The putative effects of chronic ingestion of either standard energy drink, MotherTM (ED), or its sugar-free formulation (sfED) on metabolic syndrome were determined in wild-type C57BL/6J mice, in comparison to a soft drink, Coca-Cola (SD), a Western-styled diet enriched in saturated fatty acids (SFA), and a combination of SFA + ED. Following 13 weeks of intervention, mice treated with ED were hyperglycaemic and hypertriglyceridaemic, indicating higher triglyceride glucose index, which was similar to the mice maintained on SD. Surprisingly, the mice maintained on sfED also showed signs of insulin resistance with hyperglycaemia, hypertriglyceridaemia, and greater triglyceride glucose index, comparable to the ED group mice. In addition, the ED mice had greater adiposity primarily due to the increase in white adipose tissue, although the body weight was comparable to the control mice receiving only water. The mice maintained on SFA diet exhibited significantly greater weight gain, body fat, cholesterol and insulin, whilst blood glucose and triglyceride concentrations remained comparable to the control mice. Collectively, these data suggest that the consumption of both standard and sugar-free forms of energy drinks induces metabolic syndrome, particularly insulin resistance.

Ingestion of Western-diets enriched in long chain saturated fatty acids (LCSFA) are associated with increased risk of blood-brain barrier (BBB) dysfunction and neurovascular inflammation. Potential mechanisms include vascular insult as a consequence of metabolic aberrations, or changes in capillary permeability resulting in brain parenchymal extravasation of pro-inflammatory molecules. Bovine dairy milk (BDM) is potentially a significant source of dietary LCSFA, however, BDM contains an array of bioactive molecules purported to have vascular anti-inflammatory properties. This study investigated the effects of full cream (4% total fat) and delipidated (skim) BDM on BBB integrity and neuroinflammation in wild-type mice. Mice consuming substantial amounts of full cream or skim BDM with LCSFA-enriched chow were dyslipidemic compared to control mice provided with standard chow and water. However, there was no evidence of BBB dysfunction or neuroinflammation indicated by parenchymal abundance of immunoglobulin G and microglial recruitment, respectively. Positive control mice maintained on an LCSFA-enriched diet derived from cocoa-butter and water, had marked BBB dysfunction, however, co-provision of both full cream and skim milk solutions effectively attenuated LCSFA-induced BBB dysfunction. In mice provided with low-fat chow and full cream BDM drinking solutions, there were substantial favorable changes in the concentration of plasma anti-inflammatory cytokines. This study suggests that consumption of BDM may confer potent vascular benefits through the neuroprotective properties exuded by the milk-fat globule membrane moiety of BDM.

Objective: Studies report that acute consumption of energy drinks transiently increases blood pressure (BP). However, few studies report the effect of chronic energy drink consumption on BP. In this study, we investigated the effects of long-term energy drink ingestion on BP in C57BL/6J normotensive wild-type mice. Research Methods and Procedures: Groups of mice were randomized to no treatment (water) (Control group), or to Mother ™ provided as a decarbonated 30% (v/v) drinking solution (Energy Drink group), sugar-free Mother ™ at 30% (Sugar-free group), Coca Cola ™ at 30% (Coke group) for a total intervention period of 13 weeks. Results: After 13 weeks of intervention, the control mice showed a modest increase in systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) by 7.1 ± 8.8, 5.8 ± 9.4, and 6.3 ± 9.1 mmHg, respectively. However, the Energy Drink significantly decreased the DBP and MAP by 18.8 ± 9.9 and 15.3 ± 9.8 mmHg, respectively. Similarly, Sugar-free group mice showed significant decrease of the SBP, DBP, and MAP by 10.85 ± 5.6, 18.7 ± 6.7, and 15.6 ± 6.1 mmHg, respectively. The SBP, DBP, and MAP in Coke mice showed no significant changes. The estimated cumulative intake of caffeine, taurine, and vitamin B3 and B5 was significantly higher in the mice of Energy Drink and Sugar-free groups compared to the Control and Coke mice. Conclusion: Collectively, the data suggest that the long-term chronic consumption of energy drinks may significantly lower the BP in normotensive mice through the actions of caffeine, taurine, and/or B-vitamins. The study findings do not support consideration of energy drinks for BP management, but rather demonstrate no long-term amplification of BP in normotensive preclinical models.

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