111 research outputs found
Acute effects of nitrate-rich beetroot juice on blood pressure, hemostasis and vascular inflammation markers in healthy older adults: A randomized, placebo-controlled crossover study
Aging is associated with a vasoconstrictive, pro-coagulant, and pro-inflammatory profile of arteries and a decline in the bioavailability of the endothelium-derived molecule nitric oxide. Dietary nitrate elicits vasodilatory, anti-coagulant and anti-inflammatory effects in younger individuals, but little is known about whether these benefits are evident in older adults. We investigated the effects of 140 mL of nitrate-rich (HI-NI; containing 12.9 mmol nitrate) versus nitrate-depleted beetroot juice (LO-NI; containing ≤0.04 mmol nitrate) on blood pressure, blood coagulation, vascular inflammation markers, plasma nitrate and nitrite before, and 3 h and 6 h after ingestion in healthy older adults (five males, seven females, mean age: 64 years, age range: 57–71 years) in a randomized, placebo-controlled, crossover study. Plasma nitrate and nitrite increased 3 and 6 h after HI-NI ingestion (p < 0.05). Systolic, diastolic and mean arterial blood pressure decreased 3 h relative to baseline after HI-NI ingestion only (p < 0.05). The number of blood monocyte-platelet aggregates decreased 3 h after HI-NI intake (p < 0.05), indicating reduced platelet activation. The number of blood CD11b-expressing granulocytes decreased 3 h following HI-NI beetroot juice intake (p < 0.05), suggesting a shift toward an anti-adhesive granulocyte phenotype. Numbers of blood CD14++CD16+ intermediate monocyte subtypes slightly increased 6 h after HI-NI beetroot juice ingestion (p < 0.05), but the clinical implications of this response are currently unclear. These findings provide new evidence for the acute effects of nitrate-rich beetroot juice on circulating immune cells and platelets. Further long-term research is warranted to determine if these effects reduce the risk of developing hypertension and vascular inflammation with aging
Targeted mitochondrial therapy using MitoQ shows equivalent renoprotection to angiotensin converting enzyme inhibition but no combined synergy in diabetes.
Mitochondrial dysfunction is a pathological mediator of diabetic kidney disease (DKD). Our objective was to test the mitochondrially targeted agent, MitoQ, alone and in combination with first line therapy for DKD. Intervention therapies (i) vehicle (D); (ii) MitoQ (DMitoQ;0.6 mg/kg/day); (iii) Ramipril (DRam;3 mg/kg/day) or (iv) combination (DCoAd) were administered to male diabetic db/db mice for 12 weeks (n = 11-13/group). Non-diabetic (C) db/m mice were followed concurrently. No therapy altered glycaemic control or body weight. By the study end, both monotherapies improved renal function, decreasing glomerular hyperfiltration and albuminuria. All therapies prevented tubulointerstitial collagen deposition, but glomerular mesangial expansion was unaffected. Renal cortical concentrations of ATP, ADP, AMP, cAMP, creatinine phosphate and ATP:AMP ratio were increased by diabetes and mostly decreased with therapy. A higher creatine phosphate:ATP ratio in diabetic kidney cortices, suggested a decrease in ATP consumption. Diabetes elevated glucose 6-phosphate, fructose 6-phosphate and oxidised (NAD+ and NADP+) and reduced (NADH) nicotinamide dinucleotides, which therapy decreased generally. Diabetes increased mitochondrial oxygen consumption (OCR) at complex II-IV. MitoQ further increased OCR but decreased ATP, suggesting mitochondrial uncoupling as its mechanism of action. MitoQ showed renoprotection equivalent to ramipril but no synergistic benefits of combining these agents were shown
Nitrate-responsive oral microbiome modulates nitric oxide homeostasis and blood pressure in humans
© 2018 The Author(s) Imbalances in the oral microbial community have been associated with reduced cardiovascular and metabolic health. A possible mechanism linking the oral microbiota to health is the nitrate (NO3-)-nitrite (NO2-)-nitric oxide (NO) pathway, which relies on oral bacteria to reduce NO3- to NO2-. NO (generated from both NO2- and L-arginine) regulates vascular endothelial function and therefore blood pressure (BP). By sequencing bacterial 16S rRNA genes we examined the relationships between the oral microbiome and physiological indices of NO bioavailability and possible changes in these variables following 10 days of NO3- (12 mmol/d) and placebo supplementation in young (18–22 yrs) and old (70–79 yrs) normotensive humans (n = 18). NO3- supplementation altered the salivary microbiome compared to placebo by increasing the relative abundance of Proteobacteria (+225%) and decreasing the relative abundance of Bacteroidetes (−46%; P < 0.05). After NO3-supplementation the relative abundances of Rothia (+127%) and Neisseria (+351%) were greater, and Prevotella (−60%) and Veillonella (−65%) were lower than in the placebo condition (all P < 0.05). NO3- supplementation increased plasma concentration of NO2- and reduced systemic blood pressure in old (70–79 yrs), but not young (18–22 yrs), participants. High abundances of Rothia and Neisseria and low abundances of Prevotella and Veillonella were correlated with greater increases in plasma [NO2-] in response to NO3- supplementation. The current findings indicate that the oral microbiome is malleable to change with increased dietary intake of inorganic NO3-, and that diet-induced changes in the oral microbial community are related to indices of NO homeostasis and vascular health in vivo
...on ISIS declaration in Mindanao by four militant groups
Dr Mark Briskey, a senior lecturer at Curtin University and expert in counter-terrorism, believes that there is a high likelihood of coordinated attacks in 2016, and the Philippines is included in the list
Bangladesh cricket tour: WA expert says terror ‘chatter’ behind cancellation
A Perth international relations expert who spent three years working with intelligence, security and police in Bangladesh said an increased level of terrorist "chatter" was behind the cancellation of the Australian cricket tour..
Lone wolf massacres are on the rise, experts warn
The number of people killed in lone wolf massacres is increasing, as is the number of incidents, in a violent trend that has national security experts worried..
Curcumin improves delayed onset muscle soreness and postexercise lactate accumulation
The efficacy of curcumin supplementation is traditionally limited due to its poor bioavailability. Despite this, curcumin has previously been shown to improve biomarkers of muscle damage. The addition of a novel drug delivery system that improves bioavailability could improve exercise recovery. The purpose of this randomized double-blind placebo-controlled study was to assess the effect of curcumin (combined with LipiSperse) when consumed as a drink on exercise recovery in recreationally trained healthy males aged 18–35 yrs. The study included 28 young healthy males with strength training experience. The participants undertook lower limb resistance exercise to exhaustion. Fourteen participants received curcumin dispersed in water pre and postexercise and 14 received a matched placebo drink. Pain (visual analogue scale), thigh circumference (TC), lactate, creatine kinase, lactate dehydrogenase, high sensitivity C-reactive protein, myoglobin, interleukin-6, interleukin-10, and tumor necrosis factor-alpha were assessed pre, postexercise and 1, 2, 3, 24, 48, and 72 h postexercise. There was less appearance of postexercise capillary lactate in the curcumin group compared to placebo (7.4 vs 8.8 mmol/L). The placebo group rated overall muscle pain as higher compared to the curcumin group at 48- and 72-h postexercise. TC was reduced in the curcumin group compared to the placebo group at 24- and 48-h postexercise. The results suggest curcumin may facilitate a quicker return to exercise training and/or allow a higher training intensity than a placebo by reducing postexercise pain, modulating inflammatory pathways and reducing lactate accumulation in an exercising population
Effect of Excitement, Fasting, and Sucrose Feeding on Porcine Muscle Phosphorylase and Post-Mortem Glycolysis b
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