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    Osmotic stress in banana is relieved by exogenous nitric oxide
    (PeerJ, Inc, 2021) Mohd Amnan MA; Pua T-L; Lau S-E; Tan BC; Yamaguchi H; Hitachi K; Tsuchida K; Komatsu S; Okpala C
    Drought is one of the severe environmental stresses threatening agriculture around the globe. Nitric oxide plays diverse roles in plant growth and defensive responses. Despite a few studies supporting the role of nitric oxide in plants under drought responses, little is known about its pivotal molecular amendment in the regulation of stress signaling. In this study, a label-free nano-liquid chromatography-mass spectrometry approach was used to determine the effects of sodium nitroprusside (SNP) on polyethylene glycol (PEG)-induced osmotic stress in banana roots. Plant treatment with SNP improved plant growth and reduced the percentage of yellow leaves. A total of 30 and 90 proteins were differentially identified in PEG+SNP against PEG and PEG+SNP against the control, respectively. The majority of proteins differing between them were related to carbohydrate and energy metabolisms. Antioxidant enzyme activities, such as superoxide dismutase and ascorbate peroxidase, decreased in SNP-treated banana roots compared to PEG-treated banana. These results suggest that the nitric oxide-induced osmotic stress tolerance could be associated with improved carbohydrate and energy metabolism capability in higher plants.
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    Effect of beetroot pomace consumption on acute blood pressure and postprandial blood glucose responses on healthy adults : a thesis presented in the partial fulfilment of the requirements for the degree of Master of Science in Nutrition and Dietetics, Massey University, Albany, New Zealand
    (Massey University, 2023) Gorbani, Elnaz
    Background: Nitrate-rich beetroot juice (BRJ) supplementation has been shown to improve blood pressure (BP) levels in younger and older adults via increased nitric oxide (NO) production leading to dilation of blood vessels. Similarly, to some extent a reduction of blood glucose (BG) levels through several different mechanisms. However, limited research exists on the by-product of beetroot juice production, beetroot pomace (BRPOM), and its role in controlling BP and BG levels. Objective: To investigate and compare the changes in BP and BG levels in a 3 h period following the ingestion of BRPOM, BRJ and placebo as part of an oral glucose tolerance test (OGTT). Methods: Following an overnight fast, twelve healthy adults consumed either BRPOM (600 mg nitrate, 10 g fibre, 75 g carbohydrate), BRJ (600 mg nitrate, <1 g fibre, 75 g carbohydrate), or placebo (0 mg nitrate, <1 g fibre, 75 g carbohydrate) 15 minutes prior to the OGTT, separated by 1-week washout periods, in a single-blind, crossover design, pilot study. Blood pressure and BG levels were measured at baseline, then every 15 minutes for BG and every hour for BP during a 3 h OGTT. Results: No significant changes in SBP for BRJ (-2.3 ± 5.56 mmHg, p = 0.174), BRPOM (-3 ± 13.4 mmHg, p = 0.456), or PLA (5.2 ± 11.3 mmHg, p = 0.142) treatment group after 3 h. However, there was a trend towards significance in the differences between the three groups (p = 0.075, η²ₚ = 0.404). Clinically meaningful reductions in SBP were observed for BRJ (-2.3 ± 5.56 mmHg) and BRPOM (-3 ± 13.4 mmHg). There were no differences (p = 0.739, η²ₚ = 0.059) in mean glucose incremental area under the curve (iAUC) between BRJ, BRPOM and PLA (232.8 ± 61.9, 242 ± 54.7 and 252.4 ± 60.6 mmol/L/min, respectively). There were no differences between BRJ, BRPOM and PLA in time to peak (p = 0.269, η²ₚ = 0.313), peak glucose levels (p = 0.241, η²ₚ = 0.247), 2 h glucose levels (p = 0.565, η²ₚ = 0.150), 3 h glucose levels (p = 0.395, η²ₚ = 0.233) and percentage increment of postprandial BG (p = 0.783, η²ₚ = 0.048). Conclusion: This pilot study with a small sample size showed a large effect size and clinically meaningful attenuations for acute SBP changes following the consumption of beetroot pomace. Further investigations would be needed to explore the applicability of these findings to hypertensive individuals. However, its impact on acute BG levels remains non-significant, possibly influenced by the small sample size and participants’ baseline normoglycaemic levels. Further research is needed to explore potential effects in a hyperglycaemic population.
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    Endothelial function and insulin sensitivity during acute non-esterified fatty acid elevation: Effects of fat composition and gender
    (Elsevier, 14/03/2015) Newens KJ; Thompson AK; Jackson KG; Williams CM
    Background and aims We have reported that adverse effects on flow-mediated dilation of an acute elevation of non-esterified fatty acids rich in saturated fat (SFA) are reversed following addition of long-chain (LC) n-3 polyunsaturated fatty acids (PUFA), and hypothesised that these effects may be mediated through alterations in insulin signalling pathways. In a subgroup, we explored the effects of raised NEFA enriched with SFA, with or without LC n-3 PUFA, on whole body insulin sensitivity (SI) and responsiveness of the endothelium to insulin infusion. Methods and results Thirty adults (mean age 27.8 y, BMI 23.2 kg/m2) consumed oral fat loads on separate occasions with continuous heparin infusion to elevate NEFA between 60 and 390 min. For the final 150 min, a hyperinsulinaemic-euglycaemic clamp was performed, whilst FMD and circulating markers of endothelial function were measured at baseline, pre-clamp (240 min) and post-clamp (390 min). NEFA elevation during the SFA-rich drinks was associated with impaired FMD (P = 0.027) whilst SFA + LC n-3 PUFA improved FMD at 240 min (P = 0.003). In males, insulin infusion attenuated the increase in FMD with SFA + LC n-3 PUFA (P = 0.049), with SI 10% greater with SFA + LC n-3 PUFA than SFA (P = 0.041). Conclusion This study provides evidence that NEFA composition during acute elevation influences both FMD and SI, with some indication of a difference by gender. However our findings are not consistent with the hypothesis that the effects of fatty acids on endothelial function and SI operate through a common pathway. This trial was registered at clinical trials.gov as NCT01351324 on 6th May 2011.