ORCID Profile
0000-0001-6337-0381
Current Organisation
University of Southampton
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Publisher: Springer Science and Business Media LLC
Date: 07-03-2018
DOI: 10.1007/S00421-018-3835-X
Abstract: The present study investigated different doses of ultraviolet-A (UV-A) light on plasma nitric oxide metabolites and cardiorespiratory variables. Ten healthy male participants completed three experimental conditions, 7 days apart. Participants were exposed to no light (CON) 10 J cm 2 (15 min) of UV-A light (UVA10) and 20 J cm 2 (30 min) of UV-A light (UVA20) in a randomized order. Plasma nitrite [NO 2 − ] and nitrate [NO 3 − ] concentrations, blood pressure (BP), and heart rate (HR) were recorded before, immediately after exposure and 30 min post-exposure. Whole body oxygen utilization ( $${{\\dot{V}}}{\\rm O}_{2}$$ V ˙ O 2 ), resting metabolic rate (RMR) and skin temperature were recorded continuously. None of the measured parameters changed significantly during CON (all P 0.05). $${{\\dot{V}}}{\\rm O}_{2}$$ V ˙ O 2 and RMR were significantly reduced immediately after UVA10 ( P 0.05) despite no change in plasma [NO 2 − ] ( P 0.05). Immediately after exposure to UVA20, plasma [NO 2 − ] was higher ( P = 0.014) and $${{\\dot{V}}}{\\rm O}_{2}$$ V ˙ O 2 and RMR tended to be lower compared to baseline ( P = 0.06). There were no differences in [NO 2 − ] or $${{\\dot{V}}}{\\rm O}_{2}$$ V ˙ O 2 at the 30 min time point in any condition. UV-A exposure did not alter systolic BP, diastolic BP or MAP (all P 0.05). UV-A light did not alter plasma [NO 3 − ] at any time point (all P 0.05). This study demonstrates that a UV-A dose of 20 J cm 2 is necessary to increase plasma [NO 2 − ] although a smaller dose is capable of reducing $${{\\dot{V}}}{\\rm O}_{2}$$ V ˙ O 2 and RMR at rest. Exposure to UV-A did not significantly reduce BP in this cohort of healthy adults. These data suggest that exposure to sunlight has a meaningful acute impact on metabolic function.
Publisher: Public Library of Science (PLoS)
Date: 14-04-2014
Publisher: Springer Science and Business Media LLC
Date: 11-11-2019
DOI: 10.1007/S00125-019-05022-5
Abstract: Exposure to sunlight has the potential to suppress metabolic dysfunction and obesity. We previously demonstrated that regular exposure to low-doses of ultraviolet radiation (UVR) reduced weight gain and signs of diabetes in male mice fed a high-fat diet, in part via release of nitric oxide from skin. Here, we explore further mechanistic pathways through which low-dose UVR exerts these beneficial effects. We fed mice with a luciferase-tagged Ucp1 gene (which encodes uncoupling protein-1 [UCP-1]), referred to here as the Ucp1 luciferase transgenic mouse ('Thermomouse') a high-fat diet and examined the effects of repeated exposure to low-dose UVR on weight gain and development of metabolic dysfunction as well as UCP-1-dependent thermogenesis in interscapular brown adipose tissue (iBAT). Repeated exposure to low-dose UVR suppressed the development of glucose intolerance and hepatic lipid accumulation via dermal release of nitric oxide while also reducing circulating IL-6 (compared with mice fed a high-fat diet only). Dietary nitrate supplementation did not mimic the effects of low-dose UVR. A single low dose of UVR increased UCP-1 expression (by more than twofold) in iBAT of mice fed a low-fat diet, 24 h after exposure. However, in mice fed a high-fat diet, there was no effect of UVR on UCP-1 expression in iBAT (compared with mock-treated mice) when measured at regular intervals over 12 weeks. More extensive circadian studies did not identify any substantial shifts in UCP-1 expression in mice exposed to low-dose UVR, although skin temperature at the interscapular site was reduced in UVR-exposed mice. The appearance of cells with a white adipocyte phenotype ('whitening') in iBAT induced by consuming the high-fat diet was suppressed by exposure to low-dose UVR in a nitric oxide-dependent fashion. Significant shifts in the expression of important core gene regulators of BAT function (Dio2, increased more than twofold), fatty acid transport (increased Fatp2 [also known as Slc27a2]), lipolysis (decreased Atgl [also known as Pnpla2]), lipogenesis (decreased Fasn) and inflammation (decreased Tnf), and proportions of macrophages (increased twofold) were observed in iBAT of mice exposed to low-dose UVR. These effects were independent of nitric oxide released from skin. Our results suggest that non-burning (low-dose) UVR suppresses the BAT 'whitening', steatotic and pro-diabetic effects of consuming a high-fat diet through skin release of nitric oxide, with some metabolic and immune pathways in iBAT regulated by UVR independently of nitric oxide.
Publisher: Elsevier BV
Date: 04-2017
DOI: 10.1016/J.NIOX.2016.12.006
Abstract: Dietary supplementation with inorganic nitrate (NO
Publisher: ACM
Date: 25-07-2019
Publisher: Canadian Urological Association Journal
Date: 20-11-2018
DOI: 10.5489/CUAJ.5658
Abstract: Introduction: Patients suffering from chronic kidney disease (CKD) experience a number of associated comorbidities, including anemia. Relative deficiency in renal erythropoietin (EPO) production is thought to be a primary cause of anemia. Interestingly, CKD patients display low levels of hydrogen sulfide (H2S), an endogenously derived renal oxygen sensor. Previous in vitro experiments have revealed that H2S-deficient renal cell lines produce less EPO than wild-type renal cell lines during hypoxia.Methods: We postulated that H2S might be a primary mediator of EPO synthesis during hypoxia, which was tested using an in vivo murine model of whole-body hypoxia and in clinical s les obtained from CKD patients.Results: Following a 72-hour period of hypoxia (11% O2), partial H2S knockout mice (lacking the H2S biosynthetic enzyme cystathionine γ-lyase [CSE]) displayed lower levels of hemoglobin, EPO and cystathionine-β-synthase (CBS) (another H2S biosynthetic enzyme) compared to wild-type mice, all of which was rescued by exogenous H2S supplementation. We also found that anemic CKD patients requiring exogenous EPO exhibited lower urinary thiosulfate levels compared to non-anemic CKD patients of similar CKD classification.Conclusions: Together, our results confirm an interplay between the actions of H2S during hypoxia and EPO production.
Publisher: Wiley
Date: 16-05-2013
DOI: 10.1111/BPH.12152
Publisher: Elsevier BV
Date: 07-2019
DOI: 10.1016/J.JSAMS.2019.01.011
Abstract: Dietary nitrate (NO Double-blind randomized crossover trial. Ten competitive male cyclists (age 34±6years, body mass 78.9±4.9kg, V⋅O Plasma [NO Pre-exercise IPC did not improve sub-maximal exercise or performance measures, either alone or in combination with dietary NO
Publisher: American Diabetes Association
Date: 27-12-2017
DOI: 10.2337/DB16-0843
Abstract: Exercise is an effective intervention for the prevention and treatment of type 2 diabetes. Skeletal muscle combines multiple signals that contribute to the beneficial effects of exercise on cardiometabolic health. Inorganic nitrate increases exercise efficiency, tolerance, and performance. The transcriptional regulator peroxisome proliferator–activated receptor γ coactivator 1α (PGC1α) coordinates the exercise-stimulated skeletal muscle fiber-type switch from glycolytic fast-twitch (type IIb) to oxidative slow-twitch (type I) and intermediate (type IIa) fibers, an effect reversed in insulin resistance and diabetes. We found that nitrate induces PGC1α expression and a switch toward type I and IIa fibers in rat muscle and myotubes in vitro. Nitrate induces the release of exercise/PGC1α-dependent myokine FNDC5/irisin and β-aminoisobutyric acid from myotubes and muscle in rats and humans. Both exercise and nitrate stimulated PGC1α-mediated γ-aminobutyric acid (GABA) secretion from muscle. Circulating GABA concentrations were increased in exercising mice and nitrate-treated rats and humans thus, GABA may function as an exercise/PGC1α-mediated myokine-like small molecule. Moreover, nitrate increased circulating growth hormone levels in humans and rodents. Nitrate induces physiological responses that mimic exercise training and may underlie the beneficial effects of this metabolite on exercise and cardiometabolic health.
Publisher: Elsevier BV
Date: 09-2017
Publisher: Elsevier BV
Date: 10-2017
Location: United Kingdom of Great Britain and Northern Ireland
Location: United States of America
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Bernadette Fernandez.