Spirulina extract improves age-induced vascular dysfunction

Vascular dysfunction is considered a hallmark of ageing that has been associated with altered vasomotor responses, in which nitric oxide (NO) and reactive oxygen species participate. The consumption of Spirulina extracts, with antioxidant properties, increased recently. Objective: This study investigates the effect of Spirulina aqueous extract (SAE) on the vascular function of the aorta from aged rats. Materials and methods: Aortic segments from aged male Sprague-Dawley rats (20–22 months old) were exposed to SAE (0.1% w/v, for 3 h) to analyse: (i) the vasodilator response induced by acetylcholine (ACh), by the NO donor sodium nitroprusside (SNP), by the carbon monoxide releasing molecule (CORM) and by the KATP channel opener, cromakalim (CK); (ii) the vasoconstrictor response induced by KCl and noradrenaline (NA); (iii) the production of NO and superoxide anion, and (iv) the expression of the p-eNOS and HO-1 proteins. Results: Incubation with SAE increased the expression of p-eNOS (1.6-fold) and HO-1 (2.0-fold), enhanced NO release (1.4-fold in basal and 1.9-fold in ACh-stimulated conditions) while decreased the production of superoxide (0.7-fold). SAE also increased the sensitivity (measured as pEC50) to ACh (control: −7.06 ± 0.11; SAE: −8.16 ± 0.21), SNP (control: −7.96 ± 0.16; SAE: −9.11 ± 0.14) and CK (control: −7.05 ± 0.39; SAE: −8.29 ± 0.53), and potentiated the response to KCl (1.3-fold) and to NA (1.7-fold). Conclusion: The antioxidant properties of SAE improved the vasomotor responses of aorta from aged rats. These results may support the use of Spirulina as a protection against vascular dysfunctionThis study was supported by grants from Comunidad de Madrid(S2013/ABI-2783,‘INSPIRA1-CM’) and Fondo Europeo de Desarrollo Regional to C. O. and M. F., the Spanish Ministerio deCiencia e Innovaci on (CTQ2017-86170-R) to C. O. and by theFondo de Investigaciones Sanitarias del Instituto de Salud Carlos III(PI19/01282) to M.

Eplerenone attenuated cardiac steatosis, apoptosis and diastolic dysfunction in experimental type-II diabetes

Cardiac steatosis and apoptosis are key processes in diabetic cardiomyopathy, but the underlying mechanisms have not been elucidated, leading to a lack of effective therapy. The mineralocorticoid receptor blocker, eplerenone, has demonstrated anti-fibrotic actions in the diabetic heart. However, its effects on the fatty-acid accumulation and apoptotic responses have not been revealed. Methods: Non-hypertensive Zucker Diabetic Fatty (ZDF) rats received eplerenone (25 mg/kg) or vehicle. Zucker Lean (ZL) rats were used as control (n = 10, each group). After 16 weeks, cardiac structure and function was examined, and plasma and hearts were isolated for biochemical and histological approaches. Cultured cardiomyocytes were used for in vitro assays to determine the direct effects of eplerenone on high fatty acid and high glucose exposed cells. Results: In contrast to ZL, ZDF rats exhibited hyperglycemia, hyperlipidemia, insulin-resistance, cardiac steatosis and diastolic dysfunction. The ZDF myocardium also showed increased mitochondrial oxidation and apoptosis. Importantly, eplerenone mitigated these events without altering hyperglycemia. In cultured cardiomyocytes, high-concentrations of palmitate stimulated the fatty-acid uptake (in detriment of glucose assimilation), accumulation of lipid metabolites, mitochondrial dysfunction, and apoptosis. Interestingly, fatty-acid uptake, ceramides formation and apoptosis were also significantly ameliorated by eplerenone. Conclusions: By blocking mineralocorticoid receptors, eplerenone may attenuate cardiac steatosis and apoptosis, and subsequent remodelling and diastolic dysfunction in obese/type-II diabetic ratsThis work was supported by national grants from Ministerio de Educación y Ciencia (SAF2009-08367), Comunidad de Madrid (CCG10-UAM/BIO-5289), FISS (PI10/00072), and a grant from by Pfizer (NY, USA), Spanish Ministry of Economy and Competitiveness (MINECO) CTQ2011-23562. These grants were used to provide consumables and animals required. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. AF received funding from the European Union Seventh Framework Programme [FP7/2007-2013] under grant agreement nº 26486

Chronic Exercise Improves Mitochondrial Function and Insulin Sensitivity in Brown Adipose Tissue

The aim of the present work was to study the consequences of chronic exercise training on factors involved in the regulation of mitochondrial remodeling and biogenesis, as well as the ability to produce energy and improve insulin sensitivity and glucose uptake in rat brown adipose tissue (BAT). Male Wistar rats were divided into two groups: (1) control group (C; n = 10) and (2) exercise-trained rats (ET; n = 10) for 8 weeks on a motor treadmill (five times per week for 50 min). Exercise training reduced body weight, plasma insulin, and oxidized LDL concentrations. Protein expression of ATP-independent metalloprotease (OMA1), short optic atrophy 1 (S-OPA1), and dynamin-related protein 1 (DRP1) in BAT increased in trained rats, and long optic atrophy 1 (L-OPA1) and mitofusin 1 (MFN1) expression decreased. BAT expression of nuclear respiratory factor type 1 (NRF1) and mitochondrial transcription factor A (TFAM), the main factors involved in mitochondrial biogenesis, was higher in trained rats compared to controls. Exercise training increased protein expression of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) and AMP-activated protein kinase (pAMPK/AMPK ratio) in BAT. In addition, training increased carnitine palmitoyltransferase II (CPT II), mitochondrial F1 ATP synthase α-chain, mitochondrial malate dehydrogenase 2 (mMDH) and uncoupling protein (UCP) 1,2,3 expression in BAT. Moreover, exercise increased insulin receptor (IR) ratio (IRA/IRB ratio), IRA-insulin-like growth factor 1 receptor (IGF-1R) hybrids and p42/44 activation, and decreased IGF-1R expression and IR substrate 1 (p-IRS-1) (S307) indicating higher insulin sensitivity and favoring glucose uptake in BAT in response to chronic exercise training. In summary, the present study indicates that chronic exercise is able to improve the energetic profile of BAT in terms of increased mitochondrial function and insulin sensitivity

Evolution of hake mislabeling niches in commercial markets

We gratefully acknowledge the Project FUO-EM-181-11 in collaboration with The Center for Public Integrity, Washington, USA, CPI, and the Principado de Asturias, Spain (Research Grant GRUPIN14-093) for their financial support. M.M.C. holds a Spanish National Grant (reference AP-2010-5211).Mislabeling of fish species at landing and along the commercial chain has been detected in many countries. In the case of hake trade, identification of different species has been and continues to be a challenge. In this work we have analyzed the evolution of commercial hake mislabeling during the last decade, focusing on the Spanish market, the world's largest one for hake. DNA-based species identification by PCR amplification and sequencing of mitochondrial genes was carried out in 234 commercial samples. The result was compared with the species stated in the product label, and with 147 samples analyzed in previous works. Significant changes were found throughout the decade for the proportion of mislabeled products, with differences between fresh and frozen products and a general decrease in frozen products. Higher mislabeling in unrecognizable versus morphologically recognizable products strongly suggests deliberate fraud. The diversity of substitute species increased significantly in the period studied, even the non-hake ones. Economic losses for the consumer, estimated from the differences in price between the stated species and their substitutes, seemed to decrease in the last years. The results were interpreted in terms of fluctuations in hake prices and annual catch. Since correct identification of fish species is essential to ensure the good management of species and to provide a reliable market to the consumers, implementing different control points from the landings to the selling points is indispensable.Depto. de Genética, Fisiología y MicrobiologíaFac. de Ciencias BiológicasTRUEpu

Proanthocyanidins block aldosterone-dependent up-regulation of cardiac gamma ENaC and Nedd4-2 inactivation via SGK1

Aldosterone plays a central role in the development of cardiac pathological states involving ion transport imbalances, especially sodium transport. We have previously demonstrated a cardioprotective effect of proanthocyanidins in aldosterone-treated rats. Our objective was to investigate for the first time the effect of proanthocyanidins on serum and glucocorticoid-regulated kinase 1 (SGK1), epithelial Na+ channel (γ-ENaC), neuronal precursor cells expressed developmentally down-regulated 4-2 (Nedd4-2) and phosphoNedd4-2 protein expression in the hearts of aldosterone-treated rats. Male Wistar rats received aldosterone (1mg kg-1day-1)+1% NaCl for 3weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5mg kg-1day-1). Hypertension and diastolic dysfunction induced by aldosterone were abolished by treatment with PRO80. Expression of fibrotic, inflammatory and oxidative mediators were increased by aldosterone-salt administration and blunted by PRO80. Antioxidant capacity was improved by PRO80. The up-regulated aldosterone mediator SGK1, ENaC and p-Nedd4-2/total Nedd4-2 ratio were blocked by PRO80. PRO80 blunted aldosterone-mineralocorticoid-mediated up-regulation of ENaC provides new mechanistic insight of the beneficial effect of proanthocyanidins preventing the cardiac alterations induced by aldosterone excess.Programa Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica de España (SAF2011-30396) y al National Health and Medical Research Council (NHMRC) of Australia (1002559)2015-1