Cycling training effects on fat metabolism blood parameters

BACKGROUND: Study the acute and middle term (4 weeks training) effect of cycling training on fat blood hematological parameters, urine, fatigue, and general health in recreational well-trained cyclists. METHODS: Nineteen cyclists underwent five blood sample collections: before and after an incremental maximal ramp test 7 days before day 0 (D-0); before and after 1 hour exhaustion trial test at baseline (D-0); and after 28 days of training (D-28). Age 34.5 years (\ub19.5); weight 74.87 kg (\ub16.6); height 177.3 cm (\ub15.2); BMI 26.3 (\ub14.9); VO2max 53.75 mL/kg/ min (\ub16.01); distance cycled 314.7 km/week (\ub1137.1). RESULTS: Acute effect was strong elevating WBC from 6.27\ub12.34 to 9.01\ub13.63 7103/\ub5L, an increase in LDL and total CHOL, in this respect, existing literature is controversial. No changes in body weight or blood pressure was observed after 1 month of regular training albeit lipid profile significantly improved, as well as GOT. CONCLUSIONS: Effect of a short incremental bout of exercise was to temporary elevated all the blood parameters except MCH and MCHC. A month of intensive training (distance cycled: 314.7\ub1137.1 km/week) significantly improved blood lipids profile with no permanent effect on WBC, blood pressure or body weight, but improved post effort lactate concentration and fatigue perception. Hematuria is confirmed to be a rare occurrence in recreational cyclists. Data can be useful for training monitoring and comparisons with similar groups of athletes, where there is a lack of information in literature and for comparing exercise effects

Nitric oxide can function as either a killer molecule or an antiapoptotic effector in cardiomyocytes

AbstractCaspase enzymes are a family of cysteine proteases that play a central role in apoptosis. Recently, it has been demonstrated that caspases can be S-nitrosylated and inhibited by nitric oxide (NO). The present report shows that in chick embryo heart cells (CEHC), NO donor molecules such as S-nitroso-N-acetylpenicillamine (SNAP), S-nitrosoglutathione, spermine-NO or sodium nitroprusside inhibit caspase activity in both basal and staurosporine-treated cells. However, the inhibitory effect of NO donors on caspase activity is accompanied by a parallel cytotoxic effect, that precludes NO to exert its antiapoptotic capability. N-Acetylcysteine (NAC) at a concentration of 10 mM blocks depletion of cellular glutathione and cell death in SNAP-treated CEHC, but it poorly affects the ability of SNAP to inhibit caspase activity. Consequently, in the presence of NAC, SNAP attenuates not only caspase activity but also cell death of staurosporine-treated CEHC. These data show that changes in the redox environment may inhibit NO-mediated toxicity, without affecting the antiapoptotic capability of NO, mediated by inhibition of caspase enzymes. NO may thus be transformed from a killer molecule into an antiapoptotic agent

Bone mineral density and hormonal status in adolescent athletic girls

The aim of this study was to determine the relationships of bone mineral density (BMD) and content (BMC) with selected fasting hormones in adolescents with different exercise training patterns. The participants were female athletes of weight-loaded (n=23) and weight-supported (n=24) sports, and 33 non-athletic girls aged 13–15 years. BMD (g/cm2) and BMC (g) at the femoral neck (FN) and lumbar spine (LS) were measured. Venous blood samples were drawn to determine the concentration of insulin-like growth factor-1 (IGF-1), IGF binding protein-3 (IGFBP-3), estradiol, visfatin, adiponectin, leptin, insulin, and glucose. After adjusting for age, height, and body mass, the relationships of BMD variables with IGF-1, IGF-1/IGFBP-3 molar ratio, estradiol, and leptin levels remained significant only in the weight-loaded sport group (r=0.41–0.60; p<0.05). Adiponectin was inversely correlated to FN and LS BMD and BMC (r=–0.47–0.62; p<0.05) in weight-supported sport group only, but after adjustments for age, height, and body mass, these associations disappeared. In this study, concentrations of visfatin, a fairly new adipocytokine, were not related to bone parameters in adolescent girls with different training patterns

Assessment of the Effects of Edible Microalgae in a Canine Gut Model

Microalgae are a source of bioactive compounds having recently been studied for their possible application as health-promoting ingredients. The aim of the study was to evaluate in an in vitro canine gut model the effects of four microalgae, Arthrospira platensis (AP), Haematococcus pluvialis (HP), Phaeodactylum tricornutum (PT) and Chlorella vulgaris (CV), on some fecal microbial populations and metabolites. The four microalgae were subjected to an in vitro digestion procedure, and subsequently, the digested biomass underwent colonic in vitro fermentation. After 6 h of incubation, PT increased propionate (+36%) and butyrate (+24%), and decreased total BCFA (-47%), isobutyrate (-52%) and isovalerate (-43%) and C. hiranonis (-0.46 log10 copies/75 ng DNA). After 24 h, PT increased propionate (+21%) and isovalerate (+10%), and decreased the abundance of Turicibacter spp. (7.18 vs. 6.69 and 6.56 log10 copies/75 ng DNA for CTRL vs. PT, respectively); moreover, after 24 h, CV decreased C. coccoides (-1.12 log10 copies/75 ng DNA) and Enterococcus spp. (-0.37 log10 copies/75 ng DNA). In conclusion, the microbial saccharolytic activities and the shift in fecal bacterial composition were less pronounced than expected, based on current literature. This study should be considered as a preliminary assessment, and future investigations are required to better understand the role of microalgae in canine nutrition

Antiapoptotic and Antiautophagic Effects of Eicosapentaenoic Acid in Cardiac Myoblasts Exposed to Palmitic Acid

Apoptosis is a programmed cell death that plays a critical role in cell homeostasis. In particular, apoptosis in cardiomyocytes is involved in several cardiovascular diseases including heart failure. Recently autophagy has emerged as an important modulator of programmed cell death pathway. Recent evidence indicates that saturated fatty acids induce cell death through apoptosis and this effect is specific for palmitate. On the other hand, n-3 polyunsaturated fatty acids (PUFAs) have been implicated in the protection against cardiovascular diseases, cardiac ischemic damage and myocardial dysfunction. In the present study we show that n-3 PUFA eicosapentaenoic acid (EPA) treatment to culture medium of H9c2 rat cardiomyoblasts protects cells against palmitate-induced apoptosis, as well as counteracts palmitate-mediated increase of autophagy. Further investigation is required to establish whether the antiautophagic effect of EPA may be involved in its cytoprotective outcome and to explore the underlying biochemical mechanisms through which palmitate and EPA control the fate of cardiac cells

MiR-494 induces metabolic changes through G6pc targeting and modulates sorafenib response in hepatocellular carcinoma

BackgroundMetabolic reprogramming is a well-known marker of cancer, and it represents an early event during hepatocellular carcinoma (HCC) development. The recent approval of several molecular targeted agents has revolutionized the management of advanced HCC patients. Nevertheless, the lack of circulating biomarkers still affects patient stratification to tailored treatments. In this context, there is an urgent need for biomarkers to aid treatment choice and for novel and more effective therapeutic combinations to avoid the development of drug-resistant phenotypes. This study aims to prove the involvement of miR-494 in metabolic reprogramming of HCC, to identify novel miRNA-based therapeutic combinations and to evaluate miR-494 potential as a circulating biomarker.MethodsBioinformatics analysis identified miR-494 metabolic targets. QPCR analysis of glucose 6-phosphatase catalytic subunit (G6pc) was performed in HCC patients and preclinical models. Functional analysis and metabolic assays assessed G6pc targeting and miR-494 involvement in metabolic changes, mitochondrial dysfunction, and ROS production in HCC cells. Live-imaging analysis evaluated the effects of miR-494/G6pc axis in cell growth of HCC cells under stressful conditions. Circulating miR-494 levels were assayed in sorafenib-treated HCC patients and DEN-HCC rats.ResultsMiR-494 induced the metabolic shift of HCC cells toward a glycolytic phenotype through G6pc targeting and HIF-1A pathway activation. MiR-494/G6pc axis played an active role in metabolic plasticity of cancer cells, leading to glycogen and lipid droplets accumulation that favored cell survival under harsh environmental conditions. High miR-494 serum levels associated with sorafenib resistance in preclinical models and in a preliminary cohort of HCC patients. An enhanced anticancer effect was observed for treatment combinations between antagomiR-494 and sorafenib or 2-deoxy-glucose in HCC cells.ConclusionsMiR-494/G6pc axis is critical for the metabolic rewiring of cancer cells and associates with poor prognosis. MiR-494 deserves attention as a candidate biomarker of likelihood of response to sorafenib to be tested in future validation studies. MiR-494 represents a promising therapeutic target for combination strategies with sorafenib or metabolic interference molecules for the treatment of HCC patients who are ineligible for immunotherapy

Structure-activity relationships of novel substituted naphthalene diimides as anticancer agents

Novel 1,4,5,8-naphthalenetetracarboxylic diimide (NDI) derivatives were synthesized and evaluated for their antiproliferative activity on a wide number of different tumor cell lines. The prototypes of the present series were derivatives 1 and 2 characterized by interesting biological profiles as anticancer agents. The present investigation expands on the study of structure-activity relationships of prototypes 1 and 2, namely, the influence of the different substituents of the phenyl rings on the biological activity. Derivatives 3-22, characterized by a different substituent on the aromatic rings and/or a different chain length varying from two to three carbon units, were synthesized and evaluated for their cytostatic and cytotoxic activities. The most interesting compound was 20, characterized by a linker of three methylene units and a 2,3,4-trimethoxy substituent on the two aromatic rings. It displayed antiproliferative activity in the submicromolar range, especially against some different cell lines, the ability to inhibit Taq polymerase and telomerase, to trigger caspase activation by a possible oxidative mechanism, to downregulate ERK 2 protein and to inhibit ERKs phosphorylation, without acting directly on microtubules and tubuline. Its theoretical recognition against duplex and quadruplex DNA structures have been compared to experimental thermodynamic measurements and by molecular modeling investigation leading to putative binding modes. Taken together these findings contribute to define this compound as potential Multitarget-Directed Ligands interacting simultaneously with different biological targets. \ua9 2012 Elsevier Masson SAS. All rights reserved