Abstracts su componenti di ENDOSILAN

Biol Trace Elem Res. 2013 Apr;152(1):105-12. doi: 10.1007/s12011-012-9593-4. Epub 2013 Jan 11.

Effects of silicon on osteoblast activity and bone mineralization of MC3T3-E1 cells. Kim EJ, Bu SY, Sung MK, Choi MK.

Source

Division of Food Science, Kongju National University, Yesan 340-702, South Korea.

Abstract

Previous studies have reported that dietary silicon (Si) intake is positively associated with bone health including bone mineral density. Although the amount of Si intake is high among trace elements in humans, how dietary Si affects bone formation at the cellular level is not well addressed. The purpose of this study was to investigate the role of Si in osteoblast activity and bone mineralization. MC3T3-E1 was cultured as mature osteoblasts and treated with sodium metasilicate (0, 1, 5, 10, 25, 50, and 100 M) as a source of Si. After 7 days of treatment, 5 and 10 M of sodium metasilicate significantly increased intracellular alkaline phosphatase activity (p < 0.05) when compared to the control. Additionally, all doses of sodium metasilicate (1, 5, 10, 25, 50, and 100 M) increased mineralized nodule formation at 14 days of differentiation as evidenced by increased Alizarin Red S staining. In the analysis of gene expression, 50 M of sodium metasilicate upregulated type I collagen (COL-I) compared to the control group. However, the increase of COL-I gene expression as a result of treatment with 1, 10, 25, and 100 M of sodium metasilicate did not reach statistical significance. mRNA expression of insulin-like growth factor-I and receptor activator of NF-B ligand was not significantly changed at any dose of sodium metasilicate (0, 1, 5, 10, 25, 50, and 100 M). In light of the results, we conclude that Si has a positive effect on bone metabolism by enhancing osteoblast mineralization activity.

Nutr Metab (Lond). 2013 Jan 8;10(1):2. doi: 10.1186/1743-7075-10-2.

Biological and therapeutic effects of ortho-silicic acid and some ortho-silicic acid-releasing compounds: New perspectives for therapy. Jurki LM, Cepanec I, Paveli SK, Paveli K.

Source

Department of Biotechnology, University of Rijeka, Radmile Mateji 2, Rijeka, HR-51000, Croatia. sandrakp@biotech.uniri.hr.

Abstract

Silicon (Si) is the most abundant element present in the Earth's crust besides oxygen. However, the exact biological roles of silicon remain unknown. Moreover, the ortho-silicic acid (H4SiO4), as a major form of bioavailable silicon for both humans and animals, has not been given adequate attention so far. Silicon has already been associated with bone mineralization, collagen synthesis, skin, hair and nails health atherosclerosis, Alzheimer disease, immune system enhancement, and with some other disorders or pharmacological effects. Beside the ortho-silicic acid and its stabilized

formulations such as choline chloride-stabilized ortho-silicic acid and sodium or potassium silicates (e.g. M2SiO3; M= Na,K), the most important sources that release ortho-silicic acid as a bioavailable form of silicon are: colloidal silicic acid (hydrated silica gel), silica gel (amorphous silicon dioxide), and zeolites. Although all these compounds are characterized by substantial water insolubility, they release small, but significant, equilibrium concentration of ortho-silicic acid (H4SiO4) in contact with water and physiological fluids. Even though certain pharmacological effects of these compounds might be attributed to specific structural characteristics that result in profound adsorption and absorption properties, they all exhibit similar pharmacological profiles readily comparable to ortho-silicic acid effects. The most unusual ortho-silicic acid-releasing agents are certain types of zeolites, a class of aluminosilicates with well described ion(cation)-exchange properties. Numerous biological activities of some types of zeolites documented so far might probably be attributable to the ortho-silicic acid-releasing property. In this review, we therefore discuss biological and potential therapeutic effects of ortho-silicic acid and ortho-silicic acid -releasing silicon compounds as its major natural sources.

Osteoporos Int. 2013 Mar;24(3):771-86. doi: 10.1007/s00198-012-2214-4. Epub 2012 Nov 14.

Skeletal effects of nutrients and nutraceuticals, beyond calcium and vitamin D. Nieves JW.

Source

Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, New York, NY 10032, USA. nievesj@helenhayeshosp.org

Abstract

There is a need to understand the role of nutrition, beyond calcium and vitamin D, in the treatment and prevention of osteoporosis in adults. Results regarding soy compounds on bone density and bone turnover are inconclusive perhaps due to differences in dose and composition or in study population characteristics. The skeletal benefit of black cohosh and red clover are unknown. Dehydroepiandrosterone (DHEA) use may benefit elderly individuals with low serum dehydroepiandrosterone-sulfate levels, but even in this group, there are inconsistent benefits to bone density (BMD). Higher fruit and vegetable intakes may relate to higher BMD. The skeletal benefit of flavonoids, carotenoids, omega-3-fatty acids, and vitamins A, C, E and K are limited to observational data or a few clinical trials, in some cases investigating pharmacologic doses. Given limited data, it would be better to get these nutrients from fruits and vegetables. Potassium bicarbonate may improve calcium homeostasis but with little impact on bone loss. High homocysteine may relate to fracture risk, but the skeletal benefit of each B vitamin is unclear. Magnesium supplementation is likely only required in persons with low magnesium levels. Data are very limited for the role of nutritional levels of boron, strontium, silicon and phosphorus in bone health. A nutrient rich diet with adequate fruits and vegetables will generally meet skeletal needs in healthy individuals. For most healthy adults, supplementation with nutrients other than calcium and vitamin D may not be required, except in those with chronic disease and the frail elderly

Am J Clin Nutr. 2005 May;81(5):1232S-1239S.

Osteoporosis: the role of micronutrients. Nieves JW.

Source

Clinical Research and Regional Bone Centers, Helen Hayes Hospital, West Haverstraw, NY, USA.

Abstract

Osteoporosis and low bone mass are currently estimated to be a major public health threat. Adequate nutrition plays a major role in the prevention and treatment of osteoporosis; the micronutrients of greatest importance are calcium and vitamin D. Calcium has been shown to have beneficial effects on bone mass at all ages, although the results are not always consistent. Higher doses than the current US recommendation (600 IU) of vitamin D in the elderly (age > or = 65 y) may actually be required for optimal bone health (800-1000 IU/d). The elderly can clearly benefit from increased vitamin D intakes; however, the potential importance of vitamin D in peak bone mass is just being investigated. Vitamin D has been related to falls, with supplementation reducing the number of falls. There are clear fracture benefits demonstrated in randomized clinical trials of calcium and vitamin D supplementation. The other micronutrient needs for optimizing bone health can be easily met by a healthy diet that is high in fruits and vegetables to ensure adequate intakes for magnesium, potassium, vitamin C, vitamin K, and other potentially important nutrients. Healthcare professionals need to be aware of the importance of adequate calcium and vitamin D intakes (easily monitored by serum 25(OH)D) for optimal bone health, as well as the prevention of falls and fractures. In addition, a healthy diet that includes 5 servings a day of fruits and vegetables should optimize the intake of micronutrients required for bone health.

Adv Exp Med Biol. 2013;775:395-403. doi: 10.1007/978-1-4614-6130-2_30.

Taurine may not alleviate hyperglycemia-mediated endoplasmic reticulum stress in human adipocytes. Kim KS, Ji HI, Yang HI.

Source

East-West Bone & Joint Disease Research Institute, Kyung Hee University Hospital at Gangdong, 149 Sangil-dong, Gangdong-gu, Seoul, 134-727, Korea, labrea46@yahoo.co.kr.

Abstract

In obesity and diabetes, adipocytes show significant endoplasmic reticulum (ER) stress. Hyperglycemia-induced ER stress has not been studied in adipocyte differentiation and adipokine expression. Taurine has been known to protect the cells against ER stress. This study examined the effect of taurine on ER stress-induced adipocyte differentiation and adipokine expression to explain the therapeutic effect of taurine on diabetes and obesity. To do this, human preadipocytes were differentiated into adipocytes, in the presence or absence of taurine, under ER stress conditions. Changes in adipokine expression in adipocytes stimulated with IL-1 were investigated in the presence or absence of taurine. Human preadipocytes were treated with thapsigargin (10 nM) or high glucose concentrations (100 mM) as ER stress inducers during differentiation into adipocytes. Thapsigargin inhibited the differentiation of adipocytes in a dose-dependent manner, but the high glucose concentration treatment did not. Taurine 100 mM treatment did not block the inhibition of differentiation of preadipcytes into adipocytes. Furthermore, the high glucose concentration treatment inhibited the expression of adiponectin and increased the expression of leptin in human adipocytes. However, taurine treatment did not affect the expression of two adipokines. In conclusion, the therapeutic mechanism of taurine in diabetes and obesity does not appear to occur

by alleviating hyperglycemia-mediated ER stress. To clarify the molecular mechanism by which taurine improves diabetic symptoms and obesity in animal models, the protective effect of taurine against hyperglycemia- or overnutrition-mediated ER stress should be further evaluated under various conditions or types of ER stress.

Amino Acids. 2012 Dec 8. [Epub ahead of print]

Potential role of taurine in the prevention of diabetes and metabolic syndrome. Imae M, Asano T, Murakami S.

Source

R&D Laboratories, Self Medication Business, Taisho Pharmaceutical Co. Ltd, 403, Yoshino-cho 1-chome, Kita-ku, Saitama-shi, Saitama, 331-9530, Japan.

Abstract

Metabolic syndrome is characterized by the cluster of a number of metabolic abnormalities in the presence of underlying insulin resistance. The prevalence of metabolic syndrome has steadily increased in all populations worldwide. Taurine (2-aminoethanesulfonic acid) is a sulfur-containing amino acid that is involved in a variety of physiological functions. Clinical and experimental studies show that taurine intake may be beneficial in the prevention of metabolic syndrome including diabetes, obesity, dyslipidemia, and hypertension. This article reviews the effect of taurine on all of the components of metabolic syndrome. In addition, the possible mechanisms by which taurine prevents diabetes and metabolic syndrome are also discussed. Further study is needed to determine the role of taurine in the development of metabolic syndrome in humans, because there is presently limited clinical data available.

Mol Vis. 2012;18:2673-86. Epub 2012 Nov 12.

Review: taurine: a "very essential" amino acid. Ripps H, Shen W.

Source

Departments of Ophthalmology and Visual Science, Anatomy and Cell Biology, Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL 60612, USA. harrripp@uic.edu

Abstract

Taurine is an organic osmolyte involved in cell volume regulation, and provides a substrate for the formation of bile salts. It plays a role in the modulation of intracellular free calcium concentration, and although it is one of the few amino acids not incorporated into proteins, taurine is one of the most abundant amino acids in the brain, retina, muscle tissue, and organs throughout the body. Taurine serves a wide variety of functions in the central nervous system, from development to cytoprotection, and taurine deficiency is associated with cardiomyopathy, renal dysfunction, developmental abnormalities, and severe damage to retinal neurons. All ocular tissues contain taurine, and quantitative analysis of ocular tissue extracts of the rat eye revealed that taurine was the most abundant amino acid in the retina, vitreous, lens, cornea, iris, and ciliary body. In the retina, taurine is critical for photoreceptor development and acts as a cytoprotectant against stress-related

neuronal damage and other pathological conditions. Despite its many functional properties, however, the cellular and biochemical mechanisms mediating the actions of taurine are not fully known. Nevertheless, considering its broad distribution, its many cytoprotective attributes, and its functional significance in cell development, nutrition, and survival, taurine is undoubtedly one of the most essential substances in the body. Interestingly, taurine satisfies many of the criteria considered essential for inclusion in the inventory of neurotransmitters, but evidence of a taurine-specific receptor has yet to be identified in the vertebrate nervous system. In this report, we present a broad overview of the functional properties of taurine, some of the consequences of taurine deficiency, and the results of studies in animal models suggesting that taurine may play a therapeutic role in the management of epilepsy and diabetes.

Adv Exp Med Biol. 2013;775:299-310. doi: 10.1007/978-1-4614-6130-2_25.

Taurine's Effects on the Neuroendocrine Functions of Pancreatic Cells. Cuttitta CM, Guariglia SR, Idrissi AE, L'amoreaux WJ.

Source

Department of Biology, College of Staten Island, Staten Island, NY, 10314, USA, christinacuttitta@gmail.com.

Abstract

Taurine plays significant physiological roles, including those involved in neurotransmission. Taurine is a potent -aminobutyric acid (GABA) agonist and alters cellular events via GABA(A) receptors. Alternately, taurine is transported into cells via the high affinity taurine transporter (TauT), where it may also play a regulatory role. We have previously demonstrated that treatment of Hit-T15 cells with 1 mM taurine for 24 h significantly decreases insulin and GABA levels. We have also demonstrated that chronic in vivo administration of taurine results in an up-regulation of glutamic acid decarboxylase (GAD), the key enzyme in GABA synthesis. Here, we wished to test if administration of 1 mM taurine for 24 h may increase release of another cell neurotransmitter somatostatin (SST) and also directly impact up-regulation of GAD synthesis. Treatment with taurine did not significantly alter levels of SST (p > 0.05) or GAD67 (p > 0.05). This suggests that taurine does not directly affect SST release, nor does it directly affect GAD synthesis. Taken together with our observation that taurine does promote GABA release via large dense-core vesicles, the data suggest that taurine may alter membrane potential, which in turn would affect calcium flux. We show here that 1 mM taurine does not alter intracellular Ca(2+) concentrations from 20 to 80 s post treatment (p > 0.05), but does increase Ca(2+) flux between 80 and 200 s post-treatment (p < 0.005). This suggests that taurine may induce a biphasic response in cells. The initial response of taurine via GABA(A) receptors hyperpolarizes cell and sequesters Ca(2+). Subsequently, taurine may affect Ca(2+) flux in long term via interaction with K(ATP) channels.

Food Funct. 2012 Dec;3(12):1251-64. doi: 10.1039/c2fo30117b.

Mechanism of the protective action of taurine in toxin and drug induced organ pathophysiology and diabetic complications: a review. Das J, Roy A, Sil PC.

Source

Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata-700054, India.

Abstract

Taurine (2-aminoethanesulfonic acid), a conditionally essential amino acid, is found in large concentrations in all mammalian tissues and is particularly abundant in aquatic foods. Taurine exhibits membrane stabilizing, osmoregulatory and cytoprotective effects, antioxidative properties, regulates intracellular Ca(2+) concentration, modulates ion movement and neurotransmitters, reduce the levels of pro-inflammatory cytokines in various organs and controls blood pressure. Recently, emerging evidence from the literature shows the effectiveness of taurine as a protective agent against several environmental toxins and drug-induced multiple organ injuries as the outcome of hepatotoxicity, nephrotoxicity, neurotoxicity, testicular toxicity and cardiotoxicity in several animal models. Besides, taurine is also effective in combating diabetes and its associated complications, including cardiomyopathy, nephropathy, neuropathy, retinopathy and atherosclerosis. These beneficial effects appear to be due to the multiple actions of taurine on cellular functions. This review summarizes the mechanism of the prophylactic role of taurine against several environmental toxins and drug-induced organ pathophysiology and diabetes.

Adv Exp Med Biol. 2013;775:53-68. doi: 10.1007/978-1-4614-6130-2_5.

The modulatory role of taurine in retinal ganglion cells. Jiang Z, Bulley S, Guzzone J, Ripps H, Shen W.

Source

Department of Biomedical Science, Charles E Schmidt College of Medicine, Florida Atlantic University, 777 Glades Road, Boca Raton, FL, 33431, USA, zjiang7@jhmi.edu.

Abstract

Taurine (2-aminoethylsuphonic acid) is present in nearly all animal tissues, and is the most abundant free amino acid in muscle, heart, CNS, and retina. Although it is known to be a major cytoprotectant and essential for normal retinal development, its role in retinal neurotransmission and modulation is not well understood. We investigated the response of taurine in retinal ganglion cells, and its effect on synaptic transmission between ganglion cells and their presynaptic neurons. We find that taurine-elicited currents in ganglion cells could be fully blocked by both strychnine and SR95531, glycine and GABA(A) receptor antagonists, respectively. This suggests that taurine-activated receptors might share the antagonists with GABA and glycine receptors. The effect of taurine at micromolar concentrations can effectively suppress spontaneous vesicle release from the presynaptic neurons, but had limited effects on light-evoked synaptic signals in ganglion cells. We also describe a metabotropic effect of taurine in the suppression of light-evoked response in ganglion cells. Clearly, taurine acts in multiple ways to modulate synaptic signals in retinal output neurons, ganglion cells.

J Food Sci. 2013 Apr 12. doi: 10.1111/1750-3841.12116. [Epub ahead of print]

Coenzyme Q10 Regulates Osteoclast and Osteoblast Differentiation.

Moon HJ, Ko WK, Jung MS, Kim JH, Lee WJ, Park KS, Heo JK, Bang JB, Kwon IK.

Source

Dept. of Maxillofacial Biomedical Engineering and Inst. of Oral Biology, School of Dentistry, Kyung Hee Univ., Seoul 130-701, Republic of Korea.

Abstract

Coenzyme Q10 (CoQ10), a powerful antioxidant, is a key component in mitochondrial bioenergy transfer, generating energy in the form of ATP. Many studies suggest that antioxidants act as inhibitors of osteoclastogenesis and we also have previously demonstrated the inhibitory effect of CoQ10 on osteoclast differentiation. Despite the significance of this effect, the molecular mechanism when CoQ10 is present at high concentrations in bone remodeling still remains to be elucidated. In this study, we investigated the inhibitory effect of CoQ10 on osteoclastogenesis and its impact on osteoblastogenesis at concentrations ranging from 10 to 100 M. We found that nontoxic CoQ10 markedly attenuated the formation of receptor activator of nuclear factor B ligand (RANKL)-induced tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells in both bone-marrow-derived monocytes (BMMs) and RAW 264.7 cells. Osteoclastogenesis with CoQ10 was significantly suppressed the gene expression of NFATc1, TRAP, and osteoclast-associated immunoglobulin-like receptor, which are genetic markers of osteoclast differentiation and scavenged intracellular reactive oxygen species, an osteoclast precursor, in a dose-dependent manner. Furthermore, CoQ10 strongly suppressed H2 O2 -induced IB, p38 signaling pathways for osteoclastogenesis. In bone formation study, CoQ10 acted to enhance the induction of osteoblastogenic biomarkers including alkaline phosphatase, type 1 collagen, bone sialoprotein, osteoblast-specific transcription factor Osterix, and Runt-related transcription factor 2 and, also promoted matrix mineralization by enhancing bone nodule formation in a dose-dependent manner. Together, CoQ10 acts as an inhibitor of RANKL-induced osteoclast differentiation and an enhancer of bone-forming osteoblast differentiation. These findings highlight the potential therapeutic applications of CoQ10 for the treatment of bone disease

Metab Syndr Relat Disord. 2013 Mar 15. [Epub ahead of print]

Coenzyme Q10 Ameliorates the Reduction in GLUT4 Transporter Expression Induced by Simvastatin in 3T3-L1 Adipocytes. Ganesan S, Ito MK.

Source

Department of Pharmacy Practice, College of Pharmacy, Oregon State University/ Oregon Health & Science University , Portland, Oregon.

Abstract

Abstract Background: Statins significantly reduce cardiovascular events in a broad population of patients with hyperlipidemia. However, a small, but significant risk of new-onset diabetes has been reported in patients treated with statins. The mechanism by which statins cause diabetes has not been elucidated and therefore preventive strategies have yet to be defined. Method: Our goal was to study the differing effects of a lipophilic (simvastatin) statin, hydrophilic (pravastatin) statin, and ezetimibe on glucose transporter-4 (GLUT4) protein expression in 3T3-L1 adipocytes. We

hypothesized that the reductions in GLUT4 protein secondary to statin treatment would be prevented when cells were co-incubated with coenzyme Q10 (CoQ10). GLUT4 protein expression was determined using the In-Cell Western technique. Confluent adipocytes were differentiated using a hormonal cocktail for 3 days; followed by treatment with simvastatin, pravastatin, ezetimibe and CoQ10. Cell morphology was observed after treatment using phase-contrast microscopy. Results: Treatment with simvastatin (P

Abstract

Low seminal plasma concentrations of coenzyme Q10 (CoQ10) have been correlated with impaired sperm parameters, but the exact mechanism remains of dominating interest. This randomised, placebo-controlled study examined the effect of CoQ10 on catalase, superoxide dismutase (SOD) and F(2) -isoprostanes in seminal plasma in infertile men and their relation with CoQ10 concentration. Sixty infertile men with idiopathic oligoasthenoteratozoospermia (OAT) were randomised to receive 200 mg d(-1) of CoQ10 or placebo for 3 months. 47 persons of them completed the study. Semen analysis, anthropometric measurements, diet and physical activity assessment were performed for subjects before and after treatment. Independent and paired t-test, chi-square test and ancova were compared outcomes of supplementation between two groups. CoQ10 levels increased from 44.74 36.47 to 68.17 42.41 ng ml(-1) following supplementation in CoQ10 (P < 0.001). CoQ10 group had higher catalase and SOD activity than the placebo group. There was a significant positive correlation between CoQ10 concentration and normal sperm morphology (P = 0.037), catalase (P = 0.041) and SOD (P < 0.001). Significant difference was shown between the mean of changes in seminal plasma 8-isoprostane in two groups (P = 0.003) after supplementation. Three-month supplementation with CoQ10 in OAT infertile men can attenuate oxidative stress in seminal plasma and improve semen parameters and antioxidant enzymes activity.

J Am Coll Cardiol. 2013 Jan 8;61(1):44-53. doi: 10.1016/j.jacc.2012.09.036. Simvastatin effects on skeletal muscle: relation to decreased mitochondrial function and glucose intolerance. Larsen S, Stride N, Hey-Mogensen M, Hansen CN, Bang LE, Bundgaard H, Nielsen LB, Helge JW, Dela F.

Source

Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. stelar@sund.ku.dk

Abstract

OBJECTIVES:

Glucose tolerance and skeletal muscle coenzyme Q(10) (Q(10)) content, mitochondrial density, and mitochondrial oxidative phosphorylation (OXPHOS) capacity were measured in simvastatin-treated patients (n = 10) and in well-matched control subjects (n = 9).

BACKGROUND:

A prevalent side effect of statin therapy is muscle pain, and yet the basic mechanism behind it remains unknown. We hypothesize that a statin-induced reduction in muscle Q(10) may attenuate mitochondrial OXPHOS capacity, which may be an underlying mechanism.

METHODS:

Plasma glucose and insulin concentrations were measured during an oral glucose tolerance test. Mitochondrial OXPHOS capacity was measured in permeabilized muscle fibers by high-resolution respirometry in a cross-sectional design. Mitochondrial content (estimated by citrate synthase [CS]

activity, cardiolipin content, and voltage-dependent anion channel [VDAC] content) as well as Q(10) content was determined.

RESULTS:

Simvastatin-treated patients had an impaired glucose tolerance and displayed a decreased insulin sensitivity index. Regarding mitochondrial studies, Q(10) content was reduced (p = 0.05), whereas mitochondrial content was similar between the groups. OXPHOS capacity was comparable between groups when complex I- and complex II-linked substrates were used alone, but when complex I + II-linked substrates were used (eliciting convergent electron input into the Q intersection [maximal ex vivo OXPHOS capacity]), a decreased (p < 0.01) capacity was observed in the patients compared with the control subjects.

CONCLUSIONS:

These simvastatin-treated patients were glucose intolerant. A decreased Q(10) content was accompanied by a decreased maximal OXPHOS capacity in the simvastatin-treated patients. It is plausible that this finding partly explains the muscle pain and exercise intolerance that many patients experience with their statin treatment.

Eur J Nutr. 2012 Oct;51(7):791-9. Epub 2011 Oct 12.

Coenzyme Q(10) supplementation ameliorates inflammatory signaling and oxidative stress associated with strenuous exercise. Daz-Castro J, Guisado R, Kajarabille N, Garca C, Guisado IM, de Teresa C, Ochoa JJ.

Source

Department of Physiology, University of Granada, Granada, Spain.

Abstract

BACKGROUND:

Exhausting exercise induces muscle damage associated with high production of free radicals and pro-inflammatory mediators.

AIM:

The objective of this study was to determine for the first time and simultaneously whether oral coenzyme Q(10) (CoQ(10)) supplementation can prevent over-expression of inflammatory mediators and oxidative stress associated with strenuous exercise.

METHODS:

The participants were classified in two groups: CoQ(10) group (CG) and placebo group (PG). The physical test consisted in a constant run (50 km) that combined several degrees of high effort (mountain run and ultra-endurance), in permanent climbing.

RESULTS:

Exercise was associated with an increase in TNF-, IL-6, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and isoprostane levels, revealing the degree of inflammation and oxidative stress induced. Oral supplementation of CoQ(10) during exercise was efficient reducing oxidative stress (decreased membrane hydroperoxides, 8-OHdG and isoprostanes generation, increased catalase, and total antioxidant status), which would lead to the maintenance of the cell integrity. Data obtained also indicate that CoQ(10) prevents over-expression of TNF- after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF. Moreover, CoQ(10) supplementation reduced creatinine production.

CONCLUSIONS:

CoQ(10) supplementation before strenuous exercise decreases the oxidative stress and modulates the inflammatory signaling, reducing the subsequent muscle damage.

Nutrition. 2008 Apr;24(4):293-9. doi: 10.1016/j.nut.2007.12.007. Epub 2008 Feb 13. Antifatigue effects of coenzyme Q10 during physical fatigue. Mizuno K, Tanaka M, Nozaki S, Mizuma H, Ataka S, Tahara T, Sugino T, Shirai T, Kajimoto Y, Kuratsune H, Kajimoto O, Watanabe Y.

Source

Department of Physiology, Osaka City University Graduate School of Medicine, Osaka, Japan. mizuno@med.osaka-cu.ac.jp

Erratum in

Nutrition. 2008 Jun;24(6):616.

Abstract

OBJECTIVE:

This study examined the effects of coenzyme Q10 administration on physical fatigue.

METHODS:

In a double-blinded, placebo-controlled, three crossover design, 17 healthy volunteers were randomized to oral coenzyme Q10 (100 or 300 mg/d) or placebo administration for 8 d. As a fatigue-inducing physical task, subjects performed workload trials on a bicycle ergometer at fixed workloads twice for 2 h and then rested for 4 h. During the physical tasks, subjects performed non-workload trials with maximum velocity for 10 s at 30 min (30-min trial) after the start of physical tasks and 30 min before the end of the tasks (210-min trial).

RESULTS:

The change in maximum velocity from the 30- to the 210-min trial in the 300-mg coenzyme Q10-administered group was higher than that in the placebo group. In addition, subjective fatigue sensation measured on a visual analog scale in the 300-mg coenzyme Q10-administered group after

the fatigue-inducing physical task and recovery period was alleviated when compared with that in the placebo group.

CONCLUSION:

Oral administration of coenzyme Q10 improved subjective fatigue sensation and physical performance during fatigue-inducing workload trials and might prevent unfavorable conditions as a result of physical fatigue.

Exp Mol Med. 2012 Nov 30;44(11):665-73. doi: 10.3858/emm.2012.44.11.075.

Taurine ameliorates hyperglycemia and dyslipidemia by reducing insulin resistance and leptin level in Otsuka Long-Evans Tokushima fatty (OLETF) rats with long-term diabetes. Kim KS, Oh da H, Kim JY, Lee BG, You JS, Chang KJ, Chung HJ, Yoo MC, Yang HI, Kang JH, Hwang YC, Ahn KJ, Chung HY, Jeong IK.

Source

East-West Bone and Joint Research Institute, Kyung Hee University Hospital at Gangdong, Korea. labrea46@yahoo.co.kr

Abstract

This study aimed to determine whether taurine supplementation improves metabolic disturbances and diabetic complications in an animal model for type 2 diabetes. We investigated whether taurine has therapeutic effects on glucose metabolism, lipid metabolism, and diabetic complications in Otsuka Long- Evans Tokushima fatty (OLETF) rats with long-term duration of diabetes. Fourteen 50-week-old OLETF rats with chronic diabetes were fed a diet supplemented with taurine (2%) or a non-supplemented control diet for 12 weeks. Taurine reduced blood glucose levels over 12 weeks, and improved OGTT outcomes at 6 weeks after taurine supplementation, in OLETF rats. Taurine significantly reduced insulin resistance but did not improve -cell function or islet mass. After 12 weeks, taurine significantly decreased serum levels of lipids such as triglyceride, cholesterol, high density lipoprotein cholesterol, and low density lipoprotein cholesterol. Taurine significantly reduced serum leptin, but not adiponectin levels. However, taurine had no therapeutic effect on damaged tissues. Taurine ameliorated hyperglycemia and dyslipidemia, at least in part, by improving insulin sensitivity and leptin modulation in OLETF rats with long-term diabetes. Additional study is needed to investigate whether taurine has the same beneficial effects in human diabetic patients.

J Ethnopharmacol. 2003 Oct;88(2-3):161-7.

Antiinflammatory and antiulcer activities of Bambusa arundinacea. Muniappan M, Sundararaj T.

Source

Department of Pharmacology, Sri Ramachandra Medical College and Research Institute (Deemed University), Porur, Chennai 600116, India. muniappan@hkmu.ac.tz

Abstract

The extracts of Bambusa arundinacea have been used in Indian folk medicine to treat various inflammatory conditions. The plant has got antiulcer activity also. It is thought that these two properties in the same extract are very much useful in the treatment of inflammatory conditions. It is well known fact that the most of the available antiinflammatory drugs are ulcerogenic. The antiinflammatory effect of the methanol extract of the leaves of Bambusa arundinacea against carrageenin-induced as well as immunologically induced paw oedema and also its antiulcer activity in albino rats have been studied and found to be significant when compared to the standard drugs. The combination of methanol extract and phenylbutazone (Non-Steroidal Antiinflammatory Agent, NSAIA) has been studied and found to be the most potent antiinflammatory activity experimentally with least toxic (no ulcerogenic) activity. Thus, the combination of herbal product (methanol extract of Bambusa arundinacea) with modern medicine (NSAIAs) will produce the best antiinflammatory drug and will be useful for long-term treatment of chronic inflammatory conditions like rheumatoid arthritis with peptic ulcer, which are common

Nutr Metab (Lond). 2013 Jan 8;10(1):2. doi: 10.1186/1743-7075-10-2.

Biological and therapeutic effects of ortho-silicic acid and some ortho-silicic acid-releasing compounds: New perspectives for therapy. Jurki LM, Cepanec I, Paveli SK, Paveli K.

Source

Department of Biotechnology, University of Rijeka, Radmile Mateji 2, Rijeka, HR-51000, Croatia. sandrakp@biotech.uniri.hr.

Abstract

Silicon (Si) is the most abundant element present in the Earth's crust besides oxygen. However, the exact biological roles of silicon remain unknown. Moreover, the ortho-silicic acid (H4SiO4), as a major form of bioavailable silicon for both humans and animals, has not been given adequate attention so far. Silicon has already been associated with bone mineralization, collagen synthesis, skin, hair and nails health atherosclerosis, Alzheimer disease, immune system enhancement, and with some other disorders or pharmacological effects. Beside the ortho-silicic acid and its stabilized formulations such as choline chloride-stabilized ortho-silicic acid and sodium or potassium silicates (e.g. M2SiO3; M= Na,K), the most important sources that release ortho-silicic acid as a bioavailable form of silicon are: colloidal silicic acid (hydrated silica gel), silica gel (amorphous silicon dioxide), and zeolites. Although all these compounds are characterized by substantial water insolubility, they release small, but significant, equilibrium concentration of ortho-silicic acid (H4SiO4) in contact with water and physiological fluids. Even though certain pharmacological effects of these compounds might be attributed to specific structural characteristics that result in profound adsorption and absorption properties, they all exhibit similar pharmacological profiles readily comparable to ortho-silicic acid effects. The most unusual ortho-silicic acid-releasing agents are certain types of zeolites, a class of aluminosilicates with well described ion(cation)-exchange properties. Numerous biological activities of some types of zeolites documented so far might probably be attributable to the ortho-silicic acid-releasing property. In this review, we therefore discuss biological and potential therapeutic effects of ortho-silicic acid and ortho-silicic acid -releasing silicon compounds as its major natural sources.

J Alzheimers Dis. 2006 Sep;10(1):17-24; discussion 29-31.

Non-invasive therapy to reduce the body burden of aluminium in Alzheimer's disease. Exley C, Korchazhkina O, Job D, Strekopytov S, Polwart A, Crome P.

Source

Birchall Centre for Inorganic Chemistry and Materials Science, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk

Abstract

There are unexplained links between human exposure to aluminium and the incidence, progression and aetiology of Alzheimer's disease. The null hypothesis which underlies any link is that there would be no Alzheimer's disease in the effective absence of a body burden of aluminium. To test this the latter would have to be reduced to and retained at a level that was commensurate with an Alzheimer's disease-free population. In the absence of recent human interference in the biogeochemical cycle of aluminium the reaction of silicic acid with aluminium has acted as a geochemical control of the biological availability of aluminium. This same mechanism might now be applied to both the removal of aluminium from the body and the reduced entry of aluminium into the body while ensuring that essential metals, such as iron, are unaffected. Based upon the premise that urinary aluminium is the best non-invasive estimate of body burden of aluminium patients with Alzheimer's disease were asked to drink 1.5 L of a silicic acid-rich mineral water each day for five days and, by comparison of their urinary excretion of aluminium pre-and post this simple procedure, the influence upon their body burden of aluminium was determined. Drinking the mineral water increased significantly (P0.05) influence upon the urinary excretion of iron (20.7 +/- 9.5 to 21.7 +/- 13.8 nmol/mmol creatinine). The reduction in urinary aluminium supported the future longer-term use of silicic acid as non-invasive therapy for reducing the body burden of aluminium in Alzheimer's disease.