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 COLI 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 1chome, 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 taurinespecific 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 posttreatment (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 taurineactivated 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<0.001) and simvastatin plus ezetimibe (P<0.001)
significantly decreased GLUT4 protein expression in the adipocytes compared to control
conditions. GLUT4 protein levels were similar to control after treatment with ezetimibe alone
(P=0.52) or pravastatin (P=0.32). There was no significant difference (P=0.098) in GLUT4 protein
levels after co-treatment with CoQ10 between any of the treatments and control conditions.
Conclusion: Our studies have shown that lipophilic statins (simvastatin) reduce the GLUT4 protein
levels in adipocytes, whereas hydrophilic statins (pravastatin) or ezetimibe do not. Co-treatment
with CoQ10 appears to prevent the reduction in GLUT4 protein levels caused by simvastatin.
Bioorg Med Chem. 2013 Apr 15;21(8):2346-54. doi: 10.1016/j.bmc.2013.01.075. Epub 2013 Feb
13.
Effects of alkyl side chain modification of coenzyme Q10 on mitochondrial respiratory chain
function and cytoprotection.
Fash DM, Khdour OM, Sahdeo SJ, Goldschmidt R, Jaruvangsanti J, Dey S, Arce PM, Collin VC,
Cortopassi GA, Hecht SM.
Source
Center for BioEnergetics, Biodesign Institute, and Department of Chemistry and Biochemistry,
Arizona State University, Tempe, AZ 85287, USA.
Abstract
The effect of the alkyl side chain length of coenzyme Q10 on mitochondrial respiratory chain
function has been investigated by the use of synthetic ubiquinone derivatives. Three analogues (3, 4
and 6) were identified that exhibited significantly improved effects on mitochondrial oxygen
consumption and mitochondrial membrane potential, and also conferred significant cytoprotection
on cultured mammalian cells in which glutathione had been depleted by treatment with diethyl
maleate. The analogues also exhibited lesser inhibition of the electron transport chain than
idebenone. The results obtained provide guidance for the design of CoQ10 analogues with
improved activity compared to that of idebenone (1), the latter of which is undergoing evaluation in
the clinic as a therapeutic agent.
Andrologia. 2013 Jan 7. doi: 10.1111/and.12062. [Epub ahead of print]
Effect of Coenzyme Q10 supplementation on antioxidant enzymes activity and oxidative stress
of seminal plasma: a double-blind randomised clinical trial.
Nadjarzadeh A, Shidfar F, Amirjannati N, Vafa MR, Motevalian SA, Gohari MR, Nazeri Kakhki
SA, Akhondi MM, Sadeghi MR.
Source
Department of Nutrition, Faculty of Health, Shahid Sadoughi University of Medical Sciences,
Yazd, Iran.

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 nonworkload 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 Q10administered 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 (P<0.001) their urinary excretion of silicic acid (34.3 +/- 15.2
to 55.7 +/- 14.2 micromol/mmol creatinine) and concomitantly reduced significantly P=0.037) their
urinary excretion of aluminium (86.0 +/- 24.3 to 62.2 +/- 23.2 nmol/mmol creatinine). The latter
was achieved without any significant (P>0.05) 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.