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"[Vitamin K and Bone Update. The biological effects of vitamin K(2) on bone quality.] - [Clin Calcium. 2009] - PubMed result
"[Vitamin K and Bone Update. The biological effects of vitamin K(2) on bone quality.]
Amizuka N, Li M, Guo Y, Liu Z, Suzuki R, Yamamoto T.
Clin Calcium. 2009 Dec;19(12):1788-96. Japanese.
PMID: 19949270
Post-transcriptional maturation with the presence of vitamin K(2) promotesgamma-carboxylation of osteocalcin, enabling further binding to hydroxyapatite, from which one could infer that vitamin K(2) increased the quality of bone matrix. For instance, vitamin K(2) rescued the impaired collagen mineralization caused by Mg insufficiency, by promoting a re-association of the process of collagen mineralization with mineralized nodules. Sodium warfarin, which antagonizes the function of vitamin K(2), reduced the binding of osteocalcin to bone matrices, and consequently resulted in crystalline particles being dispersed throughout the osteoid without forming mineralized nodules. Therefore,gamma-carboxylated Gla proteins mediated by vitamin K(2) appear to play a pivotal role in normal mineralization in bone."
Vitamin D and mortality in older men and women. - Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. - Wiley InterScience :: Article :: HTML Full Text
Vitamin D and mortality in older men and women.
Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, van Dam RM, Dekker JM.
Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18.
PMID: 19226272
DOI: 10.1111/j.1365-2265.2009.03548.x
Conclusions Low 25(OH)D levels are associated with all-cause mortality and even more pronounced with cardiovascular mortality, but it remains unclear whether vitamin D deficiency is a cause or a consequence of a poor health status. Therefore, intervention studies are warranted to evaluate whether vitamin D supplementation reduces mortality and cardiovascular diseases.
Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women
Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women.
Semba RD, Houston DK, Ferrucci L, Cappola AR, Sun K, Guralnik JM, Fried LP.
Nutr Res. 2009 Aug;29(8):525-30.
PMID: 19761886
doi:10.1016/j.nutres.2009.07.007
Older community-dwelling women with low 25(OH)D levels are at an increased risk of death.
Vitamin D and aging. [J Steroid Biochem Mol Biol. 2009] - PubMed result
Vitamin D and aging.
Tuohimaa P.
J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84. Review.
PMID: 19444937
Induction of Ovarian Cancer Cell Apoptosis by 1,25-Dihydroxyvitamin D3 through the Down-regulation of Telomerase — JBC
Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase.
Jiang F, Bao J, Li P, Nicosia SV, Bai W.
J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12.
PMID: 15485861
doi: 10.1074/jbc.M410395200
Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression.
Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85–90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene.
It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chromosome ends and leads to the genomic instability a
A vitamin D nutritional cornucopia: new insights concerning the serum 25-hydroxyvitamin D status of the US population -- Norman 88 (6): 1455 -- American Journal of Clinical Nutrition
A vitamin D nutritional cornucopia: new insights concerning the serum 25-hydroxyvitamin D status of the US population.
Norman AW.
Am J Clin Nutr. 2008 Dec;88(6):1455-6.
PMID: 19064502
doi:10.3945/ajcn.2008.27049
In summary, the report of Looker et al should be required reading for all nutritionists, clinicians, and vitamin D aficionados who are decision makers with regard to 25(OH)D assays, vitamin D nutritional policy, and the care of patients with vitamin D–related diseases.
Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004 -- Looker et al. 88 (6): 1519 -- American Journal of Clinical Nutrition
Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004.
Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA.
Am J Clin Nutr. 2008 Dec;88(6):1519-27.
PMID: 19064511
doi:10.3945/ajcn.2008.26182
Conclusions: Overall, mean serum 25(OH)D was lower in 2000–2004 than 1988–1994. Assay changes unrelated to changes in vitamin D status accounted for much of the difference in most population groups. In an adult subgroup, combined changes in BMI, milk intake, and sun protection appeared to contribute to a real decline in vitamin D status.
In summary, age-standardized mean serum 25(OH)D concentrations based on observed values were significantly lower in 2000–2004 than in 1988–1994 in all groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. However, mean serum 25(OH)D concentrations remained significantly lower in males (except Mexican Americans) in NHANES 2000–2004 than in NHANES III, even after adjustment for assay differences. This remaining difference likely represents a real decline in vitamin D status. Changes in BMI, milk intake, and sun protection appeared to contribute to this decline in a subgroup of non-Hispanic white adults. The possibility that trends in overweight, sun protection, and milk intake may continue supports the need to continue monitoring the serum 25(OH)D status of the population
The Effect of Vitamin D2 and Vitamin D3 on Intestinal Calcium Absorption in Nigerian Children with Rickets -- Thacher et al. 94 (9): 3314 -- Journal of Clinical Endocrinology & Metabolism
The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets.
Thacher TD, Obadofin MO, O'Brien KO, Abrams SA.
J Clin Endocrinol Metab. 2009 Sep;94(9):3314-21. Epub 2009 Jun 30.
PMID: 19567516
Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption
Developmental toxicity evaluation of berberine in rats and mice. Gloria D. Jahnke. 2006; Birth Defects Research Part B: Developmental and Reproductive Toxicology - Wiley InterScience
Developmental toxicity evaluation of berberine in rats and mice.
Jahnke GD, Price CJ, Marr MC, Myers CB, George JD.
Birth Defects Res B Dev Reprod Toxicol. 2006 Jun;77(3):195-206.
PMID: 16634078
DOI: 10.1002/bdrb.20075
BACKGROUND: Berberine, a plant alkaloid, is found in some herbal teas and health-related products. It is a component of goldenseal, an herbal supplement. Berberine chloride dihydrate (BCD) was evaluated for developmental toxicity in rats and mice.
METHODS: Berberine chloride dihydrate was administered in the feed to timed-mated Sprague-Dawley (CD) rats (0, 3625, 7250, or 14,500 ppm; on gestational days [GD] 6-20), and Swiss Albino (CD-1) mice (0, 3500, 5250, or 7000 ppm; on GD 6-17). Ingested doses were 0, 282, 531, and 1313 mg/kg/day (rats) and 0, 569, 841, and 1155 mg/kg/day (mice).
RESULTS:There were no maternal deaths. The rat maternal lowest observed adverse effect level (LOAEL), based on reduced maternal weight gain, was 7250 ppm. The rat developmental toxicity LOAEL, based on reduced fetal body weight per litter, was 14,500 ppm. In the mouse study, equivocal maternal and developmental toxicity LOAELs were 5250 ppm. Due to scattering of feed in the high dose groups, a gavage study at 1000 mg/kg/day was conducted in both species.
CONCLUSIONS: In rats, maternal, but not fetal adverse effects were noted. The maternal toxicity LOAEL remained at 7250 ppm (531 mg/kg/day) based on the feed study and the developmental toxicity NOAEL was raised to 1000 mg/kg/day BCD based on the gavage study. In the mouse, 33% of the treated females died. Surviving animals had increased relative water intake, and average fetal body weight per litter decreased 5-6% with no change in live litter size. The maternal toxicity LOAEL remained at 5250 ppm (841 mg/kg/day) BCD, based on increased water consumption. The developmental toxicity LOAEL was raised to 1000 mg/kg/day BCD based on decreased fetal body weight.
Mechanisms of Berberine (Natural Yellow 18)-Induced Mitochondrial Dysfunction: Interaction with the Adenine Nucleotide Translocator -- Pereira et al. 105 (2): 408 -- Toxicological Sciences
Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator.
Pereira CV, Machado NG, Oliveira PJ.
Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3.
PMID: 18599498
doi: 10.1124/jpet.107.128017
The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study.
Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs.
In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.
Mitochondrially Targeted Effects of Berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 Mouse Melanoma Cells: Comparison with Direct Effects on Isolated Mitochondrial Fractions - JPET
Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions.
Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ.
J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17.
PMID: 17704354
doi: 10.1124/jpet.107.128017
The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic “natural” over-the-counter medication.
Berberine Inhibits Metastasis of Nasopharyngeal Carcinoma 5-8F Cells by Targeting Rho Kinase-mediated Ezrin Phosphorylation at Threonine 567 - JBC
Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567.
Tang F, Wang D, Duan C, Huang D, Wu Y, Chen Y, Wang W, Xie C, Meng J, Wang L, Wu B, Liu S, Tian D, Zhu F, He Z, Deng F, Cao Y.
J Biol Chem. 2009 Oct 2;284(40):27456-66. Epub 2009 Aug 3.
PMID: 19651779
Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells — Mol Cancer Ther
Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells.
Mantena SK, Sharma SD, Katiyar SK.
Mol Cancer Ther. 2006 Feb;5(2):296-308.
PMID: 16505103
doi: 10.1158/1535-7163.MCT-05-0448
The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy.
The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time.
In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.
Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-κB, u-PA and MMP-2 and -9
Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-kappaB, u-PA and MMP-2 and -9.
Ho YT, Yang JS, Li TC, Lin JJ, Lin JG, Lai KC, Ma CY, Wood WG, Chung JG.
Cancer Lett. 2009 Jul 8;279(2):155-62. Epub 2009 Feb 28.
PMID: 19251361
doi:10.1016/j.canlet.2009.01.033
There is increasing evidence that urokinase-type plasminogen activator (u-PA) and matrix metalloproteinases (MMPs) play an important role in cancer metastasis and angiogenesis. Inhibition of u-PA and MMPs could suppress migration and invasion of cancer cells. Berberine, one of the main constituents of the plant Rhizoma coptidis, is a type of isoquinoline alkaloid, reported to have anti-cancer effects in different human cancer cell lines. There is however, no available information on effects of berberine on migration and invasion of human tongue cancer cells. Here, we report that berberine inhibited migration and invasion of human SCC-4 tongue squamous carcinoma cells. This action was mediated by the p-JNK, p-ERK, p-p38, IκK and NF-κB signaling pathways resulting in inhibition of MMP-2 and -9 in human SCC-4 tongue squamous carcinoma cells. Our Western blowing analysis also showed that berberine inhibited the levels of urokinase-plasminogen activator (u-PA). These results suggest that berberine down-regulates u-PA, MMP-2 and -9 expressions in SCC-4 cells through the FAK, IKK and NF-κB mediated pathways and a novel function of berberine is to inhibit the invasive capacity of malignant cells.
Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP -- Mantena et al. 27 (10): 2018 --
Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP.
Mantena SK, Sharma SD, Katiyar SK.
Carcinogenesis. 2006 Oct;27(10):2018-27. Epub 2006 Apr 18.
PMID: 16621886
doi:10.1093/carcin/bgl043
In the present investigation, we show that berberine, which is present abundantly in Berberis plant species, significantly inhibits the viability, proliferation and induces cell death in human epidermoid carcinoma A431 cells (Figure 1), but this effect was not found in normal human epidermal keratinocytes under the identical conditions, except for a non-significant reduction in cell viability at higher concentrations of berberine (50 and 75 µM) and treatment of cells for a longer period of time (72 h). These data suggested that berberine may be examined as an effective chemotherapeutic agent against non-melanoma skin cancers.
In conclusion, our study indicates that berberine inhibits growth, induces G1 arrest and apoptotic cell death of human epidermoid carcinoma A431 cells. We also provide mechanistic evidences that berberine-induced apoptosis in human epidermoid carcinoma cells is mediated through disruption of mitochondrial membrane potential and activation of caspase 3 pathway, although other pathways may have a role and that require further investigation. Moreover, further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the prevention of non-melanoma skin cancers.
A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs. - Anti-Cancer Drugs
A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs.
Sun Y, Xun K, Wang Y, Chen X.
Anticancer Drugs. 2009 Oct;20(9):757-69.
PMID: 19704371
Berberine and Coptidis Rhizoma as novel antineoplastic agents: A review of traditional use and biomedical investigations - ScienceDirect - Journal of Ethnopharmacology
Berberine and Coptidis rhizoma as novel antineoplastic agents: a review of traditional use and biomedical investigations.
Tang J, Feng Y, Tsao S, Wang N, Curtain R, Wang Y.
J Ethnopharmacol. 2009 Oct 29;126(1):5-17. Epub 2009 Aug 15.
PMID: 19686830
doi:10.1016/j.jep.2009.08.009
Conclusions
The modern evidences of treating cancer with Huanglian and berberine have a strong linkage with traditional concept and rules of using Huanglian in CM practice. As anticancer candidates with low toxicity, berberine and its altered structure, as well as Huanglian and its formulae, will attract scientists to pursue the potential anticancer effects and the mechanisms by using technologies of genomics, proteomics and other advanced approaches. On the other hand, relatively few in vivo studies have been conducted on anticancer effects of Huanglian and berberine. The clinical application of berberine or Huanglian as novel cancer therapeutic agents requires in vivo validations and further investigations of their anticancer mechanisms.
Is a lower dose of vitamin D supplementation enough to increase 25(OH)D status in a sunny country? - Eur J Nutr. 2009 Nov 28. - SpringerLink - Journal Article
Is a lower dose of vitamin D supplementation enough to increase 25(OH)D status in a sunny country?
Pignotti GA, Genaro PS, Pinheiro MM, Szejnfeld VL, Martini LA.
Eur J Nutr. 2009 Nov 28. [Epub ahead of print]
PMID: 19946776
CONCLUSION: The dose given (400 IU/day) was not enough to achieve 25(OH)D concentration, considered optimal for bone health.
The effect of omega-3 FAs on tumour angiogenesis and their therapeutic potential
The effect of omega-3 FAs on tumour angiogenesis and their therapeutic potential.
Spencer L, Mann C, Metcalfe M, Webb M, Pollard C, Spencer D, Berry D, Steward W, Dennison A.
Eur J Cancer. 2009 Aug;45(12):2077-86. Epub 2009 Jun 1. Review.
PMID: 19493674
Omega-3 fatty acid (omega-3 FA) consumption has long been associated with a lower incidence of colon, breast and prostate cancers in many human populations. Human trials have demonstrated omega-3 FA to have profound anti-inflammatory effects in those with cancer. In vitro and small animal studies have yielded a strong body of evidence establishing omega-3 FA as having anti-inflammatory, anti-apoptotic, anti-proliferative and anti-angiogenic effects. This review explores the evidence and the mechanisms by which omega-3 FA may act as angiogenesis inhibitors and identifies opportunities for original research trialling omega-3 FAs as anti-cancer agents in humans. The conclusions drawn from this review suggest that omega-3 FAs in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found principally in oily fish have potent anti-angiogenic effects inhibiting production of many important angiogenic mediators namely; Vascular Endothelial Growth Factor (VEGF), Platelet-Derived Growth Factor (PDGF), Platelet-Derived Endothelial Cell Growth Factor (PDECGF), cyclo-oxygenase 2 (COX-2), prostaglandin-E2 (PGE2), nitric oxide, Nuclear Factor Kappa Beta (NFKB), matrix metalloproteinases and beta-catenin
Fatty fish and fish omega-3 fatty acid intakes decrease the breast cancer risk: a case-control study
Fatty fish and fish omega-3 fatty acid intakes decrease the breast cancer risk: a case-control study.
Kim J, Lim SY, Shin A, Sung MK, Ro J, Kang HS, Lee KS, Kim SW, Lee ES.
BMC Cancer. 2009 Jun 30;9:216.
PMID: 19566923
doi: 10.1186/1471-2407-9-216
Conclusion
These results suggest that high consumption of fatty fish is associated with a reduced risk for breast cancer, and that the intake of omega-3 fatty acids from fish is inversely associated with postmenopausal breast cancer risk
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