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For all the health conscious people, athletes, sportsmen, budding bodybuilders and gym rats out there, you can get the best multivitamin supplements from sport nutrition stores at a location near to you. These multivitamin and multimineral supplements are available for you at pocket friendly rates, you need not worry about its high prices. Having the right diet and supplements is the best way to lead a healthy life.

Anticancer properties of Ganoderma lucidum methanol extracts in vitro and in vivo. Harhaji Trajković LM, Mijatović SA, Maksimović-Ivanić DD, Stojanović ID, Momcilović MB, Tufegdzić SJ, Maksimović VM, Marjanović ZS, Stosić-Grujicić SD. Nutr Cancer. 2009;61(5):696-707. PMID: 19838944 DOI: 10.1080/01635580902898743 Anticancer activities of various extracts of the medicinal mushroom, Ganoderma lucidum, have been widely demonstrated and are mainly associated with the presence of different bioactive polysaccharides and triterpenoids. We have evaluated and compared in vitro and in vivo the antitumor effects of two preparations from Ganoderma lucidum: a methanol extract containing total terpenoids (GLme) and a purified methanol extract containing mainly acidic terpenoids (GLpme). Both extracts inhibited tumor growth of B16 mouse melanoma cells inoculated subcutaneously into syngeneic C57BL/6 mice and reduced viability of B16 cells in vitro, whereby GLme exhibited stronger effect. Furthermore, anticancer activity of GLme was demonstrated for the first time against two other rodent tumor cell lines, L929-mouse fibrosarcoma and C6-rat astrocytoma. The mechanism of antitumor activity of GLme comprised inhibition of cell proliferation and induction of caspase-dependent apoptotic cell death mediated by upregulated p53 and inhibited Bcl-2 expression. Moreover, the antitumor effect of the GLme was associated with intensified production of reactive oxygen species, whereas their neutralization by the antioxidant, N-acetyl cysteine, resulted in partial recovery of cell viability. Thus, our results suggest that GLme might be a good candidate for treatment of diverse forms of cancers.

"(NaturalNews) A research team from the University of Washington (UW) recently published a study in Physiology & Behavior revealing that moderate consumption of fructose- and high fructose corn syrup-sweetened beverages leads to significant alterations of lipid metabolization in the liver. Conducted on rats, the study also noted marked increases in both cholesterol and triglyceride levels in rats that fed on fructose-sweetened beverages. Fructose is a monosaccharide sugar that is found in various fruits. It is a simple sugar that is often promoted as being a healthy "fruit" sugar, however the reality is that fructose is just one component of the complex sugar composition that occurs naturally in fruit. Most granulated fructose available today, called crystalline fructose, is derived from fructose-enriched corn syrup. Similarly, high fructose corn syrup is a fructose-enriched form of highly-processed corn syrup that is commonly found in soda, ketchup, candy, dressings, and many other processed foods. The biggest concern about fructose is the fact that, unlike sucrose, it passes undigested through the small intestine where it enters the portal vein and heads directly to the liver. "

Coconut kernel protein modifies the effect of coconut oil on serum lipids. Padmakumaran Nair KG, Rajamohan T, Kurup PA. Plant Foods Hum Nutr. 1999;53(2):133-44. PMID: 10472790 DOI: 10.1023/A:1008078103299 Feeding coconut kernel along with coconut oil in human volunteers has been found to reduce serum total and LDL cholesterol when compared to feeding coconut oil alone. This effect of the kernel was also observed in rats. Since many plant proteins have been reported to exert a cholesterol lowering effect, a study was carried out on the effect of isolated kernel protein in rats. Feeding kernel protein resulted in lower levels of cholesterol, phospholipids and triglycerides in the serum and most tissues when compared to casein fed animals. rats fed kernel protein had (1) increased hepatic degradation of cholesterol to bile acids, (2) increased hepatic cholesterol biosynthesis, and (3) decreased esterification of free cholesterol. In the intestine, however, cholesterogenesis was decreased. The kernel protein also caused decreased lipogenesis in the liver and intestine. This beneficial effect of the kernel protein is attributed to its very low lysine/arginine ratio 2.13% lysine and 24.5% arginine....

Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Nevin KG, Rajamohan T. Clin Biochem. 2004 Sep;37(9):830-5. PMID: 15329324 doi:10.1016/j.clinbiochem.2004.04.010 Conclusion: The results demonstrated the potential beneficiary effect of virgin coconut oil in lowering lipid levels in serum and tissues and LDL oxidation by physiological oxidants. This property of VCO may be attributed to the biologically active polyphenol components present in the oil

Tissue phylloquinone and menaquinones in rats are affected by age and gender. Huber AM, Davidson KW, O'Brien-Morse ME, Sadowski JA. J Nutr. 1999 May;129(5):1039-44. PMID: 10222397 The results suggest that in extrahepatic tissues, certain menaquinones may be the predominant form of vitamin K. The specific tissue distribution and the general decline of MK-4 and MK-6 in extrahepatic tissues during aging suggest a vitamin K tissue dynamic that is affected not only by diet, but also by gender, age and the specific roles of phylloquinone, MK-4 and MK-6 in metabolism. All of these factors must be taken into account in establishing the nutrient requirement for vitamin K.

Age and dietary form of vitamin K affect menaquinone-4 concentrations in male Fischer 344 rats. Booth SL, Peterson JW, Smith D, Shea MK, Chamberland J, Crivello N. J Nutr. 2008 Mar;138(3):492-6. PMID: 18287355 These data suggest that dihydrophylloquinone, which differs from phylloquinone in its side phytyl chain, is absorbed but its intake results in less MK-4 in certain tissues. Dihydrophylloquinone may be used in models for the study of tissue-specific vitamin K deficiency

Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. Davidson RT, Foley AL, Engelke JA, Suttie JW. J Nutr. 1998 Feb;128(2):220-3. PMID: 9446847 These data offer conclusive proof that the tissue-specific formation of MK-4 from K is a metabolic transformation that does not require bacterial transformation to menadione as an intermediate in the process

Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations. Czernik M, Sroka J, Madeja Z, Czyz J. Cell Mol Biol Lett. 2008;13(3):327-38. Epub 2008 Feb 21. PMID: 18292973 DOI: 10.2478/s11658-008-0003-z This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

Berberine reduces the hypoxic-ischemic insult in rat pup brain. Benaissa F, Mohseni-Rad H, Rahimi-Moghaddam P, Mahmoudian M. Acta Physiol Hung. 2009 Jun;96(2):213-20. PMID: 19457765 DOI: 10.1556/APhysiol.96.2009.2.6 Pathologic review of the samples obtained from rats treated with different doses of berberine in comparison with samples from pups treated by normal saline showed that there was a significant reduction of brain injury and edema in the rats treated with berberine. Our study also demonstrates that berberine reduces brain ischemic-hypoxic injury dose-dependently. Therefore, beberine may be considered as useful anti-stroke agent.

Effect of vitamin K2 (menaquinone-7) in fermented soybean (natto) on bone loss in ovariectomized rats. Yamaguchi M, Taguchi H, Gao YH, Igarashi A, Tsukamoto Y. J Bone Miner Metab. 1999;17(1):23-9. PMID: 10084398 This study demonstrates that the intake of dietary MK-7 has a preventive effect on bone loss caused by OVX. This effect may be partly caused by MK-4, which is formed by degradation of MK-7.

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.

Egg yolk proteins suppress azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colon of rats. Ishikawa S, Asano T, Takenoshita S, Nozawa Y, Arihara K, Itoh M. Nutr Res. 2009 Jan;29(1):64-9. PMID: 19185779 These results indicate that dietary egg yolk proteins have a preventive effect on AOM-induced large bowel carcinogenesis in rats; it exerts this effect by altering cell proliferation through SCFA production. This study suggests that the consumption of egg yolk proteins might be protective against colon carcinogenesis.

Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats. Lavigne C, Tremblay F, Asselin G, Jacques H, Marette A. Am J Physiol Endocrinol Metab. 2001 Jul;281(1):E62-71. PMID: 11404223 These data demonstrate that feeding cod protein prevents obesity-induced muscle insulin resistance in high fat-fed obese rats at least in part through a direct action of amino acids on insulin-stimulated glucose uptake in skeletal muscle cells.

"We've been having an interesting discussion in the comments about a recently published paper by Dr. Stephen C. Benoit and colleagues (free full text). They showed that a butter-rich diet causes weight gain and insulin resistance in rats, compared to a low-fat diet or a diet based on olive oil. They published a thorough description of the diets' compositions, which is very much appreciated! They went on to show that infusing palmitic acid (a 16-carbon saturated fat) directly into the brain of rats also caused insulin resistance relative to oleic acid (an 18-carbon monounsaturated fat, like in olive oil). Here's a representation of palmitic acid. The COOH end is the acid end, and the squiggly line is the fatty end. Thus it's called a "fatty acid", various forms of which are the fat currency of the body."

Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Schurgers LJ, Spronk HM, Soute BA, Schiffers PM, DeMey JG, Vermeer C. Blood. 2007 Apr 1;109(7):2823-31. PMID: 17138823 DOI 10.1182/blood-2006-07-035345. This is the first study in rats demonstrating that AC and the resulting decreased arterial distensibility are reversible by high-VK intake

Phytase activity in the human and rat small intestine. Iqbal TH, Lewis KO, Cooper BT. Gut. 1994 Sep;35(9):1233-6. PMID: 7959229

I'm always on the lookout for foods rich in vitamin K2 MK-4, because it's so important and so rare in the modern food system. I heard some internet rumors that marrow might be rich in fat-soluble vitamins. Google let me down, so I decided to look through the rat studies on K2 MK-4 in which they looked at its tissue distribution. I found one that looked at the K2 MK-4 content in different tissues of rats fed vitamin K1. Marrow was rich in K2, along with testes. It contains 10-20 times more MK-4 than liver by weight, and more than any of the other organs they tested (serum, liver, spleen, kidney, heart, testes, marrow, brain) except testes. They didn't include values for salivary gland and pancreas, the two richest sources.

Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. Vieth R, Milojevic S, Peltekova V. J Nutr. 2000 Mar;130(3):578-84. PMID: 10702588 We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite. When viewed from a perspective that starts with higher vitamin D nutrition, the results indicate that low vitamin D nutrition may bring about a form of resistance to 1,25(OH)2D. This situation would explain why, in humans, nutritional rickets and osteomalacia are commonly associated with normal or increased levels of 1,25(OH)2D (Chesney et al. 1981Citation , Eastwood et al. 1979Citation , Garabedian et al. 1983Citation ,Rasmussen et al. 1980Citation )-these are not like the low hormone levels associated with any other endocrine-deficiency disorder. A connection between lower vitamin D nutrition and vitamin D resistance helps to explain why the supposedly inactive compound 25(OH)D is more relevant in diagnosing nutritional rickets than is the active hormone 1,25(OH)2D. If the features of improved vitamin D nutrition shown here were demonstrated for any newly synthesized compound, the compound would be classified as a noncalcemic 1,25(OH)2D analogue (Brown et al. 1989Citation , Finch et al. 1999Citation , Goff et al. 1993Citation , Koshizuka et al. 1999Citation ). Thus, we contend that 25(OH)D or a metabolite of it other than 1,25(OH)2D exists as a physiological and biologically-active noncalcemic vitamin D metabolite whose effects require further examination, particularly in relationship to studies involving the synthetic analogs of 1,25(OH)2D.

Various selected vegetables, fruits, mushrooms and red wine residue inhibit bone resorption in rats. Mühlbauer RC, Lozano A, Reinli A, Wetli H. J Nutr. 2003 Nov;133(11):3592-7. PMID: 14608079