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Researchers link calorie intake to cell lifespan, cancer development (w/ Video)
"Researchers from the University of Alabama at Birmingham (UAB) have discovered that restricting consumption of glucose, the most common dietary sugar, can extend the life of healthy human-lung cells and speed the death of precancerous human-lung cells, reducing cancer's spread and growth rate.
The research has wide-ranging potential in age-related science, including ways in which calorie-intake restriction can benefit longevity and help prevent diseases like cancer that have been linked to aging, said principal investigator Trygve Tollefsbol, Ph.D., D.O., a professor in the Department of Biology.
"These results further verify the potential health benefits of controlling calorie intake." Tollefsbol said. "Our research indicates that calorie reduction extends the lifespan of healthy human cells and aids the body's natural ability to kill off cancer-forming cells.
Calorie intake linked to cell lifespan, cancer development
"ScienceDaily (Dec. 17, 2009) — Researchers from the University of Alabama at Birmingham (UAB) have discovered that restricting consumption of glucose, the most common dietary sugar, can extend the life of healthy human-lung cells and speed the death of precancerous human-lung cells, reducing cancer's spread and growth rate.
The research has wide-ranging potential in age-related science, including ways in which calorie-intake restriction can benefit longevity and help prevent diseases like cancer that have been linked to aging, said principal investigator Trygve Tollefsbol, Ph.D., D.O., a professor in the Department of Biology.
"These results further verify the potential health benefits of controlling calorie intake." Tollefsbol said. "Our research indicates that calorie reduction extends the lifespan of healthy human cells and aids the body's natural ability to kill off cancer-forming cells.""
Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations. - Cell Mol Biol Lett. 2008 - SpringerLink - Journal Article
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.
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
Cell - Dietary and Genetic Control of Glucose Transporter 2 Glycosylation Promotes Insulin Secretion in Suppressing Diabetes
Dietary and genetic control of glucose transporter 2 glycosylation promotes insulin secretion in suppressing diabetes.
Ohtsubo K, Takamatsu S, Minowa MT, Yoshida A, Takeuchi M, Marth JD.
Cell. 2005 Dec 29;123(7):1307-21.
PMID: 16377570
Hypovitaminosis D is associated with insulin resistance and {beta} cell dysfunction -- Chiu et al. 79 (5): 820 -- American Journal of Clinical Nutrition
Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction.
Chiu KC, Chu A, Go VL, Saad MF.
Am J Clin Nutr. 2004 May;79(5):820-5.
PMID: 15113720
Conclusions: The data show a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher risk of insulin resistance and the metabolic syndrome. Further studies are required to explore the underlying mechanisms.
1,25(OH)2 Vitamin D Inhibits Foam Cell Formation and Suppresses Macrophage Cholesterol Uptake in Patients With Type 2 Diabetes Mellitus -- Oh et al. 120 (8): 687 -- Circulation
1,25(OH)2 vitamin d inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus.
Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, Proctor BM, Petty M, Chen Z, Schechtman KB, Bernal-Mizrachi L, Bernal-Mizrachi C.
Circulation. 2009 Aug 25;120(8):687-98. Epub 2009 Aug 10.
PMID: 19667238
doi: 10.1161/CIRCULATIONAHA.109.856070
Conclusion— These results identify reduced vitamin D receptor signaling as a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disease in diabetic subjects.
AP Biology | MIT OpenCourseWare - Free Online MIT Course Materials for High School
We have selected relevant material from MIT's introductory courses to support students as they study and educators as they teach the AP® Biology curriculum.
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