scholarly journals Calorie restriction and cancer prevention: metabolic and molecular mechanisms

2010 ◽  
Vol 31 (2) ◽  
pp. 89-98 ◽  
Author(s):  
Valter D. Longo ◽  
Luigi Fontana
Keyword(s):  
Cancer Prevention ◽  
Calorie Restriction ◽  
Molecular Mechanisms

Molecular Mechanisms of Cancer Prevention by Selenium Compounds

2001 ◽  
Vol 40 (1) ◽  
pp. 42-49 ◽  
Author(s):  
Janis Fleming ◽  
Aurnab Ghose ◽  
Paul R. Harrison
Keyword(s):  
Cancer Prevention ◽  
Molecular Mechanisms ◽  
Selenium Compounds

Molecular mechanisms of life- and health-span extension: role of calorie restriction and exercise intervention

2007 ◽  
Vol 32 (5) ◽  
pp. 954-966 ◽  
Author(s):  
Christy S. Carter ◽  
Tim Hofer ◽  
Arnold Y. Seo ◽  
Christian Leeuwenburgh
Keyword(s):  
Life Span ◽  
Calorie Restriction ◽  
Aging Process ◽  
Molecular Mechanisms ◽  
Geriatric Medicine ◽  
Functional Decline ◽  
Intervention Strategies ◽  
Health Span ◽  
Structural Deterioration ◽  
Age Related

The aging process results in a gradual and progressive structural deterioration of biomolecular and cellular compartments and is associated with many pathological conditions, including cardiovascular disease, stroke, Alzheimer’s disease, osteoporosis, sarcopenia, and liver dysfunction. Concomitantly, each of these conditions is associated with progressive functional decline, loss of independence, and ultimately disability. Because disabled individuals require care in outpatient or home care settings, and in light of the social, emotional, and fiscal burden associated with caring for an ever-increasing elderly population, research in geriatric medicine has recently focused on the biological mechanisms that are involved in the progression towards functional decline and disability to better design treatment and intervention strategies. Although not completely understood, the mechanisms underlying the aging process may partly involve inflammatory processes, oxidative damage, mitochondrial dysfunction, and apoptotic tissue degeneration. These hypotheses are based on epidemiological evidence and data from animal models of aging, as well as interventional studies. Findings from these studies have identified possible strategies to decrease the incidence of age-related diseases and delay the aging process. For example, lifelong exercise is known to extend mean life-span, whereas calorie restriction (CR) increases both mean and maximum life-span in a variety of species. Optimal application of these intervention strategies in the elderly may positively affect health-related outcomes and possibly longevity. Therefore, the scope of this article is to (i) provide an interpretation of various theories of aging from a “health-span” perspective; (ii) describe interventional testing in animals (CR and exercise); and (iii) provide a translational interpretation of these data.

Polymethoxyflavones: Chemistry and Molecular Mechanisms for Cancer Prevention and Treatment

2019 ◽  
Vol 5 (2) ◽  
pp. 98-113 ◽  
Author(s):  
Yen-Chen Tung ◽  
Ya-Chun Chou ◽  
Wei-Lun Hung ◽  
An-Chin Cheng ◽  
Roch-Chui Yu ◽  
...  
Keyword(s):  
Cancer Prevention ◽  
Molecular Mechanisms ◽  
Prevention And Treatment

scholarly journals Molecular Mechanisms Linking Exercise to Cancer Prevention and Treatment

2018 ◽  
Vol 27 (1) ◽  
pp. 10-21 ◽  
Author(s):  
Pernille Hojman ◽  
Julie Gehl ◽  
Jesper F. Christensen ◽  
Bente K. Pedersen
Keyword(s):  
Cancer Prevention ◽  
Molecular Mechanisms ◽  
Prevention And Treatment

scholarly journals Intrauterine calorie restriction affects placental DNA methylation and gene expression

2013 ◽  
Vol 45 (14) ◽  
pp. 565-576 ◽  
Author(s):  
Pao-Yang Chen ◽  
Amit Ganguly ◽  
Liudmilla Rubbi ◽  
Luz D. Orozco ◽  
Marco Morselli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Chronic Diseases ◽  
Calorie Restriction ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Specific Effects ◽  
Differentially Methylated Genes ◽  
Critical Organ ◽  
Successive Generations

Maternal nutrient restriction causes the development of adult onset chronic diseases in the intrauterine growth restricted (IUGR) fetus. Investigations in mice have shown that either protein or calorie restriction during pregnancy leads to glucose intolerance, increased fat mass, and hypercholesterolemia in adult male offspring. Some of these phenotypes are shown to persist in successive generations. The molecular mechanisms underlying IUGR remain unclear. The placenta is a critical organ for mediating changes in the environment and the development of embryos. To shed light on molecular mechanisms that might affect placental responses to differing environments we examined placentas from mice that had been exposed to different diets. We measured gene expression and whole genome DNA methylation in both male and female placentas of mice exposed to either caloric restriction or ad libitum diets. We observed several differentially expressed pathways associated with IUGR phenotypes and, most importantly, a significant decrease in the overall methylation between these groups as well as sex-specific effects that are more pronounced in males. In addition, a set of significantly differentially methylated genes that are enriched for known imprinted genes were identified, suggesting that imprinted loci may be particularly susceptible to diet effects. Lastly, we identified several differentially methylated microRNAs that target genes associated with immunological, metabolic, gastrointestinal, cardiovascular, and neurological chronic diseases, as well as genes responsible for transplacental nutrient transfer and fetal development.

scholarly journals Does Calorie Restriction Modulate Inflammaging via FoxO Transcription Factors?

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1959
Author(s):  
Sang-Eun Kim ◽  
Ryoichi Mori ◽  
Isao Shimokawa
Keyword(s):  
Transcription Factors ◽  
Calorie Restriction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Functional Decline ◽  
Cell Lineage ◽  
Myeloid Cell ◽  
The Body ◽  
Pyrin Domain ◽  
Foxo Transcription Factors

Calorie restriction (CR) has been shown to extend lifespan and retard aging-related functional decline in animals. Previously, we found that the anti-neoplastic and lifespan-extending effects of CR in mice are regulated by forkhead box O transcription factors (FoxO1 and FoxO3), located downstream of growth hormone (GH)–insulin-like growth factor (IGF)-1 signaling, in an isoform-specific manner. Inflammaging is a term coined to represent that persistent low-level of inflammation underlies the progression of aging and related diseases. Attenuation of inflammaging in the body may underlie the effects of CR. Recent studies have also identified cellular senescence and activation of the nucleotide-binding domain, leucine-rich-containing family, pyrin-domain-containing-3 (NLRP3) inflammasome as causative factors of inflammaging. In this paper, we reviewed the current knowledge of the molecular mechanisms linking the effects of CR with the formation of inflammasomes, particularly focusing on possible relations with FoxO3. Inflammation in the brain that affects adult neurogenesis and lifespan was also reviewed as evidence of inflammaging. A recent progress of microRNA research was described as regulatory circuits of initiation and propagation of inflammaging. Finally, we briefly introduced our preliminary results obtained from the mouse models, in which Foxo1 and Foxo3 genes were conditionally knocked out in the myeloid cell lineage.

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