ArticleAge (Dordrecht, Netherlands)2011
Caloric restriction attenuates the age-associated increase of adipose-derived stem cells but further reduces their proliferative capacity.
Article in Age (Dordrecht, Netherlands), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- The impact of dietary restriction on transcriptional profiles of hematopoietic stem cells in aged female mice.Biogerontology · 2025Article
- The Role of Intermittent Energy Restriction Diet on Metabolic Profile and Weight Loss among Obese Adults.Nutrients · 2022Review
- Changes in Regenerative Capacity through Lifespan.International journal of molecular sciences · 2015Review
- SRT2104 extends survival of male mice on a standard diet and preserves bone and muscle mass.Aging cell · 2014Article
- The Impact of Obesity on Autophagy in Human Adipose-Derived Mesenchymal Stromal Cells.Cell transplantationArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
White adipose tissue is a promising source of mesenchymal stem cells. Currently, little is known about the effect of age and caloric restriction (CR) on adipose-derived stem cells (ASC). This is important for three reasons: firstly, age and CR cause extensive remodeling of WAT; it is currently unknown how this remodeling affects the resident stem cell population. Secondly, stem cell senescence has been theorized as one of the causes of aging and could reduce the utility of a stem cell as a reagent. Thirdly, the mechanism by which CR extends lifespan is currently not known, one theory postulates that CR maintains the resident stem cell population in youthful "fit" state. For the purpose of this study, we define ASC as lineage negative (lin(-))/CD34(+(low))/CD31(-). We show that aging increases the abundance of ASC and the expression of Cdkn2a 9.8-fold and Isl1 60.6-fold. This would suggest that aging causes an accumulation of non-replicative ASC. CR reduced the percentage of ASC in the lin(-) SVF while also reducing colony forming ability. Therefore, CR appears to have anti-proliferative effects on ASC that may be advantageous from the perspective of cancer, but our data raises the possibility that it may be disadvantageous for regenerative medicine applications.
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Registered trials
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