Fat cells are not as good as thin stem cells

Strong AL, Bowles AC, Wise RM, Morand JP, Dutreil MF, Gimble JM, Bunnell BA.Human adipose stromal/stem cells from obese donors show reduced efficacy in halting disease progression in the experimental autoimmune encephalomyelitis model of multiple sclerosis.Stem Cells. 2015. doi: 10.1002/stem.2272. [Epub ahead of print]

Multiple sclerosis is an autoimmune disease that affects the white matter of the central nervous system and involves inflammation and demyelination. The recent advances in our understanding of adipose-derived stromal/stem cells (ASCs) and the utilization of these cells in clinical settings to treat diseases have made it essential to identify the most effective ASCs for therapy. Studies have not yet investigated the impact of obesity on the therapeutic efficacy of ASCs. Obesity is characterized by adipocyte hyperplasia and hypertrophy and can extend to metabolic and endocrine dysfunction. Investigating the impact obesity has on ASC biology will determine whether these cells are suitable for use in regenerative medicine. The therapeutic efficacy of ASCs isolated from lean subjects (body mass index <25; lnASCs) and obese subjects (body mass index >30; obASCs) were determined in murine experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. Compared to the EAE disease-modifying effects of lnASCs, obASCs consistently failed to alleviate clinical symptoms or inhibit inflammation in the central nervous system. When activated, obASCs expressed higher mRNA levels of several pro-inflammatory cytokines compared to lnASCs. Additionally, conditioned media collected from the obASCs markedly enhanced the proliferation and differentiation of T cells; whereas, conditioned media from lnASC did not. These results indicate that obesity reduces, or eliminates, the anti-inflammatory effects of human ASCs such that they may not be a suitable cell source for the treatment of autoimmune diseases. The data suggests that donor demographics may be particularly important when identifying suitable stem cells for treatment.

So after tucking into our christmas lunch we may add a few pounds/kilos. What this study does is looks at stem cells from fat cells from fat people and says they don’t work unlike stem cells from thin people. This may be because they produce pro-inflammatory factors.

The question is, Is this why we are interested in stem cells? 

Don’t we want them to repair as there are plenty of treatments to deal with the immune response. Do stem cells do this any better..generally the answer is no.

So we will be hearing about 

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