It seems that our friend C3KO city mouse has found his country mouse cousin: C5L2KO. In keeping with the Star Wars saga, albeit stretching things a bit with this one, I've found the depiction of our new friend!
To catch up, C3KO is a knockout mouse lacking the ability to produce Complement 3 (C3) protein which is a precursor for production of acylation stimulating protein, ASP. Therefore C3KO is ASP deficient. The result of this genetic mutation is to produce a mouse that is resistant to obesity, and essentially an ASP equivalent of insulin deficiency -- Type 1 diabetes. If you've not read about C3KO, here are the links to the two relevant installments in this series:
Fat Tissue Regulation ~ Part II: Meet C3KO
Fat Tissue Regulation ~ Part III: C3KO Meets Obi No Leptinobi
Fat Tissue Regulation ~ Part II: Meet C3KO
Fat Tissue Regulation ~ Part III: C3KO Meets Obi No Leptinobi
It is known that fat tissue expresses insulin receptors. Indeed this has been exploited to more clearly elucidate the roll of insulin acting on fat tissue in the form of insulin receptor knockout mice, the FIRKO mouse (F = fat specific, IR = insulin receptor) to be exact. As it is less well characterized, ASP action on fat tissue is not universally well known or acknowledged. Indeed ASP is pretty much a TWICHOOB's worst nightmare. It seems silly to me to even be having this part of the discussion because it is absolutely not controversial that ASP plays a critical role in clearing dietary fat into the adipose tissue. Or, we are to believe the fat tissue itself manufactures such a hormone for no purpose related controlling its own function. Huh? In any case, one piece of the puzzle that was missing was how ASP works and the absence of an identified receptor. This piece of the puzzle was found in 2005 by Katherine Cianflone's group.
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