Although limited information is available for the precise cause of death for these ob/ob obese mice, it may be speculated that obesity-associated tumorigenesis (e.g., colon and skin cancer), chronic inflammation, immune deficiency and cardiovascular complications are among the leading causes of death in these mice [39].
The subcellular localization of HSLtes is not known, but based on studies performed in HSL null mice it can be speculated that HSLtes is indirectly associated with the membrane in haploid germ cells, where it controls cholesterol deposition and thus membrane fluidity [25].
It can be speculated that this specific growth factor response is due to our cell system, because most cells used in previous studies are mouse osteoblasts from calvaria.
It is speculated that this mouse model may have NPC2 independent mechanisms or might have developed alternative mechanisms to form papillae.
In mice it was speculated that the lacking PITX3 function in muscles is perhaps completely compensated by the maintenance of PITX2 expression [41].
Therefore, it is speculated that generation of adipocytes in FcorKO mice is decreased due to activation of Foxo1.
Thus, it has been speculated that miR-128-2 miR-128-2 miR-128-2 in obese mice, might confereductionnce tobservedsin and induce cancer.
In an animal study with normal, wild-type mice, it was speculated that elevated plasma PS concentrations after PS feeding could be atherogenic because these concentrations were correlated with impaired endothelial vasorelaxation in situ (25).
Since Compound K was detected in blood after oral administration of ginsenoside Rb1 to mice, it has been speculated that it is probably the major form of protopanaxadiol saponin absorbed by the intestine.
Eldecalcitol increased bone formation at the periosteal surface of SAM/P6 mice, and it is speculated that eldecalcitol activates Wnt signaling and/or growth factor signaling via enhanced muscle function [ 31].
