New LSJL and IGF-2 related study by Zhang and Yokota

Lengthening of mouse hind limbs with local administration of insulin-like growth factor 2

"C57/BL/6 mice (∼ 8 weeks old) were used in this study, and the mice were separated into two groups: an IGF2-treated group and a placebo group. In the IGF2-treated group, IGF2 was locally administered into the distal epiphysis of the left femur, and the right femur was used as a contralateral control. In the placebo group, saline was administered to the left femur as a vehicle control. The left and right tibiae, without any direct intervention, were employed as negative controls. The dosage of IGF2 was 100 μg/kg/day for 5 consecutive days, and bone samples were harvested on Day 14. Microcomputed tomography images did not show any anomaly at the IGF2 or saline injection sites.
In comparison with the vehicle control as well as the contralateral control, the results revealed that IGF2 significantly lengthened the treated femur, with an elevation of bone mineral density (BMD) as well as bone mineral content (BMC). The increase in the femoral length of the IGF2-treated left limb was 1.6% (p < 0.05) to the vehicle control, and 1.7% (p < 0.05) to the contralateral control. However, the length, BMD, and BMC of the tibiae were not affected by administration of IGF2 or saline. Western blotting analysis demonstrated that this administration of IGF2 upregulated phosphorylation of an extracellular signal-regulated kinase in the treated femur."

LSJL knee loading was actually more effective than IGF2 lengthening both the tibia and femur and by a greater amount.  The fact that LSJL lengthened both is actually mentioned as a downside as they are developing this as a method to treat limb length discrepencies.  With LSJL there was an increase in the contralateral limb but only the local limb was increased with IGF2.

"IGF2 activates transforming growth factor beta (TGFb) and extracellular signal-regulated kinase (ERK) signaling"<-both of these are likely activated by LSJL as well.  An increase in ERK1/2-p was validated by this study.

"Both IGF1 and IGF2 bind to IGF receptor 1, but only IGF receptor 2 can be bound by IGF2 and not by IGF1. They are reported to be able to recruit primary osteoblastic cells, and regulate proliferation and differentiation of chondrocytes in the growth plate."

"a C28/I2 chondrocyte cell line that administration of IGF2 (5 hours at 10–100 ng/ml) activates TGFb signaling"

It would suck if they abondoned LSJL for IGF-2. Maybe someone other than me can email Ping Zhang and ask if the results of this study means that they're not researching their lateral joint loading method? And we still don't know if IGF2 results in adult height increase than an increase in height velocity.  The scientists allude to testing IGF2 on mature skeletons in the future.

Look at the growth plate in figure 2 C, you can see that the growth plate is open at the end at the computer screen's left whereas it is fused at the end of all other growth plates.  Therefore IGF-2 may have an anti-fusion effect.  Could this effect occur in the adult plate?  Unfortunately there are no before pictures.  The IGF2 bone is much more porous than the other bones.

The scientists state that 8 week old mice are equivalent to twelve year olds.