As far as increase in adiposity this has been directly addressed on three counts:
1. r-ala lowers plasma insulin response (both directly through action on pancreas and through glucose clearance)
2. r-ala inhibits adipogenesis via the MaPK pathway and ppar-y antagonism
3. animals treated with r-ala show decreases in adiposity, both lean and obese models.
btw- if fat cells are insulin resistant, as noted in the glut-4 study cited in the IGF-1 thread, the result is poor glucose clear, hypergylcemia and adiposity. as a note if your fat cells were to lack an insulin receptor as that FIRKO mice did the effects are increased insulin sensitivity in both muscle and the fat tissues that they do have.
as a further note all cells store glycogen and utilize glucose, even adipocytes, in fact their uptake of glucose increase leptin levels.