In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis?

I believe it is related to the fact that the enzyme HMG-CoA lyase is regulated by glucagon (activates) and insulin (inactivates). It appears that this extra step was added so the pathway can be hormonally regulated.

After further checking, I found that HMG-CoA synthase rather than HMG-CoA lyase is the enzyme which is regulated. This enzyme also plays a vital role in cholesterol synthesis. HMG so produced can either form mevalonate, which leads to cholesterol synthesis, or form acetoacetate. Therefore if acetoacetyl CoA were directly hydrolyzed, it would short circuit the cholesterol pathway.

The enzyme can be regulated by succinylation. Its synthesis can be regulated by several transcription factors. Evidence suggests that hormones play a role in each of these processes. References: Harris, et al., Journal of Investigative Dermatology 114(1) 83-87 (2001); F.G. Haggart, Biochem. J. Mar. 5, 338 (pt. 3) 569-582 (1999); Quant, P.A. et al. Eur. J. Biochem. 187, 169-174 (1987)

Most Biochemistry texts today list HMG-CoA as the source of acetoacetate with no mention of direct hydrolysis of acetoacetyl-CoA. This suggests that if direct hydrolysis of acetoacetyl-CoA does occur, it probably plays a very minor role.