Once released into the blood stream, PTH has a very short life span; levels fall by half in less than 5 minutes due to uptake and cleavage in the liver and kidneys. The fragments are referred to as C-terminal fragments and are variably sized, missing anywhere from 6 amino acids to more than half the N-terminal portion of the molecule. C-terminal fragments have a longer half-life , exist in much higher concentrations, and are eventually cleared by the kidneys. Although it was originally thought that the C-terminal fragments were inactive, it now appears that certain fragments may have biologic activities that are able to oppose those of intact PTH.
Cholesterol biosynthesis has been exhaustively studied in animals. All steps occur in the cytosol. The starting material is citrate, which is exported by the mitochondrion when metabolic fuels are high. It is converted into acetyl-CoA, ADP, CO 2 , and oxaloacetate by ATP-citrate lyase, together with ATP and CoASH as substrates. Three acetyl-CoAs are converted inoto HMG-CoA by the cytosolic isoforms of thiolase and 3-hydroxy-3-methylglutaryl-CoA synthase. The HMG-CoA is then reduced by NADPH to mevalonate by HMG-CoA reductase, the rate controlling enzyme of cholesterol biosynthesis. This enzyme has 8 helical domains anchoring it in the Golgi membrane of the ER;  the catalytic domain is in the cytosol. It is strongly inhibited by the statins , a class of drugs based on a mold metabolite which, at least at one time, were the largest selling class of drugs in the world. Mevalonate is acted of by a series of 3 kinases to give the highly labile 1,2-diphosphomevalonate-3-phosphate, which is acted on by a lyase to give phosphate, CO 2 , and isopentenyl diphosphate . Isopentenyl diphosphate isomerase converts the latter to the less stable dimethylallyl diphosphate . Farnesyl diphosphate synthase takes one DMAPP and two IPP to give the C 15 metabolite farnesyl diphosphate . There are a large number of additional steps to generate cholesterol from IPP, the ubiquitous precursor of all isoprenoids.
Using RNA-seq analysis, we identified 455 up-regulated and 314 down-regulated genes in JH-deprived fat bodies further treated with methoprene for 24 h ( Fig. 2A , Table S1 ). Gene ontology analysis showed that the up-regulated genes were significantly enriched in cellular metabolic processes, response to stimuli, development, and cellular process regulation ( Fig. 2B ). KEGG pathway analysis showed that DNA replication was on the top of up-regulated pathways ( Fig. 2C ). Subsequent real-time semi-quantitative reverse transcription PCR (qRT-PCR) confirmed that the expression of all 16 genes in the DNA replication pathway were up-regulated in methoprene-treated ( Fig. 2D ), but not acetone-treated ( Fig. S2 ) fat bodies when compared to the precocene treatment.