In Drosophila melanogaster, Hmgcr is the homolog of Human HMGCR, and plays crucial roles in regulating energy metabolism and food intake but also sleep homeostasis through the central mechanisms according to these studies , https://www.mdpi.com/2073-4409/11/6/970 and https://www.mdpi.com/1424-8247/15/1/79 Click on genes, proteins and metabolites below to link to respective articles.

[11] These drugs include rosuvastatin (CRESTOR), lovastatin (Mevacor), atorvastatin (Lipitor), pravastatin (Pravachol), fluvastatin (Lescol), pitavastatin (Livalo), and simvastatin (Zocor).

[12] Red yeast rice extract, one of the fungal sources from which the statins were discovered, contains several naturally occurring cholesterol-lowering molecules known as monacolins.

[14] Statins, HMG-CoA reductase inhibitors, are competent in lowering cholesterol levels and reducing cardiac-related diseases.

SREBP-2 activation for cholesterol homeostasis is crucial for the upregulation of low density lipoprotein (LDL) receptor (LDLR).

In many studies, lipophilic statins are shown as more diabetogenic, possibly due to the fact that they can easily diffuse into cells and inhibit the production of isoprenoids which become more potent.

[17] Statins have been shown to have anti-inflammatory properties,[18] most likely as a result of their ability to limit production of key downstream isoprenoids that are required for portions of the inflammatory response.

It can be noted that blocking of isoprenoid synthesis by statins has shown promise in treating a mouse model of multiple sclerosis, an inflammatory autoimmune disease.

Inhibition of its activity and the concomitant lack of isoprenoids that yields can lead to germ cell migration defects[21] as well as intracerebral hemorrhage.

This protein binds to the sterol regulatory element (SRE), located on the 5' end of the reductase gene after controlled proteolytic processing.

When cholesterol levels rise, Insigs retains the SCAP-SREBP complex in the ER membrane by preventing its incorporation into COPII vesicles.

An excellent review on regulation of the mevalonate pathway by Nobel Laureates Joseph Goldstein and Michael Brown adds specifics: HMG-CoA reductase is phosphorylated and inactivated by an AMP-activated protein kinase, which also phosphorylates and inactivates acetyl-CoA carboxylase, the rate-limiting enzyme of fatty acid biosynthesis.

[37] Thus, both pathways utilizing acetyl-CoA for lipid synthesis are inactivated when energy charge is low in the cell, and concentrations of AMP rise.