Recently, a specific peptide inhibitor for ATGL was isolated from white blood cells, specifically mononuclear cells. This peptide was originally identifed as being involved in the regulation of the G 0 to G 1 transition of the cell cycle . This peptide was, therefore, called G0G1 switch protein 2 (G0S2). The protein is found in numerous tissues, with highest concentrations in adipose tissue and liver. In adipose tissue G0S2 expression is very low during fasting but increases after feeding. Conversely, fasting or PPARα-agonists increase hepatic G0S2 expression. The protein has been shown to localize to LDs, cytoplasm, ER, and mitochondria. These different subcellular localizations likely relate to multiple functions for G0S2 in regulating lipolysis, the cell cycle , and, possibly, apoptosis via its ability to interact with the mitochondrial antiapoptotic factor Bcl-2. With respect to ATGL regulation, the binding of the enzyme to LDs and subsequent is dependent on a physical interaction between the N-terminal region of G0S2 and the patatin domain of ATGL.
Actovegin is a deproteinated, pyrogen- and antigen-free hemodialysate of calf blood. It is manufactured from calf blood in several steps by ultrafiltration: here, the manufacturer uses different cut off sieves: first, an ultrafiltration step employing a cut off of 6 kD is performed, followed by a vacuum distillation step and removal of the precipitate by filtration ( urn) and titration to pH . Afterwards, the product is subjected to sterile filtration with prefilters of pm and pm and stored at 2-6 °C for more than 14 days and subsequently filtered ( pm) and again titrated to pH . After subsequent pH titration steps, the product is again subject to filtration (7 pm and pm) and another ultrafiltration step with a lOkDa cut off, followed by sterile filtration with prefilters of pm and pm. After another storage period at 2-6 °C for more than 56 days, the final precipitate is removed by filtration ( pm) and diluted to a nominal concentration to 200 mg/ml dry weight. Finally, deproteinization is completed by sterile filtration with prefilters of pm and pm. The analysis of the final product shows that it contains a mixture of natural substances: both inorganic components like common blood electrolytes (. chloride, phosphate, sodium, potassium, calcium, and magnesium, several sources for nitrogen, amino acids, peptides, glucose, acetate and lactate) and organic components like amino acids, a number oligopeptides, nucleosides, glycosphingolipids and products of the intermediary metabolism. 
Metabolism of ethanol by CYP2E1 also results in a significant increase in free radical and acetaldehyde production which, in turn, diminish reduced glutathione (GSH) and other defense systems against oxidative stress leading to further hepatocyte damage. Increased activity of CYP2E1 results in accelerated production of lipid hydroperoxides (designated LOOH in the Figure above) and is a significant contributor to the development of nonalcoholic fatty liver disease, NAFLD and nonalcoholic steatohepatitis, NASH. Both NAFLD and NASH are commonly associated with obesity , type 2 diabetes , and hyperlipidemia. Along with increased CYP2E1 activity there is an induction of microsomal enzymes involved in lipoprotein production, resulting in hyperlipemia which contributes to the development of NAFLD and NASH (discussed in more detail below).