DGATs, lipid droplets and the biology of triglyceride storage

Robert Farese, Sloan Kettering Institute and Memorial Sloan Kettering Cancer Center, New York, USA, describes the catalysis of TG synthesis by diacylglycerol acyltransferase 1 and 2 (DGAT 1 and DGAT 2) in the endoplasmic reticulum and the packaging of TG into lipid droplets, and discusses recent studies targeting DGAT 2 to reduce TG and improve liver function in patients with metabolic dysfunction-associated steatotic liver disease (MAFLD).

Making the diagnosis of monogenic vs polygenic SHTG: Does it matter for drug therapy?

Robert Eckel, University of Colorado, Aurora, USA, explains that as the first novel TG lowering agents complete clinical trials and are approved, the importance of differentiating between monogenic and polygenic causes of severe hypertriglyceridaemia becomes increasingly important. He discusses the similarities and differences between the European and North American diagnostic scoring systems for familial chylomicronaemia syndrome.

Making the diagnosis of monogenic vs polygenic SHTG: Does it matter for nutritional therapy?

Alice Lichtenstein, Tufts University, Boston, USA, shows why a very low fat diet (10-15%) is key to management of monogenic severe hypertriglyceridaemia (SHTG), along with meeting essential fatty acid and fat soluble vitamin requirements, avoiding simple carbohydrates, and reducing alcohol. For those with polygenic SHTG, the emphasis is on a healthy weight, minimising alcohol intake and consuming moderate amounts of ‘healthy’ unsaturated fat.