Further long-term follow-up studies are required to validate ELF as a monitoring tool. Disclosures: Patrick J. McKiernan – Advisory Committees or Review Panels: Swedish Orphan Biovitrum AB The following people have nothing to disclose: Jeremy K. Rajanayagam, Andrew W. Lee “
“ABC, adenosine tri-phosphate

binding cassette; AMP, adenosine monophosphate; AMPK, AMP-activated selleck chemicals llc protein kinase; ANGPTL3, angiopoetin-like 3; CPT1a, carnitine palmitoyltransferase 1a; CROT, carnitine O-acetyltransferase; GPAM, glycerol-3-phosphate acyltransferase 1; HADHB, hydroxyacyl-CoA dehydrogenase beta subunit; HDL, high-density lipoprotein; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; Huh7, human hepatocarcinoma cell line; LPL, lipoprotein lipase;

miRNA, microRNA; PPAR, proliferator-activated receptor; TSP-1, thrombospondin-1. MicroRNAs (miRNAs) are endogenous ∼22 nucleotide (nt) RNAs that play essential gene-regulatory roles in animals and plants by pairing messenger RNAs (mRNAs) of protein-coding genes to direct their posttranscriptional repression by translational inhibition, deadenylation, and mRNA decay.1-3 The human genome is thought to encode over 1,000 miRNAs that regulate the expression of more than 60% of genes. Interestingly, a single miRNA may target multiple genes, potentially providing simultaneous regulation of the genes involved in a physiological pathway. In fact, the BGB324 in vitro complexity in higher organisms is thought to be achieved through sophisticated control and coordinated mechanisms carried out by noncoding

cAMP RNAs including miRNAs. MiRNAs have recently emerged as key regulators of lipid metabolism, playing major roles in regulating cholesterol and fatty acid metabolism.4 Among these, miR-122 was the most widely studied miRNA and the first described for its role in regulating total serum cholesterol and hepatic metabolism.5, 6 miR-122 is highly expressed in the liver, and it is estimated to account for ∼75% of all liver miRNAs. Inhibition of miR-122 using antisense oligonucleotides significantly reduces plasma cholesterol levels and reverses hepatic steatosis in mice fed a high-fat diet.6 Similarly, silencing of miR-122 in nonhuman primates results in a significant reduction in plasma cholesterol.7 In addition to miR-122, miR-33a/b have recently been discovered as main regulators of lipid homeostasis. miR-33a/b are miRNAs encoded in intron 16 and 17 of the Srebp-2 and Srebp-1 genes, respectively.8-13 miR-33a/b are cotranscribed with their host genes and target genes involved in cellular cholesterol export, including the adenosine triphosphate binding cassette (ABC) transporters ABCA1 and ABCG1, and fatty acid metabolism, including carnitine O-acetyltransferase (CROT), carnitine palmitoyltransferase 1a (CPT1a), hydroxyacyl-CoA dehydrogenase beta subunit (HADHB), and AMP-activated protein kinase (AMPK).