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Genes involved in fat metabolism refers to a comprehensive set of genetic loci that encode the proteins responsible for the synthesis, transport, and breakdown of lipids in human physiology [1]. These genes include enzymes such as HMG-CoA Reductase (HMGCR) and Fatty Acid Synthase (FASN), as well as master transcriptional regulators like the Peroxisome Proliferator-Activated Receptors (PPARs) and Sterol Regulatory Element-Binding Proteins (SREBPs) [2]. The primary biological function of this gene set is to maintain lipid homeostasis, provide energy through beta-oxidation, and synthesize essential components for cellular membranes and signaling molecules [3]. Dysregulation of these genetic pathways is a primary driver of metabolic syndrome, obesity, non-alcoholic fatty liver disease (NAFLD), and atherosclerosis [4]. Therapeutic intervention is highly diverse, involving drugs that inhibit cholesterol synthesis (statins), enhance fatty acid oxidation (fibrates), or reduce fat absorption (orlistat) [5]. Because the term describes a broad biological process involving hundreds of distinct proteins rather than a single receptor or enzyme, it is considered a pathway-level classification rather than a discrete therapeutic target. [1] National Center for Biotechnology Information (NCBI) Genes and Disease; [2] UniProt Consortium; [3] StatPearls: Lipid Metabolism; [4] Nature Reviews Endocrinology: Lipid metabolism in disease; [5] PubChem: Lipid Modulating Agents.
HMG-CoA reductase inhibition, PPAR activation, Niemann-Pick C1-Like 1 (NPC1L1) inhibition, Gastric and pancreatic lipase inhibition, PCSK9 inhibition
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