De Novo Lipogenesis
De Novo Lipogenesis - Related Videos
12:11
Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes
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Cited by 39 •
2015
De novo lipogenesis and β-fatty acid oxidation constitute key metabolic pathways in hepatocyte, pathways that are perturbed in several metabolic disorders, including fatty liver disease. Here we demonstrate isolation of mouse primary hepatocytes and describe quantification of β-fatty acid oxidation and lipogenesis.
05:51
A Strategy to Identify de Novo Mutations in Common Disorders such as Autism and Schizophrenia
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Cited by 11 •
2011
Molecular genetic strategy for finding de novo mutations causing common disorders such as autism and schizophrenia.
10:41
Leveraging CyVerse Resources for De Novo Comparative Transcriptomics of Underserved (Non-model) Organisms
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Cited by 7 •
2017
This protocol outlines a comparative de novo transcriptome assembly and annotation workflow for novice bioinformaticians. The workflow is available for free entirely through CyVerse and connected by the Data Store. Command line and graphical user interfaces are used, but all code needed is available to copy and paste.
07:10
Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
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2025
This protocol describes an in vitro system to model de novo lytic infection of Kaposi's sarcoma-associated herpesvirus using BAC16-derived virions. The method enables investigation of early viral replication and dissemination. Infectious virus production is quantified by GFP-based infectious units assays and real-time PCR of encapsidated viral genomes.
08:48
Generating De Novo Antigen-specific Human T Cell Receptors by Retroviral Transduction of Centric Hemichain
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Cited by 3 •
2016
Herein we describe a novel method to generate antigen-specific T cell receptors (TCRs) by pairing the TCRα or TCRβ of an existing TCR, possessing the antigen-specificity of interest, with complementary hemichain of the peripheral T cell receptor repertoire. The de novo generated TCRs retain antigen-specificity with varying affinity.
FAQs
Acetyl-CoA carboxylase performs the committed conversion of glucose-derived acetyl-CoA into malonyl-CoA. Fatty acid synthase then uses acetyl-derived and malonyl-derived units to assemble palmitate. This division of labor connects precursor processing with chain construction, allowing cells to channel excess carbohydrate carbon toward a fatty acid that can later be modified or incorporated into triglyceride.
Malonyl-CoA links cytosolic acetyl-CoA availability to fatty acid chain synthesis. Its formation by acetyl-CoA carboxylase creates the substrate required for fatty acid synthase to extend the developing fatty acid chain toward palmitate. Because this intermediate sits between precursor supply and product formation, its production is an important control point for studying pathway activity.
Insulin and carbohydrate-responsive signaling adjust pathway activity according to nutritional and energetic conditions. When carbohydrate or energy intake exceeds immediate cellular needs, these signals support routing glucose-derived carbon into fatty acid synthesis. Examining this regulation helps explain why the liver and adipose tissue respond differently across metabolic states and how excess nutrient availability affects lipid storage.
The liver and adipose tissue are central tissues for examining this pathway because the overview identifies both as sites where its regulation and activity are relevant. Liver-focused studies can address conversion of excess carbohydrate into fatty acids, whereas adipose-focused studies can consider subsequent storage as triglyceride. Comparing these tissues clarifies tissue-specific roles in energy balance.
This pathway becomes especially informative when researchers examine conditions involving excess carbohydrate or energy intake, since synthesis can increase when immediate cellular needs are already met. Its study provides a framework for investigating how nutrient surplus becomes stored lipid and supports research on obesity, fatty liver disease, diabetes, and broader metabolic adaptation.
Research on de novo lipogenesis can connect nutrient conditions, signaling, fatty acid production, and triglyceride storage within a single metabolic framework. It helps explain how cells manage energy balance and how altered handling of excess carbohydrate may relate to obesity, fatty liver disease, or diabetes. The pathway also offers context for studying metabolic adaptation across tissues.