Ketogenic diet fat threshold analysis in wild-type mice

Validation Score: 0.900 Price: $0.50 metabolic disease C57BL/6J wild-type mice Status: proposed

What This Experiment Tests

Validation experiment designed to validate causal mechanisms targeting Hmgcs2, Cd36, Cpt1a, Acat1 in C57BL/6J wild-type mice. Primary outcome: β-hydroxybutyrate levels and ketogenesis gene expression

Description

This experiment evaluated multiple ketogenic diet formulations with varying fat content (80-95%) in C57BL/6J wild-type mice to determine the fat threshold required for sustained ketosis. Researchers measured plasma, hepatic, and intestinal β-hydroxybutyrate (BHB) levels and assessed expression of ketogenesis and fatty acid oxidation genes including Cd36, Cpt1a, Acat1, and Hmgcs2. Body weight, adipose distribution, and liver morphology were monitored. The study found that only diets exceeding 85% fat induced robust ketogenesis with elevated BHB and hepatic upregulation of key metabolic genes, while moderate KDs (80-85%) failed to trigger ketosis and resembled standard high-fat feeding.

TARGET GENE
Hmgcs2, Cd36, Cpt1a, Acat1
MODEL SYSTEM
C57BL/6J wild-type mice
ESTIMATED COST
$0
TIMELINE
0 months
PATHWAY
ketogenesis, fatty acid oxidation
SOURCE
extracted_from_pmid_41156456
PRIMARY OUTCOME
β-hydroxybutyrate levels and ketogenesis gene expression

Scoring Dimensions

Info Gain 0.00 (25%) Feasibility 0.00 (20%) Hyp Coverage 0.00 (20%) Cost Effect. 0.00 (15%) Novelty 0.00 (10%) Ethical Safety 0.00 (10%) 0.900 composite

📖 Wiki Pages

cd36geneCD36 Protein (Cluster of Differentiation 36)proteinResearchersindexamyloid-beta-cellular-uptakemechanismAmyloid-beta Cellular Uptake PathwaymechanismLipid-Loaded Microglia (Foam Cells)cellInflammaging in NeurodegenerationmechanismMicroglia Activation MechanismmechanismMicroglial Phagocytosis in Neurodegenerationmechanismamyloid-responsive-microgliacell_typeneuroinflammationmechanismPPAR Signaling Pathway in NeurodegenerationmechanismMicroglia-Targeted Nanoparticles for CNS DeliveryideaPhagocytosis Modulation TherapytherapeuticMicroglia in Chronic Neuroinflammationcell

Protocol

Multiple KD formulations (80-95% fat) feeding with measurement of plasma, hepatic, and intestinal BHB levels and gene expression analysis

Expected Outcomes

Identification of fat threshold for sustained ketosis and associated metabolic changes

Success Criteria

Elevated BHB levels and upregulation of ketogenesis genes

Related Hypotheses (4)

Ketone Utilization Index as Metabolic Flexibility Biomarker0.829
Biphasic Ketogenic Intervention Protocol0.773
The Glial Ketone Metabolic Shunt Hypothesis0.608
Temporal Metabolic Window Therapy0.525

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