40 kcal% Fat, 20 kcal% Fructose and 2 % Cholesterol Diet
40 kcal% Fat, 20 kcal% Fructose, and 2% Cholesterol Diet is a high-fat, high-fructose, and high-cholesterol diet that can be used to establish models of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Designed with similarities to Research Diets, Inc.formula D09100310.
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Induced Disease Models
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
Induction of Non-alcoholic Fatty Liver Disease (NAFLD)[1].
Administration: fed • every day for 25 weeks.
1) Blood samples were collected from all mice at 0 wk (right before starting 40 kcal% Fat, 20 kcal% Fructose and 2% Cholesterol Diet diet) and 25 wk (terminal stage) after 5 h fasting to evaluate biochemical changes in serum.
2) Change the diet every 2-3 days, discarding old feed.
3) Store refrigerated.
Histopathology: Induces hepatic steatosis and increase the amount of large fat droplets (LDF).
Serum biochemical: Significantly increases serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), low-density lipoprotein (LDL), and triglyceride levels. Furthermore, liver total cholesterol (TC) and liver free cholesterol (FC) are increased. and hepatic triglyceride levels are also elevated.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Appearance Solid
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Color Green to dark green
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SMILES
[40 kcal% Fat, 20 kcal% Fructose and 2 % Cholesterol Diet]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
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Data Sheet (272 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Soo-Mi Kweon, et al. Heterozygous midnolin knockout attenuates severity of nonalcoholic fatty liver disease in mice fed a Western-style diet high in fat, cholesterol, and fructose. Am J Physiol Gastrointest Liver Physiol . 2023 Aug 1;325(2):G147-G157. [Content Brief]
[2]. Zhang L, et al. High-Carbohydrate Diet Consumption Poses a More Severe Liver Cholesterol Deposition than a High-Fat and High-Calorie Diet in Mice. Int J Mol Sci. 2023 Sep 28;24(19):14700. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)