TD.88137 - Western Diet (Stocked)

TD.88137 was developed more than 35 years ago, incorporating characteristics of a "western diet" that promotes and accelerates the development of atherosclerosis in ApoE and Ldlr deficient mouse models. The key factors driving phenotype development include cholesterol, saturated fat (comprising over 60% of the total fat), along with high total fat (45% kcal), 0.2% total cholesterol, and sucrose (34% wt/wt), which promote fat synthesis.

Extensively cited, TD.88137 remains one of our most widely used high-fat diets. Popular modifications of TD.88137 involve adjusting the concentrations of total cholesterol, fat, and/or sucrose. With its multifaceted nature, TD.88137 has also been used in diet induced obesity and MASLD research.

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Atherogenic

ApoE Deficient Models

After 10 days, animals exhibit increased total adipose tissue, heavier liver weight, and overall weight gain compared to control animals¹
In 3 weeks, plasma cholesterol triples to >1500 mg/dL^2,3
Within 6-10 weeks, foam cell and lesion development occurs; following 15 weeks fibrous plaque formation and fibrous cap development is observed^2,4

Ldlr Deficient Models

In 2 weeks, plasma cholesterol increases to >800 mg/dL and triglycerides increases to >300 mg/dL⁶
In 8 weeks, foamy macrophages and atherosclerosis is reported⁷
Within 6-10 weeks, foam cells, hyperglycemia, hyperinsulinemia, dyslipidemia, and lesion development is observed^8,9
In 16 weeks, atherosclerotic lesions and hypertension are observed¹⁰

Reference List

Diet Induced Obesity

C57BL/6 Models

After 3 weeks, male and female mice had greater inflammatory cell infiltration around airways and blood vessels, a more severe degree of inflammation, and more pronounced neutrophilic infiltration in lung tissues compared to control groups¹¹
After 4 weeks, male and female mice developed obesity, increased sphingolipids and pro-inflammatory cytokine circulation (males only)¹²
After 8 weeks, increased circulating non-esterified free fatty acids, triglycerides, CD4+ and CD8+ T cells were reported¹³
After 14 weeks, females exhibited significant increases in body weight compared to control mice¹⁴

Reference List

MASLD*

C57BL/6 Models

After 8 weeks, maternal fed diet increased hepatic macrophage infiltration, inflammation in bone marrow-derived macrophages, fibrosis genes, and macrophage immune tolerance adult offspring¹⁵
After 20 weeks, male mice exhibited increased free fatty acid circulation and mild steatosis¹⁶
After 52 weeks, males developed obesity, liver injury, dyslipidemia, and insulin resistance¹⁷

* Primarily for MASLD; for MASH-like phenotype expression, feed more than 36 weeks

Reference List

Control Diets

The magnitude of differences observed between control and experimental groups may be influenced by the choice of control diet, as natural ingredient diets (chow) may be associated with greater inter-individual variability in body weight compared to purified diets.

Ingredient matched, low fat purified diets

The diets below control for the type of ingredients (ingredient-matched), non-nutritive components, and the source and level of specific nutrients.

Diet	Kcal/g	Fat, % by weight	%, Kcal from fat	Fat sources, % by weight	Sucrose, % by weight
TD.05230	3.7	5.2	12.6	3.7% milk fat, 1.3% soybean oil	34.1
TD.08485	3.6	5.2	13.0	3.7% milk fat, 1.3% soybean oil	12.0

Natural ingredient diets

These diets, also known as standard diets or chows, vary in the source and amount of nutrients, as well as the presence of non-nutritive factors (like phytates or phytoestrogens), when compared to TD.88137. Natural ingredient diets limit inferences to differences in dietary pattern versus specific dietary components.

To explore available options, please visit our standard natural ingredient diets.