The new total Western diet for rodents does not induce an overweight phenotype or alter parameters of metabolic syndrome in mice

Monsanto, Stephany P.; Hintze, Korry; Ward, Robert E.; Larson, Deanna; Lefevre, Michael; Benninghoff, Abby D.

doi:10.1016/j.nutres.2016.06.002

Cited by 23 publications

(39 citation statements)

References 31 publications

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“…As the potential interactions between diet and GTE were the key parameters of interest and because AOM is known to decrease body weight [28], these data were segregated by carcinogen treatment and analyzed separately by two-way ANOVA with appropriate posthoc tests. Consumption of TWD did not significantly affect body weight compared to mice fed AIN93G, an effect previously observed in C57BL/6J mice fed AIN93G and TWD for a similar timeframe [30]. Significant main effects of GTE on body weight (p = 0.0030 and 0.0131 for sham-and AOMinitiated mice, respectively) were likely driven by the marked decrease in body weight in mice fed the TWD (Fig 2C and D).…”

Section: Food Intake Gte Intake and Body Weightsupporting

confidence: 68%

Consumption of the total Western diet differentially affects the response to green tea in rodent models of chronic disease compared to the AIN93G diet

Ward

Benninghoff

Healy

et al. 2017

Molecular Nutrition Food Res

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Section: Food Intake Gte Intake and Body Weightsupporting

confidence: 68%

Consumption of the total Western diet differentially affects the response to green tea in rodent models of chronic disease compared to the AIN93G diet

Ward

Benninghoff

Healy

et al. 2017

Molecular Nutrition Food Res

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“…Major groupings include transcripts associated with cellular response to cytokine-mediated cell signaling and the STAT cascade (blue), antigen processing (yellow), cellular protein catabolic processes (red), regulation of granulocyte chemotaxis (green and purple). As we reported previously, mice consuming the DIO diet acquired an obesity/metabolic syndrome phenotype whereas consumption of the TWD did not significantly alter any biomarkers of metabolic health [36], a somewhat surprising observation considering that the TWD diet contains substantially more fat than the AIN93G diet (35% compared to 17% of total kcal, respectively). Thus, the colon tumor-promoting effect of the TWD was unrelated to a metabolic syndrome phenotype or systemic inflammation induced by consumption of a high fat diet.…”

Section: Experiments E: Immune-and Cancer-related Gene Expression and supporting

confidence: 66%

Consumption of the Total Western Diet Promotes Colitis and Inflammation-Associated Colorectal Cancer in Mice

et al. 2020

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Consumption of a Western type diet is a known risk factor for colorectal cancer. Our group previously developed the total Western diet (TWD) for rodents with energy and nutrient profiles that emulate a typical Western diet. In this study, we tested the hypothesis that consumption of the TWD would enhance colitis, delay recovery from gut injury and promote colon tumorigenesis.In multiple experiments using the azoxymethane + dextran sodium sulfate or Apc Min/+ mouse models of colitis-associated colorectal carcinogenesis (CAC), we determined that mice fed TWD experienced more severe and more prolonged colitis compared to their counterparts fed the standard AIN93G diet, ultimately leading to markedly enhanced colon tumorigenesis. Additionally, this increased tumor response was attributed to the micronutrient fraction of the TWD, and restoration of calcium and vitamin D to standard amounts ameliorated the tumor-promoting effects of TWD. Finally, exposure to the TWD elicited large scale, dynamic changes in mRNA signatures of colon mucosa associated with interferon (IFN) response, inflammation, innate immunity, adaptive immunity, and antigen processing pathways, among others. Taken together, these observations indicate that consumption of the TWD markedly enhanced colitis, delayed recovery from gut injury, and enhanced colon tumorigenesis likely via extensive changes in expression of immune-related genes in the colon mucosa.Nutrients 2020, 12, 544 2 of 35 characterizes these conditions is now recognized as an important factor in CRC due to its involvement in the disruption of the same oncogenic pathways that are disrupted in CRC [5]. The mutation of genes involved in the maintenance of the intestinal mucosal barrier that protects the intestinal wall from bacterial invasion contributes to both Crohn's and UC [6,7].Dysfunction of the intestinal mucosal barrier leads to sustained damage of gut epithelial cells. This chronic injury to the gut triggers a compensatory immune response characterized by the up-regulation of cell proliferation and anti-apoptotic pathways that promote cell survival [8]. Various molecules are involved in the activation of such pathways, including transcription factors (e.g., NF-κB, and STAT3) and various inflammatory cytokines (e.g., IL-6 and TNF-α), which are normally secreted during an inflammatory response. The resulting compensatory cell regeneration results in increased rates of mitosis that, when chronically active, increase DNA mutation rates [8,9]. Not only can this process promote the disruption of oncogenic pathways, but it can also provide cancerous cells with a nurturing environment due to the increased availability of proliferative and survival signals. This notion is supported by an animal study by Tanaka et al. [10], in which a combined treatment of the chemical carcinogen azoxymethane (AOM) with the inflammatory agent dextran sodium sulfate (DSS) significantly increased intestinal tumorigenesis in CD-1 mice. The AOM + DSS model yields a consistent, reproducible colon cancer outcome ...

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“…Surprisingly, TWD-fed mice did not show increase in energy intake, fat mass and BW and failed to acquire an MetS phenotype. 45 Hence, dietary micronutrients may play a major role in the hyperphagic response, increasing weight gain in mice. 45 Another attempt to more realistically replicate the human WD pattern in rodents involves the use of a new prototypic animal WD formulated with high amounts of simple CHO, salt and fat (42.5% kcal from fat), along with a low-fibre percentage.…”

Section: Diet As a Driving Force For The Continuum Of Obesity-relatmentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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Diet is a critical element determining human health and diseases, and unbalanced food habits are major risk factors for the development of obesity and related metabolic disorders. Despite technological and pharmacological advances, as well as intensification of awareness campaigns, the prevalence of metabolic disorders worldwide is still increasing. Thus, novel therapeutic approaches with increased efficacy are urgently required, which often depends on cellular and molecular investigations using robust animal models. In the absence of perfect rodent models, those induced by excessive consumption of fat and sugars better replicate the key aspects that are the root causes of human metabolic diseases. However, the results obtained using these models cannot be directly compared, particularly because of the use of different dietary protocols, and animal species and strains, among other confounding factors. This review article revisits diet-induced models of obesity and related metabolic disorders, namely, metabolic syndrome, prediabetes, diabetes and nonalcoholic fatty liver disease. A critical analysis focused on the main pathophysiological features of rodent models, as opposed to the criteria defined for humans, is provided as a practical guide with a translational perspective for the establishment of animal models of obesity-related metabolic diseases.

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The new total Western diet for rodents does not induce an overweight phenotype or alter parameters of metabolic syndrome in mice

Cited by 23 publications

References 31 publications

Consumption of the total Western diet differentially affects the response to green tea in rodent models of chronic disease compared to the AIN93G diet

Consumption of the total Western diet differentially affects the response to green tea in rodent models of chronic disease compared to the AIN93G diet

Consumption of the Total Western Diet Promotes Colitis and Inflammation-Associated Colorectal Cancer in Mice

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

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