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Obesity and DiabetesDiabetic Wound HealingDiet-Induced NASH (AMLN)
Metabolic DiseaseBioModels has extensive experience with a variety of preclinical animal models that capture critical mechanisms of metabolic disease.
Assess your experimental materials for efficacy and mechanism of action in BioModels’ preclinical obesity models. Obesity is characterized by having excess body fat and is a medical problem that can lead to heart disease, diabetes, high blood pressure, as well as a number of other pathologies. With the advent of new GLP-1 agonists, obesity research has never been more active. BioModels’ obesity models capture a spectrum of disease mechanisms, allowing you to select the model most relevant for your hypothesis. The BioModels team is experienced with numerous preclinical obesity models, including genetic and diet-induced (DIO) models.
Experimental endpoints for these models include:
Assess your experimental materials for efficacy in BioModels’ established diabetic wound healing models. Diabetes mellitus defines a group of metabolic disorders characterized by chronic hyperglycemia due to impaired insulin secretion systems or dysregulated insulin sensitivity in an individual. The global prevalence of diabetes and diabetes-related complications (e.g. diabetic ulcers) has increased exponentially over the past several decades, creating a clear need for the development of novel therapeutics in this space.
BioModels has experience with a variety of in vivo models to simulate Type I and Type II diabetes as well as the diabetic wound healing process that can be used to validate compounds in a pre-clinical setting with customizable, experimental endpoints such as:
Assess your experimental materials for efficacy and mechanism of action in BioModels’ Diet-Induced NASH model. Nonalcoholic steatohepatitis (NASH), the most severe form of nonalcoholic fatty liver disease (NAFLD), is a condition in which the liver builds up excessive fat deposits, potentially resulting in fibrosis, cirrhosis, and hepatocellular carcinoma.
Experimental endpoints for these models include:
Study Models
There are several well characterized, genetic rodent models of obesity that can be used to identify factors that are contributing to obesity and to assess novel therapeutics for their potential in treating this metabolic disorder. Additionally, many of these models also exhibit spontaneous Type 1 and Type 2 diabetes and display delayed wound healing. Some of these preclinical models include Zucker rats (T1D), ZDF rats (T2D), ob/ob mice (T2D) and db/db mice (T2D). BioModels can provide the expertise necessary to design and execute an obesity study that is customized to meet your specific needs with flexible experimental endpoints.
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Macronutrients of rodent chow can be manipulated to introduce specific levels of dietary fat. Rodents placed on a diet that provides at least 30% of total daily energy intake from fat provide a translational preclinical model of obesity (western diet). These models can be used to identify specific mechanistic factors that are contributing to diet-induced obesity and to assess novel therapeutics (e.g- GLP-1 agonists) for their potential in treating this metabolic disorder. BioModels can provide the expertise necessary to design and execute a diet induced obesity model that is customized to meet your specific needs with flexible experimental endpoints.
Animals maintained on a control or high-fat diet are weight daily, and percent weight change as compared to Day 0 is calculated. The AUC is calculated to compare treatment arms and is shown in the inset. (***p<0.001).
Animals maintained on a control or high-fat diet underwent a dual-energy X-ray absorptiometry (DEXA) scan to assess bone density, bone mineral content, and bone area. (**p<0.01).
Animals maintained on a control or high-fat diet underwent a dual-energy X-ray absorptiometry (DEXA) scan to assess lean tissue mass, fat tissue mass, and percent body fat. (***p<0.001; ****p<0.0001).
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The Streptozotocin-induced diabetes model is a well published diabetes model in the field that is frequently used in preclinical drug development. Streptozotocin is an antibiotic derived from Streptomyces achromogenes that preferentially targets and destroys insulin-secreting pancreatic β cells and can be used to induce a hyperglycemic state in rodents. These models are characterized by altered blood glucose and insulin levels and can be used to assess disease pathology or to screen potential therapeutic compounds.
Streptozotocin-induced animals are weighed daily, and percent body weight change relative to Day 0 is calculated. The AUC is calculated to compare groups and is shown in the inset. (****p<0.0001).
Blood glucose levels are monitored using a blood glucose reader. The AUC is calculated to compare groups and is shown in the inset. (*p<0.05; ****p<0.0001).
Day 14 Blood glucose and blood insulin levels were measured via glucose monitor and ELISA, respectively. (****p<0.0001).
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Study Models
There are several well characterized, genetic rodent preclinical models of spontaneous Type I and Type II diabetes including the Zucker fatty rat (T1D), the ZDF rat (T2D), the ob/ob mouse (T2D), and the db/db mouse (T2D) that recapitulate autoimmune aspects of the human disease. Often, animals with these genetic backgrounds display delays in wound healing. Both splinted and non-splinted diabetic wound healing models are available. Splinted models allow you to test your treatment in the absence of wound contraction that is often observed in rodents. BioModels has the expertise and experience to help you select the model that will be most appropriate for your goals of testing novel therapeutics, assessing specific mechanisms of the metabolic disorder, or addressing certain medical complications that arise in diabetic patients.
Animals with splinted wounds are weighed daily and percent body weight change relative to Day 0 is calculated. The AUC is calculated to compare groups and is shown in the inset. (****p<0.0001).
Pre-study and terminal blood glucose levels were measured via glucose monitor. (****p<0.0001).
Wound healing is measured with calipers three times per week during study. The AUC is calculated to compare groups and is shown in the inset. (***p<0.001).
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Study Models
Feeding mice an Amylin liver NASH (AMLN) diet leads to obesity, fatty liver, and after longer amounts of time, both liver inflammation and fibrosis. Animals maintained on this diet are a widely used model for nonalcoholic steatohepatitis (NASH). This model is often referred to as the Gubran Amylin NASH (GAN) diet of obesity/NASH.
Liver samples from control and NASH diet-fed animals (either 40 or 53 weeks on diet) are processed for histopathology for determination of NAFLD Activity Score (H&E) and collagen content (PSR). Sum of steatosis grade (0-3), lobular inflammation (0-3), and ballooning degeneration (0-2) was calculated with a total range of 0-8 to determine NAFLD Activity Score. Central vein (C) and portal tract (P) are indicated. Macrovesicular (black arrow) and microvesicular (black arrowhead) steatosis are indicated. Percent collagen (PSR) positive area was calculated by taking the quotient of total positive area (um2) over the total area of the hepatic ROI (um2). (**p<0.01 compared to the control diet group). Histopathology performed by Dallas Tissue Research.
NASH diet-fed animals (either 40 or 53 weeks on diet) and control-diet fed animals had body composition analysis performed using a DEXA Scanner. Increases in Fat and Total Tissue are observed in NASH Diet-fed animals (*p<0.05 compared to the control diet group).
NASH diet-fed animals (either 40 or 53 weeks on diet) and control-diet fed animals had blood collected and assessed for levels of Alanine transaminase (ALT), Aspartate transaminase (AST), and Alkaline.
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