Ace Therapeutics is a dedicated preclinical contract research provider specializing in obesity research. Our commitment lies in designing and executing rigorous, scientifically driven studies using established animal models to support early-stage drug discovery. One of our core service offerings involves the utilization of the ob/ob Mouse Model, a well-recognized genetic model of leptin-deficient obesity. This model is instrumental in simulating key aspects of metabolic dysregulation, providing a robust platform for evaluating potential therapeutic interventions in obesity research.
The ob/ob Mouse Model is characterized by a mutation in the leptin gene, leading to a state of leptin deficiency. This genetic alteration results in hyperphagia, marked weight gain, and metabolic disturbances that mimic several aspects of human obesity. By leveraging this model, researchers can gain valuable insights into the pathophysiology of obesity and explore the underlying mechanisms contributing to metabolic dysfunction.
Key advantages of the ob/ob Mouse Model include:
Fig.1. Liver glucose metabolism in the Lep ob/ob (ob/ob) obesity and type II diabetes mouse model. (Williams, H. C. et al. 2020)
Ace Therapeutics designs studies to address your specific research objectives, ensuring alignment with therapeutic mechanisms and regulatory expectations.
Below is a summary of key model validation data for the DIO Mouse Model, outlining observed changes in critical metabolic and physiological parameters that confirm its effectiveness in mimicking obesity phenotypes:
Parameter | Observed Change | Validation Notes |
Weight Gain | Significant increase relative to controls | Consistent weight gain attributed to hyperphagia |
Adiposity | Marked increase in fat mass | Quantifiable through imaging and post-study analysis |
Glucose Tolerance | Impaired compared to lean controls | Reflects metabolic dysfunction typical of obesity |
Insulin Sensitivity | Reduced sensitivity observed | Indicative of the insulin resistance seen in leptin deficiency |
Serum Lipids | Elevated cholesterol and triglycerides | Critical for assessing dyslipidemia |
Note: Values and observations are averages derived from multiple validation studies and can vary based on experimental conditions.
Ace Therapeutics offers a suite of complementary models to address diverse research needs:
Our services facilitate the evaluation of diverse therapeutic modalities:
What distinguishes the ob/ob mouse model from other obesity models?
The ob/ob mouse lacks functional leptin, leading to spontaneous obesity without dietary manipulation. This genetic model is ideal for studying leptin-independent pathways and severe metabolic dysfunction.
How does the ob/ob Mouse Model benefit preclinical studies?
This model provides an in vivo platform that closely mimics aspects of leptin-deficient obesity observed in humans. Its well-characterized metabolic profile allows researchers to evaluate the efficacy and safety of potential therapeutic compounds in a controlled environment.
How does Ace Therapeutics ensure study relevance to human obesity?
We focus on translational endpoints such as glucose homeostasis, lipid metabolism, and adipose tissue biology—key factors in human obesity. Our protocols are designed to mirror clinical dosing and therapeutic scenarios.
Can you accommodate studies combining the ob/ob model with other interventions?
Yes. We design studies integrating genetic models with dietary or pharmacological challenges to evaluate combination therapies or multifactorial mechanisms.
What types of studies can Ace Therapeutics conduct using the ob/ob Mouse Model?
Our services encompass a broad range of preclinical studies, including metabolic assessments, dose-response evaluations, and detailed biochemical and histopathological analyses. We tailor each study to address specific research questions and experimental endpoints.
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