Type 2 Diabetes Mellitus Model

healthy young cynomolgus monkeys, male/female, adult, pre-screening 1.HGHFD feeding (12 months) 2.HGHFD feeding + STZ (6 months)

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Product Introduction

Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance and a progressive decline in pancreatic beta-cell function, leading to hyperglycemia. Unlike Type 1 diabetes, where insulin deficiency is the primary issue, T2DM is often associated with an initial period of compensatory hyperinsulinemia, followed by beta-cell exhaustion. T2DM is commonly associated with obesity, particularly central obesity, and is strongly linked to lifestyle factors such as a sedentary lifestyle and poor diet. It is the most prevalent form of diabetes, affecting millions of people worldwide and contributing to the development of serious complications such as cardiovascular disease, neuropathy, nephropathy, and retinopathy.

Cause: The development of T2DM is multifactorial, involving a combination of genetic, environmental, and lifestyle factors. The primary mechanisms include insulin resistance in peripheral tissues (particularly muscle, fat, and liver), which forces the pancreas to produce more insulin to maintain normal blood glucose levels. Over time, this compensatory mechanism fails, leading to a progressive decline in beta-cell function and subsequent hyperglycemia.

Genetic predisposition plays a significant role in T2DM, with several genes implicated in increasing susceptibility to the condition, particularly those involved in insulin signaling, beta-cell function, and glucose metabolism. Environmental factors, including poor diet (high in sugars and fats), obesity, and lack of physical activity, are major contributors to insulin resistance. Other risk factors include age, ethnicity, and the presence of comorbidities such as hypertension and dyslipidemia.

Diagnosing T2DM typically involves blood tests to measure fasting blood glucose, hemoglobin A1c, and an oral glucose tolerance test. Management of T2DM focuses on lifestyle interventions, such as diet and exercise, alongside pharmacological therapies like metformin, insulin, GLP-1 receptor agonists, and SGLT2 inhibitors to control blood sugar levels and prevent complications.

Advantages of Non-Human Primate (NHP) Models for T2DM Research:

1.Similar Metabolic Physiology to Humans: NHPs have a metabolic system that closely resembles that of humans, including insulin production, insulin resistance mechanisms, and glucose metabolism. This makes them highly relevant models for studying the pathophysiology of T2DM and evaluating the effects of therapies aimed at improving insulin sensitivity or beta-cell function.

2.Diet-Induced Diabetes Modeling: NHPs can develop T2DM when exposed to diets high in sugars and fats, similar to humans. This allows researchers to study diet-induced obesity, insulin resistance, and the progression of T2DM in a manner that is directly translatable to human populations at risk for the disease.

3.Longer Lifespan for Chronic Studies: The longer lifespan of NHPs compared to rodents enables long-term studies on the progression of T2DM and the effects of sustained interventions. This is particularly important for investigating chronic complications of diabetes and for testing the long-term efficacy and safety of new treatments.

4.Better Immune and Inflammatory Response Representation: T2DM is increasingly recognized as an inflammatory disease, and NHPs have an immune system that more accurately mimics the human immune response compared to rodents. This allows for more relevant studies of the interplay between inflammation, obesity, and insulin resistance in T2DM.

Advantages of NHP Models Compared to Mouse Models for T2DM Research:

1.Closer Similarity in Insulin Resistance and Beta-Cell Function: NHPs exhibit insulin resistance and beta-cell dysfunction in a manner that is much more similar to humans than mice. In mice, T2DM often requires genetic modifications to induce insulin resistance or beta-cell failure, and these models may not fully replicate the human disease.

2.More Relevant Metabolic and Obesity-Related Studies: NHPs develop diet-induced obesity and insulin resistance similarly to humans, whereas mice often do not develop the full spectrum of metabolic syndrome features, such as atherosclerosis and severe hyperglycemia, without genetic engineering. This makes NHPs more suitable for studying the effects of diet and lifestyle on T2DM.

3.Better Modeling of Long-Term Disease Progression: NHPs, with their longer lifespan and physiological similarities to humans, are better suited for studying the long-term progression of T2DM and its complications, such as cardiovascular disease and nephropathy. Mouse models often have shorter lifespans and may not accurately mimic the chronic nature of human T2DM.

4.More Accurate Testing of Therapeutic Interventions: Due to their similar physiology, NHPs are more reliable for testing new pharmacological therapies, including those targeting insulin resistance, beta-cell preservation, and glucose regulation. Findings from NHP models are more likely to be translatable to human clinical trials compared to those from mouse models, which often have differing responses to diabetes medications.