Dysglycemia and Dyslipidemia Models in Nonhuman Primates: Part IV. Pancreatic Beta Cell Dysfunction and Diabetes Progression

Abstract

Diabetes mellitus, hyperglycemia and polyuria, results from the body either producing insufficient insulin or using the produced insulin inefficiently to metabolize glucose. Type I diabetes mellitus (T1DM) is recognized as reduction of beta-cell mass mostly due to autoimmune destruction. However, insulin resistance and beta-cell dysfunction or loss are potentially the main causes of Type II diabetes mellitus (T2DM). Due to long-term hyperglycemia and microvascular impairment, complications are common, including heart, kidney, liver and other organs. Therefore, diabetic patients have the overall high risk of dying prematurely by heart attack, stroke, liver dysfunction and kidney failure. Diabetes has become one of the major global threats to human health. Development of safe and potent therapeutics is thus urgently needed. Animal models remain irreplaceable for discovering, validating and optimizing novel therapeutics for their safe use in clinics. Selection of appropriate animal models is critical for obtaining crucial data to translate preclinical research to clinical trial. It has been recognized that the pancreas structure and pathophysiology in rodents greatly differ from those in humans, but in nonhuman primates (NHPs) are more similar to humans. Many researchers have used spontaneously developed or drug-induced diabetic NHPs as the models to investigate diabetes progression and novel therapies. This article summarized some characteristics of the disease progression in a large pool of diabetic NHPs.