Abstract
About 40% of the world’s population is overweight or obese and exist at risk of developing type 2 diabetes mellitus (T2D). Obesity is a leading pathogenic factor for developing insulin resistance (IR). It is well established that IR and a progressive decline in functional β-cell mass are hallmarks of developing T2D. In order to mitigate the global prevalence of T2D, we must carefully select the appropriate animal models to explore the cellular and molecular mechanisms of T2D, and to optimize novel therapeutics for their safe use in humans. Flavonoids, a group of polyphenols, have drawn great interest for their various health benefits, and have been identified in naturally occurring anti-diabetic compounds. Results from many clinical and animal studies demonstrate that dietary intake of flavonoids might prove helpful in preventing T2D. In this review, we discuss the currently available rodent animal models of T2D and analyze the advantages, the limitations of each T2D model, and highlight the potential anti-diabetic effects of flavonoids as well as the mechanisms of their actions.
Highlights
A lack of functional leptin in these animals causes hyperphagia and subsequent obesity. These models include the Lepob/ob mouse [38,39,40], which is deficient in leptin, and the Leprdb/db mouse and Zucker Diabetic Fatty (ZDF) rat, which are deficient in the leptin receptor [41,42]
ZDF rats derived from a mutation in the Zucker Fatty (ZF) rat strains exhibit less obesity than the ZF rats but have more severe insulin resistance (IR), which they are unable to compensate for due to increased apoptosis levels in β-cells; they are widely used for research on type 2 diabetes mellitus (T2D) [51]
T2D is increasing in prevalence worldwide, and is strongly associated with obesity and IR, as well as defects in pancreatic β-cell function and mass, precipitating a disease characterized by impeding the critical regulatory influence of insulin on glucose, lipid and protein metabolism [69]
Summary
Diabetes mellitus is a chronic metabolic disease that is characterized by a relative lack of insulin, resulting in hyperglycemia. T2D is characterized insulin (IR) and theofpancreatic β-cell failure to sufficiently T2D are determine an individual’s response environmental changes, the main drivers of the animal global the rise in obesity, a sedentary lifestyle,toenergy-dense diets, and population ageing. Epidemic aretothe rise inmodels obesity, lifestyle, energy-dense diets,animal and population models ofofT2D tend include of a IRsedentary and/or models of β-cell failure. The β-cell compensates increasing the release several genetic predisposition and environmental factors. Glucose-sensitive tissues, includingenvironment, liver, muscle, and adipocytes, unable to accommodate the release preserves the hyperglycemic leading toare increased glucose concentration. Persistent glucose release preserves the hyperglycemic environment, leading to T2D
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