Abstract
Type II diabetes mellitus (T2DM) is a multifactorial disease involving complex genetic and environmental interactions. No single animal model has so far mirrored all the characteristics or complications of diabetes in humans. Since this disease represents a chronic nutritional insult based on a diet bearing a high glycemic load, the ideal model should recapitulate the underlying dietary issues. Most rodent models have three shortcomings: (1) they are genetically or chemically modified to produce diabetes; (2) unlike humans, most require high-fat feeding; (3) and they take too long to develop diabetes. By contrast, Nile rats develop diabetes rapidly (8–10 weeks) with high-carbohydrate (hiCHO) diets, similar to humans, and are protected by high fat (with low glycemic load) intake. This review describes diabetes progression in the Nile rat, including various aspects of breeding, feeding, and handling for best experimental outcomes. The diabetes is characterized by a striking genetic permissiveness influencing hyperphagia and hyperinsulinemia; random blood glucose is the best index of disease progression; and kidney failure with chronic morbidity and death are outcomes, all of which mimic uncontrolled T2DM in humans. Non-alcoholic fatty liver disease (NAFLD), also described in diabetic humans, results from hepatic triglyceride and cholesterol accumulation associated with rising blood glucose. Protection is afforded by low glycemic load diets rich in certain fibers or polyphenols. Accordingly, the Nile rat provides a unique opportunity to identify the nutritional factors and underlying genetic and molecular mechanisms that characterize human T2DM.
Highlights
The current increase in metabolic syndrome (MetS) and type 2 diabetes (T2DM) in the world population emphasizes the urgent need to understand the causes and mechanisms underlying the onset and progression of these metabolic disorders
MetS is characterized by insulin resistance with hyperinsulinemia, hypertension, depressed high-density lipoprotein (HDL), increased visceral adiposity, and fatty liver with increased plasma triglycerides (TG), which lead to rising blood glucose and T2DM if sustained [1,2]
Thisbeisathought the specificaseffects against Nile rat may in part reflectiontoofreflect the microbiome, the of microbiota because can metabolize estrogen-like compounds into biologically active forms and testosterone), promote sex hormones symptoms in males are exacerbated during puberty
Summary
The current increase in metabolic syndrome (MetS) and type 2 diabetes (T2DM) in the world population emphasizes the urgent need to understand the causes and mechanisms underlying the onset and progression of these metabolic disorders. Many models depend on specific genetic or chemical manipulations to induce symptoms, whereas gene x diet interactions (i.e., between susceptibility genes and a diabetogenic nutritional environment) are implicated in the human disease via an interaction similar to the etiology of T2DM and MetS in the Nile rat (Arvicanthis niloticus) [28]. This overview compares a selection of commonly used rodent models of MetS and T2DM, including the metagenetic physiology of diabetes in the Nile rat and how this model best fulfills the various criteria necessary for effective study of the onset and progression of the disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
