Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Feb 28;11(3):530.
doi: 10.3390/nu11030530.

In Vivo Rodent Models of Type 2 Diabetes and Their Usefulness for Evaluating Flavonoid Bioactivity

Jia-You Fang  1   2   3   4 , Chih-Hung Lin  5 , Tse-Hung Huang  6   7   8   9 , Shih-Yi Chuang  10
Affiliations
Review

In Vivo Rodent Models of Type 2 Diabetes and Their Usefulness for Evaluating Flavonoid Bioactivity

Jia-You Fang et al. Nutrients. .

Erratum in

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.

Keywords: animal model; antioxidant; flavonoid; type 2 diabetes.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.

Figures

Figure 1
Figure 1
Pathology of T2D. β cell dysfunction and insulin resistance occurs following insult from several genetic predisposition and environmental factors. Initially the β-cell compensates by increasing the release of insulin; however, over time this compensatory mechanism fails and reduction in β-cell mass is evident. The reduced plasma insulin results in an increase in glucose levels. Glucose-sensitive tissues, including liver, muscle, and adipocytes, are unable to accommodate the increased glucose concentration. Persistent glucose release preserves the hyperglycemic environment, leading ultimately to T2D.
Figure 2
Figure 2
Major advantages and disadvantages of different classes of animal models used in T2D research.
See this image and copyright information in PMC

References

    1. American Diabetes Association Diagnosis and classification of diabetes mellitus. Diabetes Care. 2010;33:S62–S69. doi: 10.2337/dc10-S062. - DOI - PMC - PubMed
    1. Bloomgarden Z. Questioning glucose measurements used in the International Diabetes Federation (IDF) Atlas. J. Diabetes. 2016;8:746–747. doi: 10.1111/1753-0407.12453. - DOI - PubMed
    1. Zheng Y., Ley S.H., Hu F.B. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat. Rev. Endocrinol. 2018;14:88–98. doi: 10.1038/nrendo.2017.151. - DOI - PubMed
    1. Atkinson M.A., Eisenbarth G.S., Michels A.W. Type 1 diabetes. Lancet. 2014;383:69–82. doi: 10.1016/S0140-6736(13)60591-7. - DOI - PMC - PubMed
    1. Schulz T.J., Zarse K., Voigt A., Urban N., Birringer M., Ristow M. Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab. 2007;6:280–293. doi: 10.1016/j.cmet.2007.08.011. - DOI - PubMed