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Review
. 2019 Aug 28;8(9):1332.
doi: 10.3390/jcm8091332.

Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome-Strategies for In Vivo Administration: Part-II

Raquel Vieira  1 , Selma B Souto  2 , Elena Sánchez-López  1   3   4 , Ana López Machado  3 , Patricia Severino  5   6 , Sajan Jose  7 , Antonello Santini  8 , Amelia M Silva  9   10 , Ana Fortuna  11   12 , Maria Luisa García  13   14 , Eliana B Souto  15   16
Affiliations
Review

Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome-Strategies for In Vivo Administration: Part-II

Raquel Vieira et al. J Clin Med. .

Abstract

Diabetes is a complex disease characterized by hyperglycemia, together with polyuria, polydipsia, and polyphagia. While Type 1 diabetes mellitus (T1DM) results from genetic, environmental, or immune dysfunction factors leading to pancreatic β-cell destruction depriving the organism from endogenous insulin, Type 2 diabetes mellitus (T2DM) is characterized by peripheral insulin resistance. Depending on the type of diabetes mellitus and drug mechanism to study, the animal model should be carefully selected among the wide variety of the currently available ones. This review discusses the most common animal models currently employed to study T1DM and T2DM. Moreover, an overview on the administration routes that could be used is also discussed.

Keywords: administration routes; animal models; diabetes mellitus; in vivo.

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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, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Streptozocin diabetes induction model (based on [17]). (A) Single-dose Streptozocin, (B) Multiple-low dose streptozocin, (C) Streptozocin mechanism on the β-cells nucleus and side effects in other organs with glucose transporter subtype 2 (GLUT-2) receptors. Streptozotocin (STZ) behaves as a glucose analogue and is transported into the pancreatic β-cell by GLUT-2. It produced DNA alkylation and over-activation of poly-ADP ribose polymerase (PARP) causing NAD+ depletion, cellular ATP reduction, and compromising insulin.
Figure 2
Figure 2
Alloxan induced diabetes mechanism (based on [46]). Alloxan is reduced to dialuric acid and re-oxidized to alloxan producing alloxan radicals and reactive oxygen species (ROS) which undergo dismutation (by superoxide dismutase, SOD) to form hydrogen peroxide (H2O2). Hydroxyl radicals (*OH) may also be formed by side reactions. These *OH cause β-cell DNA fragmentation, leading to apoptosis.
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