The Influence of Genetic Background on the Susceptibility of Inbred Mice to Streptozotocin-induced Diabetes

Wolf, J; Lilly, Frank; Shin, Seung-Il

doi:10.2337/diab.33.6.567

Cited by 25 publications

(1 citation statement)

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“…Studies using STZ, HFD and high-fat high-sucrose diet induced rodent models have also been carried out to examine maternal pathologies during late onset of DM during pregnancy or GDM that may affect fetal outcomes (Pasek & Gannon, 2013; Pennington et al, 2017). Additionally, the influence of specific genetic background on the propensity to develop each types of diabetes is also being recognized in mouse models (Wolf et al, 1984; Leiter, 1989).…”

Section: Rodent Models To Study Mechanisms Associated With Matdmmentioning

confidence: 99%

Maternal hyperglycemia and fetal cardiac development: Clinical impact and underlying mechanisms

Basu

Garg

2018

Birth Defects Research

126

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Congenital heart disease (CHD) is the most common type of birth defect and is both a significant pediatric and adult health problem, in light of a growing population of survivors. The etiology of CHD has been considered to be multifactorial with genetic and environmental factors playing important roles. The combination of advances in cardiac developmental biology, which have resulted in the elucidation of molecular pathways regulating normal cardiac morphogenesis, and genome sequencing technology have allowed the discovery of numerous genetic contributors of CHD ranging from chromosomal abnormalities to single gene variants. On the other hand, mechanistic details of the contribution of environmental factors to CHD remain unknown. Maternal diabetes mellitus (matDM) is a well-established and increasingly prevalent environmental risk factor for CHD, but the underlying etiologic mechanisms by which pre-gestational matDM increases the vulnerability of embryos to cardiac malformations remains largely elusive. Here, we will briefly discuss the multifactorial etiology of CHD with a focus on the epidemiologic link between matDM and CHD. We will describe the animal models used to study the underlying mechanisms between matDM and CHD and review the numerous cellular and molecular pathways affected by maternal hyperglycemia in the developing heart. Lastly, we discuss how this increased understanding may open the door for the development of novel prevention strategies to reduce the incidence of CHD in this high-risk population.

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Section: Rodent Models To Study Mechanisms Associated With Matdmmentioning

confidence: 99%

Maternal hyperglycemia and fetal cardiac development: Clinical impact and underlying mechanisms

Basu

Garg

2018

Birth Defects Research

126

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Selective immunomodulation by the autoimmunity-inducing xenobiotics streptozotocin and HgCl2

et al. 1998

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Exposure to certain drugs and environmental chemicals can provoke the onset of autoimmune disease in susceptible individuals by releasing (self) epitopes for which tolerance has not been established, while simultaneously providing the necessary adjuvant activity. The resulting response type is influenced by the genotype of exposed individuals and relates to susceptibility to the adverse immune effects of the chemicals. Here, we assessed the modulatory role of the chemical compounds themselves. A single injection of streptozotocin (STZ) increased the number of CD8+ cells, macrophages, apoptotic cells, and IFN-gamma-producing T helper and T cytotoxic cells, whereas the number of CD4+ cells and B cells was reduced in the draining lymph node. Coinjection with the reporter antigen TNP-OVA resulted in primary and secondary production of TNP-specific antibodies that were predominantly of IgG2a and IgG2b isotype, whereas STZ did not enhance priming for delayed-type hypersensitivity (DTH) responses to TNP-OVA. Injection of HgCl2 on the other hand, reduced the number of IFN-gamma-producing cells, induced accumulation of B cells and CD4+ and CD8+ T cells, enhanced IgG1 and IgE production to TNP-OVA, and primed for secondary IgG1 and IgE production as well as for DTH reactions. Together these results indicate that a single injection of STZ stimulates type-1 responses, whereas HgCl2 enhanced mixed type-1 and -2 responses in BALB/c mice. These response types match the (auto)immune effects elicited to unknown (auto)antigens following multiple injections of these chemicals.

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Mouse Models for Studying Diabetic Nephropathy

Chow

Allen

2015

CP Mouse Biology

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Diabetic nephropathy (DN) is a term used to describe kidney damage cause by diabetes. With DN as one of the leading causes of end-stage renal disease worldwide, there is a strong need for appropriate animal models to study DN pathogenesis and develop therapeutic strategies. To date, most experiments are carried out in mouse models as opposed to other species for several reasons including lower cost, ease of handling, and easy manipulation of the mouse genome to generate transgenic and knockout animals. This unit provides detailed insights and technical knowledge in setting up one of the most widely used models of DN, the streptozotocin (STZ)-induced model. This model has been extensively exploited to study the mechanism of diabetic renal injury. The advantages and limitations of the STZ model and the availability of other genetic models of DN are also discussed.

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The Influence of Genetic Background on the Susceptibility of Inbred Mice to Streptozotocin-induced Diabetes

Cited by 25 publications

References 0 publications

Maternal hyperglycemia and fetal cardiac development: Clinical impact and underlying mechanisms

Maternal hyperglycemia and fetal cardiac development: Clinical impact and underlying mechanisms

Selective immunomodulation by the autoimmunity-inducing xenobiotics streptozotocin and HgCl2

Mouse Models for Studying Diabetic Nephropathy

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