ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are useful for a wide range od studies including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. Alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose, and become hyperinsulinemic . ALS/LtJ mice contain genes predisposing to both experimentally-induced type 1 and spontaneously-developing type 2 diabetes mellitus. ALS/Lt mice exhibit significantly lower antioxidant defenses than do ALR/Lt. ALS/Lt is a useful control strain for comparing inbred strain susceptibility to free radical-mediated damage.
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to three months of age and for Gnat2cpfl3, cone photoreceptor function loss 3, which affects bright light (photopic) vision.
ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males, which exhibit impaired glucose tolerance in the presence of low plasma insulin concentrations, alloxan-untreated ALS/LtJ males become hyperinsulinemic by 10 weeks of age and maintain hyperinsulinemia as they age. Four untreated males and three females in a research colony have spontaneously developed type 2 diabetes between nine to 32 weeks of age (EH Leiter, unpublished observations). ALS/LtJ mice thus contain genes predisposing to both experimentally-inducedtype 1 and spontaneously-developing type 2 diabetes mellitus. Since ALS/Lt mice exhibit significantly lower antioxidant defenses than do ALR/Lt, yet the two strains are closely related, ALS/Lt is a useful control strain for comparing inbred strain susceptibility to free radical-mediated damage.
Alloxan is a pancreatic beta cell-selective toxin that induces diabetes in rodents by generating cytotoxic free radicals. The ALS (alloxan-induced diabetes-susceptible) inbred strain was created in Japan by selective inbreeding of Crj:CD-1 (ICR) mice with selection for susceptibility to diabetes development after administration of alloxan at doses representing the ED50 for the original Crj:CD-1 strain (45 mg/kg in males, 47 mg/kg in females). These dosages are lower than what is necessary to elicit a strong diabetogenic response in most inbred strains, typically 60mg/kg. After a litter was born and weaned, the parents and some of the progeny were alloxan-treated to select for high versus low [ALR (alloxan-induced diabetes-resistant)] incidence lines based on blood glucose levels at 7 days post treatment. ALS and ALR inbred strains were obtained from Japan by Dr. EH Leiter (Lt) at The Jackson Laboratory in 1996. ALS/Lt and ALR/Lt mice were transferred to the production colony in 1998.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|Strain of Origin||multiple strains|
|Allele Name||cone photoreceptor function loss 3|
|Allele Synonym(s)||no cones|
|Gene Symbol and Name||Gnat2, guanine nucleotide binding protein, alpha transducing 2|
|Gene Synonym(s)||ACHM4; AW490837; GNATC; Gnat-2; Gnat-2; Gt-2; Tcalpha; expressed sequence AW490837|
|Strain of Origin||various|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of
each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders
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