ALS/LtJ and ALR/LtJ (Stock No. <a href="https://www.jax.org/strain/003070">003070</a>) 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 <i>H2<sup>nb1</sup></i> 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females in a research colony have spontaneously developed type 2 diabetes between nine to 32 weeks of age (EH Leiter, unpublished observations).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.

ALS/LtJ and ALR/LtJ (Stock No. <a href="https://www.jax.org/strain/003070">003070</a>) 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.

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