In Vivo Pharmacology Services at JAX performs efficacy studies using the spontaneous NOD/ShiLtJ (001976) and STZ-inducible Type 1 Diabetes mouse models.
Type 1 diabetes (T1D), also called insulin-dependent diabetes mellitus (IDDM), is characterized by the autoimmune destruction of pancreatic beta cells. As a result, patients produce inadequate amounts of insulin. In Vivo Pharmacology Services at JAX performs efficacy studies using the spontaneous NOD/ShiLtJ (001976) and STZ-inducible Type 1 Diabetes mouse models.
|Phenotype||STZ Models C57BL/6J (JR# 000664) Inducible||NOD/ShiLtJ (JR# 001976) Spontaneous||Method|
|Pancreatic Lymph Node Phenotyping||x||✓||Flow Cytometry|
|Serum Cytokines||x||✓||Meso Scale Discovery|
|Pancreatic Islet Phenotyping||✓||✓||qPCR/Simple Wes|
|Pancreatic B-Cell Apoptosis||✓||✓||TUNEL IHC|
|Diabetic Retinopathy||✓||x||Retinal Flat Mount Staining and Microscopy|
|Diabetic Nephropathy||✓||x||Urine ACR/Kidney Pathology|
Figure 1. STZ induces Type 1 Diabetes in C57BL/6J male mice. STZ-treated mice (n=8) exhibited higher blood glucose levels compared with vehicle-treated mice (n=4). *p<0.05; **p<0.01.
Figure 2. Oral glucose tolerance test and serum insulin assessment in STZ-induced Type 1 Diabetes mice. On study day 21, blood glucose levels were determined prior (T0) and after 15, 30, 60 and 120 min post-glucose administration in STZ-induced Type 1 Diabetes and non-diabetic control mice. STZ-treated mice exhibited higher blood glucose levels compared to vehicle-treated mice. ** p<0.01. Sera insulin was determined at 0 and 5 min post glucose administration. STZ-treated mice exhibited lower serum insulin values compared to vehicle- treated mice.
Figure 4. Diabetes Incidence. DIDS treatment decreases blood glucose levels and delays the onset of diabetes.
Figure 5. Blood Glucose. anti-CD3 treatment in NOD/ShiLtJ diabetic mice decreases blood glucose levels.