Teglicar (oral, 80 mg/kg, once a day, for 30 days or infusion, 5.3 mg/kg/h, for 3 h) reduces the endogenous glucose production (262%) without affecting peripheral glucose utilization in SD rats[1].
Teglicar (gavage, 50 mg/kg, single or long-term 100 mg/kg/day for 30 days) not affects heart 2-[3H]deoxyglucose uptake in C57BL6/J mice[1].
Teglicar (gavage, 50 mg/kg, twice a day, for 45 days) reduces postabsorptive glycemia (238%), water consumption (231%), and fructosamine (230%) in db/db mice[1].
Teglicar (30 mg/kg, twice a day, for 26 days) normalized glycemia (219%) and insulinemia (253%) and increases HTGC but not affects liver and peripheral insulin sensitivity in high-fat diet C57BL/6J mice[1].
Teglicar (oral, 50 μM, was added to the surface of fly food, 1, 8, 12, and 15 days) ameliorates the neurodegenerative phenotype in a drosophila Huntington's Disease Model by acting on the expression of carnitine-related genes[2].
| Animal Model: | SD rats[1] |
| Dosage: | 80 mg/kg, 5.3 mg/kg |
| Administration: | oral, 80 mg/kg, once a day, for 30 days or infusion, 5.3 mg/kg/h, for 3 h |
| Result: | Reduced basal insulin levels, showed a higher triglyceride and low glycogen content in the liver, without any change in liver weight.
Showed a rapid drop in glycemia, suppressed EGP (EGP2) diminished by 62% and not affected peripheral glucose utilization (GU).
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| Animal Model: | C57BL6/J mice[1] |
| Dosage: | 50 mg/kg, 100 mg/kg |
| Administration: | gavage, 50 mg/kg, single or long-term 100 mg/kg/day for 30 days. |
| Result: | Did not modify etomoxir-induced M-CPT1 inhibition and failed to determine significant changes in 2-DG heart uptake, heart weights, and triglyceride content. |
| Animal Model: | db/db mice[1] |
| Dosage: | 50 mg/kg |
| Administration: | gavage, 50 mg/kg, twice a day, for 45 days |
| Result: | Induced a significant reduction of postabsorptive serum glucose, reduced serum fructosamine and average daily water consumption, increased Serum FFAs, but did not change insulin levels, triglycerides, alanine aminotransferase, also induced a significant reduction of glucose AUC during ITT.
Did not induce any variation in the content of PPAR-α and its target gene product MCAD and peroxisomal b-oxidation in liver and heart of db/db mice.
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| Animal Model: | High-fat diet C57BL/6J mice[1] |
| Dosage: | 30 mg/kg |
| Administration: | 30 mg/kg, twice a day, for 26 days |
| Result: | Did not affect food intake, did not change body weight and serum FFAs and triglycerides and did not affect glucose intolerant. |
