AI Article Synopsis
- The study examined how the lack of adiponectin affects PPARα expression and its possible role in diabetes using adiponectin knockout mice.
- Adiponectin knockout mice were created and tested at 10 weeks old for glucose and insulin tolerance, along with organ sampling to analyze various biochemical markers.
- Results showed that these mice had poor glucose tolerance and higher insulin resistance, likely due to decreased PPARα levels and increased concentrations of TNFα and free fatty acids.
Article Abstract
Expression of peroxisome proliferator-activated receptor (PPAR) α was investigated in adiponectin knockout mice to elucidate the relationship between PPARα and adiponectin deficiency-induced diabetes. Adiponectin knockout (Adp) mice were generated by gene targeting. Glucose tolerance test (GTT), insulin tolerance test (ITT), and organ sampling were performed in Adp mice at the age of 10 weeks. PPARα, insulin, triglyceride, free fatty acid (FFA), and tumor necrosis factor α (TNFα) were analyzed from the sampled organs. Adp mice showed impaired glucose tolerance and insulin resistance. Additionally, PPARα levels were decreased and plasma concentration of triglyceride, FFA and TNFα were increased. These data may indicate that insulin resistance in Adp mice is likely caused by an increase in concentrations of TNFα and FFA via downregulation of PPARα.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5938197 | PMC |
| http://dx.doi.org/10.1292/jvms.17-0641 | DOI Listing |
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