General Information:
Id: | 407 |
Diseases: |
Diabetes mellitus, type II
- [OMIM]
Fatty liver disease, nonalcoholic Insulin resistance |
Rattus norvegicus | |
male | |
adenoviral construct to overexpress hepatic GPAT1 (Ad-GPAT1) | |
article | |
Reference: | Nagle CA et al.(2007) Hepatic overexpression of glycerol-sn-3-phosphate acyltransferase 1 in rats causes insulin resistance J. Biol. Chem. 282 [PMID: 17389595] |
Interaction Information:
Comment | Hepatic overexpression of GPAT causes hepatic steatosis, hypertriglyceridemia, and muscle TAG accumulation. |
Formal Description Interaction-ID: 1752 |
|
Comment | Hepatic overexpression of GPAT causes hepatic steatosis, hypertriglyceridemia, and muscle TAG accumulation. |
Formal Description Interaction-ID: 1771 |
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Comment | Hepatic overexpression of GPAT1 causes insulin resistance, liver was the predominant site of insulin resistance. |
Formal Description Interaction-ID: 1788 |
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Comment | Rats overexpressing GPAT1 had 2.5-fold higher hepatic glucose-output than controls during a hyperinsulinemic-euglycemic clamp. |
Formal Description Interaction-ID: 1789 |
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Comment | Hepatic diacylglycerol and lysophosphatidate were elevated in Ad-GPAT1 rats, suggesting a role for these lipid metabolites in the development of hepatic insulin resistance, and hepatic protein kinase C-epsilon was activated, providing a potential mechanism for insulin resistance. |
Formal Description Interaction-ID: 1790 |
|
Comment | Hepatic diacylglycerol and lysophosphatidate were elevated in Ad-GPAT1 rats, suggesting a role for these lipid metabolites in the development of hepatic insulin resistance, and hepatic protein kinase C-epsilon was activated, providing a potential mechanism for insulin resistance. |
Formal Description Interaction-ID: 1791 |
|
Comment | Ad-GPAT1-treated rats had 50% lower hepatic NF-kappa-B activity and no difference in expression of tumor necrosis factor-alpha and interleukin-beta, consistent with hepatic insulin resistance in the absence of increased hepatic inflammation. |
Formal Description Interaction-ID: 1793 |
|
Drugbank entries | Show/Hide entries for TNF |
Comment | Ad-GPAT1-treated rats had 50% lower hepatic NF-kappa-B activity and no difference in expression of tumor necrosis factor-alpha and interleukin-beta, consistent with hepatic insulin resistance in the absence of increased hepatic inflammation. |
Formal Description Interaction-ID: 1796 |
|
Drugbank entries | Show/Hide entries for IL1B |
Comment | Ad-GPAT1-treated rats had 50% lower hepatic NF-kappa-B activity and no difference in expression of tumor necrosis factor-alpha and interleukin-beta, consistent with hepatic insulin resistance in the absence of increased hepatic inflammation. |
Formal Description Interaction-ID: 1797 |
|
Comment | Ad-GPAT1-treated rats had 50% lower hepatic NF-kappa-B activity and no difference in expression of tumor necrosis factor-alpha and interleukin-beta, consistent with hepatic insulin resistance in the absence of increased hepatic inflammation. |
Formal Description Interaction-ID: 1798 |
|
Comment | In rats overexpressing hepatic GPAT1 the glycogen synthesis and uptake of 2-deoxyglucose were reduced in skeletal muscle, suggesting mild peripheral insulin resistance associated with a higher content of skeletal muscle triacylglycerol. |
Formal Description Interaction-ID: 1799 |
gene/protein decreases_activity of process |
Comment | In rats overexpressing hepatic GPAT1 the glycogen synthesis and uptake of 2-deoxyglucose were reduced in skeletal muscle, suggesting mild peripheral insulin resistance associated with a higher content of skeletal muscle triacylglycerol. |
Formal Description Interaction-ID: 12710 |
gene/protein increases_quantity of drug/chemical compound |