CIDeRplusGeneral Information:
| Id: | 419 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mus musculus | |
| female | |
| GPAT1-/- mouse | |
| BTO:0000759 liver | |
| article | |
| Reference: | Hammond LE et al.(2007) Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice Exp. Mol. Pathol. 82: 210-219 [PMID: 17258706] |
Interaction Information:
| Comment | Liver mitochondria from GPAT1-/- mice have 20% higher rates of reactive oxygen species (ROS) production and peroxidation. |
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Formal Description Interaction-ID: 1831 |
gene/protein affects_quantity of drug/chemical compound Reactive oxygen species |
| Comment | The fatty acid composition of liver mitochondrial phospholipids is altered in GPAT1-/- mice. |
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Formal Description Interaction-ID: 1838 |
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| Comment | Despite the alterations in mitochondrial phospholipid fatty acid composition, liver mitochondrial morphology was not affected in the GPAT1-/- mice, there was no infiltration by inflammatory cells, the mitochondrial quantity did not differ, and the glycogen content was similar, the lipid droplets were less prominent, reflecting the lower hepatic triacylglycerol content. |
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Formal Description Interaction-ID: 1839 |
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| Comment | Despite the alterations in mitochondrial phospholipid fatty acid composition, liver mitochondrial morphology was not affected in the GPAT1-/- mice, there was no infiltration by inflammatory cells, the mitochondrial quantity did not differ, and the glycogen content was similar, the lipid droplets were less prominent, reflecting the lower hepatic triacylglycerol content. |
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Formal Description Interaction-ID: 1843 |
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| Comment | Despite the alterations in mitochondrial phospholipid fatty acid composition, liver mitochondrial morphology was not affected in the GPAT1-/- mice, there was no infiltration by inflammatory cells, the mitochondrial quantity did not differ, and the glycogen content was similar, the lipid droplets were less prominent, reflecting the lower hepatic triacylglycerol content. |
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Formal Description Interaction-ID: 1844 |
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| Comment | Despite the alterations in mitochondrial phospholipid fatty acid composition, liver mitochondrial morphology was not affected in the GPAT1-/- mice, there was no infiltration by inflammatory cells, the mitochondrial quantity did not differ, and the glycogen content was similar, the lipid droplets were less prominent, reflecting the lower hepatic triacylglycerol content. |
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Formal Description Interaction-ID: 1847 |
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| Comment | Despite the alterations in mitochondrial phospholipid fatty acid composition, liver mitochondrial morphology was not affected in the GPAT1-/- mice, there was no infiltration by inflammatory cells, the mitochondrial quantity did not differ, and the glycogen content was similar, the lipid droplets were less prominent, reflecting the lower hepatic triacylglycerol content. |
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Formal Description Interaction-ID: 1849 |
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| Comment | Liver mitochondria from GPAT1-/- mice are more sensitive to Ca2+-induced opening of the permeability transition pore. |
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Formal Description Interaction-ID: 1852 |
gene/protein affects_activity of complex/PPI Mitochondrial permeability transition pore complex |
| Comment | GPAT1-/- mice exhibit increased hepatocellular apoptosis and proliferation, but there was no difference in liver weight between wild-type and GPAT1-/- mice which suggested that the increase in apoptosis was balanced by hepatocellular proliferation. |
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Formal Description Interaction-ID: 1853 |
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| Comment | GPAT1-/- mice exhibit increased hepatocellular apoptosis and proliferation, but there was no difference in liver weight between wild-type and GPAT1-/- mice which suggested that the increase in apoptosis was balanced by hepatocellular proliferation. |
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Formal Description Interaction-ID: 1855 |
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| Comment | GPAT1-/- mice exhibit increased hepatocellular apoptosis and proliferation, but there was no difference in liver weight between wild-type and GPAT1-/- mice which suggested that the increase in apoptosis was balanced by hepatocellular proliferation. |
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Formal Description Interaction-ID: 1856 |
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