EC Number   |
General Information |
Reference |
|---|
   3.1.1.34 | evolution |
phylogenetic tree based on lipoprotein lipase amino acid sequences |
749731 |
| 3.1.1.34 | malfunction |
acute hypoxia strongly inhibits lipoprotein lipase activity in differentiated human preadipocytes and increases non-esterified fatty acid release, adversely affecting postprandial lipemia. In differentiated preadipocytes, acute hypoxia induces a 6fold reduction in lipoprotein lipase activity. Acute intermittent hypoxia increases circulating plasma non-esterified fatty acid in young healthy men, but does not seem to affect postprandial triglyceride levels, nor subcutaneous abdominal adipose tissue lipoprotein lipase activity and adipocyte lipolysis. The reduction in adipose tissue LPL activity appears to be explained by the upregulation of an important posttranslational repressor of LPL, angiopoietin-like protein 4 (ANGPTL4) |
751424 |
| 3.1.1.34 | malfunction |
lipoprotein lipase (LPL) is increased during the onset of remyelination, which is associated with an anti-inflammatory reparative microglial phenotype, and may facilitate the uptake of myelin-derived lipids in the CNS |
750657 |
| 3.1.1.34 | malfunction |
lipoprotein lipase (LPL)-deficient cells show dramatically reduced expression of anti-inflammatory markers, YM1, and arginase 1 and increased expression of pro-inflammatory markers, such as iNOS compared to wild-type cells. LPL is increased during the onset of remyelination, which is associated with an anti-inflammatory reparative microglial phenotype, and may facilitate the uptake of myelin-derived lipids in the CNS |
-, 750657 |
| 3.1.1.34 | malfunction |
lipoprotein lipase knock-out mice die 18 h after birth, probably because of hypoglycemia |
715633 |
| 3.1.1.34 | malfunction |
selective loss of adipocyte enzyme in mice leads to mild hypertriglyceridemia. Enzyme-deficient mice display a profound increase in de novo lipogenesis-fatty acids, especially palmitoleate and myristoleate in brown adipose tissue and white adipose tissue depots while essential dietary fatty acids are markedly decreased. High fat diet-fed enzyme-deficient mice exhibit less adiposity and improved plasma adipokines but not increased glucose tolerance |
729291 |
| 3.1.1.34 | metabolism |
lipoprotein lipase (LPL) is a key enzyme in lipid deposition and metabolism. Nutritional regulation of LPL in redlip mullet |
749731 |
| 3.1.1.34 | metabolism |
lipoprotein lipase is a major enzyme in lipid metabolism responsible for the hydrolysis of the core triglycerides in chylomicrons and very low density lipoprotein and subsequent release of free fatty acids |
715633 |
| 3.1.1.34 | metabolism |
the phosphoinositide-3-kinase pathway is involved in the regulation of LPL gene transcription through Sp1/Sp3, signalling pathways that impact on the IFN-mediated regulation of Sp1/Sp3 binding and LPL gene transcription in macrophages, overview. The synergism between IFN- and TNF- on LPL gene transcription is not mediated at the level of Sp1/Sp3 DNA binding |
708067 |
| 3.1.1.34 | more |
enzyme ligand interaction analysis by isothermal titration calorimetry (ITC) using human plasma as substrate. ITC can be used for quantitative measurements of LPL activity and interactions under in vivo-like conditions, for comparisons of the properties of plasma samples from patients and control subjects as substrates for LPL, as well as for testing of drug candidates, method evaluation, overview |
751275 |
