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LPL encodes lipoprotein lipase, which is expressed in heart, muscle, and adipose tissue. LPL functions as a homodimer, and has the dual functions of triglyceride hydrolase and ligand/bridging factor for receptor-mediated lipoprotein uptake. Severe mutations that cause LPL deficiency result in type I hyperlipoproteinemia, while less extreme mutations in LPL are linked to many disorders of lipoprotein metabolism. , quantitative-transmission/disequilibrium-test analyses showed that there was linkage between DBP and two single nucleotide polymorphisms in the LPL gene. APOC3, LPL and GpIIIa genes were found to be associated with BP levels. The contributions of these genes, although modest, are consistent with the polygenic nature of blood pressure levels. Activity may explain the difference in LDL lipoprotein size in diabetic and nondiabetic people. Beta-cell LPL has two physiologically relevant effects in islets, the inverse regulation of glucose metabolism and the independent mediation of insulin secretion through effects distal to membrane depolarization. Data show that human lipoprotein lipase significantly inhibited spontaneous human natural killer cells, but not lymphokine-activated killer cytotoxic activity against bovine pulmonary endothelial cells. Early recognition of severe hypertriglyceridemia in pregnancy may be caused by heterozygosity of this enzyme. H+ allele of the lipoprotein lipase gene HindIII polymorphism is associated with higher plasma triglyceride and lower HDL-cholesterol levels in Chinese patients with early-onset diabetes. In Japanese, poorly controlled type 2 diabetic men had more unfavorable lipid profile than did women counterparts, which may be associated with decreased plasma LPL levels. In Polish LPL-H (G) allele carriers, obesity correlated with free fatty acid tolerance in males, and insulin resistance in females. In the ET state, only the gender difference in mLPL mRNA persisted. FAT/CD36 protein in muscle was higher in women than in men, irrespective of training status. Increased LPL activity improves insulin resistance and reduces adipose accumulation in transgenic rabbits. Increased expression after weight loss may contribute to lower plasma ldl cholesterol and triglycerides in obese premenopausal women. LPL 44X alleles were associated with moderately increased LDL peak particle size. LPL could play a key role in the differentiation of Neuro-2A cells and in the pathophysiological effects of oxidative stress in several neurodegenerative disorders. LPL enzyme activities in 28 healthy subjects with well-controlled Type 1 diabetes, and their relationship with Lp(A-I) and Lp(A-I,A-II). LPL enzyme deficiency causes elevated plasma triglyceride level and subsequent insulin resistance; increased free fatty acids combined with insulin resistance promote gluconeogenesis and hyperglycemia, a vicious circle leading to type 2 diabetes. LPL gene and associated regions might contribute to individual blood pressure variation and hypertension in the Chinese population. LPL has a role in atherosclerosis, chylomicronaemia, obesity, Alzheimer's disease, and dyslipidaemia associated with diabetes, insulin resistance, and infection [review]. LPL is bound to postprandial triglyceride-rich lipoproteins and mediates their hepatic clearance in vivo. LPL lipolysis of emulsion triolein was retarded in chylomicron-free human plasma compared with the hydrolysis activated by isolated apolipoprotein C-II. LPL may represent a link between low adiponectin levels and dyslipidemia in both nondiabetic individuals and patients with type 2 diabetes. LPL-mediated fatty acid uptake is an inefficient process, but may be more efficient in muscle than in adipose tissue. Lipoprotein lipase gene polymorphisms might be involved in predisposition to coronary artery disease. Low mass in preheparin serum of type 2 diabetes mellitus patients and its recovery with insulin therapy. Macrophage LPL activity correlated with body mass index and fat mass. Incubation of patient macrophages with IGF-I for 24 h or differentiation of monocytes from GH-deficient patients into macrophages in presence of this growth factor decreased LPL. Maturation of lipoprotein lipase in the endoplasmic reticulum. Muscle can synthesize tethered, dimeric LpL, but efficient production of this enzyme leading to secretion, and physiological function appears to favor secretion of a noncovalent dimer composed of monomeric subunits. Peroxisome proliferator-activated receptor (PPARalpha and PPARgamma) agonists decrease lipoprotein lipase secretion and glycated LDL uptake by human macrophages. SNP analysis did not provide substantial evidence of an association between polymorphisms in the LPL gene and hypertension status and/or blood pressure levels in Chinese. Single Nucleotide Polymorphisms in Lipoprotein Lipase gene is associated with variation in plasma triglyceride levels Coronary Arteriosclerosis. Spontaneously occurring dissociation of LPL dimer into monomers is accelerated in exon 5 mutants, resulting in conformational changes which result in loss of LPL catalytic activity. TRL-bound LPL activity increases in the postprandial state and is strongly reduced in type 2 diabetes, contributing to postprandial hypertriglyceridemia. The Expression of LPL mRNA as well as protein was highly restricted to leukemic B cells. The LPL D9N genotype was a significant predictor of both baseline carotid plaque area and progression. Heterozygotes for the N9 allele had higher values than did LPL D9/D9 homozygotes. D9N genotype may be a determinant of atherosclerosis. The S447X mutation is associated with anti-atherogenic effects on TG and HDL cholesterol in both genders, and with a moderate protective effect on risk of ischemic heart disease in men. The lipoprotein lipase allele significantly increases the risk of developing Alzheimer's disease , and the risk is mostly associated with the H+H+ genotype. The polymorphisms of intron 8 in lipoprotein lipase influence the blood-lipid metabolism, induce blood vessel rebuilding and play an important role in the invasion and development of Essential Hypertension. These results by showing modulation of association between S447X variant of the LPL gene and serum TG by C-514T variant of the HL gene underscore the importance of gene-gene interactions in the assessment of genetic effects on complex traits. Variants in gene relate to presence and degree of microalbuminuria in Type II diabetes. Variation in the LPL gene plays a role in determining insulin resistance in Mexican Americans. W86R mutation was the reason for the production of nonfunctional LPL and consequently triacylglycerol (TG) exceeding 15 mmol/l. X447 allele at the LPL locus is common and associated with a less atherogenic lipid profile in Asian populations. Both hyperglycemia and hyperinsulinemia plus hyperglycemia reduced LPL activity to 60 %. Conclude that type IIB VLDL-1 and VLDL-2 induce triglyceride accumulation in monocyte-macrophages primarily by the lipolytic action of LPL, which may involve stabilization and activation of the enzyme, rather than modulation of enzyme production. Data indicate an important role of endoplasmic reticulum-based chaperones for the folding/dimerization of lipoprotein lipase. Did not find significant effects of lipoprotein lipase HindIII or PvuII polymorphisms on the fasting lipids but HindIII variation was associated with higher triglyceride postprandial peak. Findings of variation near the LPL gene support the proposition that a region near the lipoprotein lipase gene or the lipoprotein lipase gene itself might contribute to the individual blood pressure variation in Chinese. High concentration of triglyceride and/or low concentration of HDL-cholesterol are associated with high blood pressure in hypertensive patients with the X447 allele of the LPL gene. Lipoprotein lipase cannot be a major factor in pathogenesis of Alzheimer's disease. Lipoprotein lipase has a protective role against coronary artery disease in Mexican-Americans. Macrophage-derived LPL in the arterial wall is pro-atherogenic, possibly via the enhancement of foam cell formation during atherogenesis. Mean LDL particle diameter was smaller in LPL N9 carriers; the LPL N9 and S291 alleles are more frequent in CHD-free men with normal HDL-C, whereas the X447 allele is less frequent; the N9 allele is associated with the LDL subclass response to gemfibrozil. Molecular modeling of its dimeric structure. Quantification of LPL and ADAM29 gene expression is a strong prognostic indicator in CLL, providing better prognostic assessment than ZAP-70 in advanced stages of the disease. Results demonstrate a direct effect of prolactin, via functional prolactin receptors, in reducing the lipoprotein lipase activity in human adipose tissue. Results imply that systemic elevation of lipoprotein lipase expression may be potentially useful for the treatment of hyperlipidemias, obesity, and insulin resistance. Results suggest that the nature of the mutation in the LPL gene modifies the relationship of HDL particle size to other metabolic variables and secondary factors such as abdominal obesity and gender. Role of Sp1 and Sp3 in interferon-gamma mediated suppression of gene transcription. Some single-nucleotide polymorphisms in the LPL gene among Chinese associated with abnormal lipid and lipoprotein profiles and predisposition to coronary heart disease, and they are gender-specific. The LPL association with lipid profile is more likely attributable to the functional S447X rather than the nonfunctional exon 10 SNP. The lipoprotein lipase X447 mutant allele may have a role in preventing myocardial infarct risk. Variation in the 3' untranslated region of LPL affects LPL expression and activity, consequently influencing risk of atherosclerosis and insulin resistance. Variations in genes affecting the removal rate of triglycerides (TG) from plasma significantly influence the lipid phenotypic expression of familial combined hyperlipidemia.
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