Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been known for more than 30 years that growth hormone has a lipolytic properties and growth hormone excess (acromegaly) and growth hormone deficiency have been reported to be associated with abnormalities in serum lipoprotein concentrations. Due to the lipolytic effect of growth hormone, its administration in man has been reported to increase plasma nonesterified fatty acid (NEFA) concentrations. Ketone body production increases during acute growth hormone excess as a result of increased NEFA concentrations; similarly, the increase in serum triglycerides may be explained by an increase in substrate (NEFA) supply to the liver for VLDL production. The effect may be enhanced by a simultaneous decrease of serum lipoprotein lipase activity. The cholesterol-lowering effect of growth hormone administration has not been investigated in detail, specifically, the effect of growth hormone on LDL kinetics is unknown. Growth hormone-excess and growth hormone deficiency have been reported to be associated with increased risk for atherosclerosis; an association with serum lipoprotein changes is likely but evidence for a causal link is yet lacking.
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PMID:Growth hormone and lipids. 180 82

Lipoprotein lipase and hepatic triglyceride lipase in postheparin plasma were measured in seven patients with active acromegaly by an immunochemical method utilizing antiserum prepared against hepatic triglyceride lipase. A mild or moderate hypertriglyceridemia was shown, with plasma triglyceride concentrations between 156 and 544 mg/dl. Lipoprotein lipase was found to be decreased in all patients (p less than 0.001). Hepatic triglyceride lipase was also low in these patients (p less than 0.001). We speculate that acromegalic hypertriglyceridemia is mediated, at least in part, by the decline in lipoprotein lipase and possibly by the decline in hepatic triglyceride lipase activities.
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PMID:Decline of postheparin plasma lipoprotein lipase in acromegalic patients. 699 60

A rare case of acromegaly developing gross hyperlipidemia not associated with overt diabetes was presented. Gross hyperlipidemia revealed type V hyperlipoproteininemia, according to agarose gel electrophoretic pattern of serum lipoprotein. Before pituitary surgery, the serum levels of cholesterol and triglyceride were 320 mg/dl and 1830 mg/dl respectively, and the basal level of growth hormone was markedly elevated, ranging from 129 to 231 ng/ml with the mean +/- SD of 168 +/- 39 ng/ml. The enzymatic activities of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were 14.2 and 1.50 mumoles/ml/hour, respectively. H-TGL activity was normal, while LPL activity was extremely low compared to those of normal subjects. After combined therapy with pituitary surgery and 60Co radiation, the serum level of growth hormone was decreased to 35.9 +/- 8.6 ng/ml in the mean +/- SD, but not normalized. However, the serum level of triglyceride was decreased and both H-TGL and LPL activities were increased to 19.3 and 2.7 mumoles/ml/hour, respectively. LPL activity was increased 79% compared to the level of pretreatment. Agarose gel electrophoretic pattern of lipoprotein changed from type V to type IV and ultracentrifugal analysis showed that very low density lipoprotein (VLDL)-cholesterol was decreased and intermediate density lipoprotein (IDL)-cholesterol, low density lipoprotein (LDL)-cholesterol and high density lipoprotein (HDL)-cholesterol were increased.
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PMID:Secondary type V hyperlipoproteinemia in an acromegalic patient without overt diabetes. 708 27

Acromegaly is associated with changes in lipoprotein metabolism and an excess in cardiovascular mortality. We have examined low density lipoprotein (LDL) subfraction distribution in 24 patients with active acromegaly and in controls matched for age, sex and body mass index. LDL was subfractionated by density gradient ultracentrifugation. The concentration of small dense LDL-III was significantly higher in the acromegalic patients compared to the controls (94.2 +/- 44.9 versus 67.2 +/- 30.4 mg/dl, P < 0.05) and there was a concomitant reduction in the intermediate subfraction LDL-II (124.8 +/- 31.3 versus 149.9 +/- 30.0 mg/dl, P < 0.05). Univariate analysis showed that both growth hormone (GH) and insulin-like growth factor (IGF)-I correlated with LDL-III and inversely with LDL-II. Acromegalic patients were found to have lower hepatic lipase (HL) and lipoprotein lipase (LPL) activities than controls (HL: 13.29 +/- 6.56 versus 21.58 +/- 7.27 micromol FFA released/ml/h, P < 0.001: LPL: 7.22 +/- 3.04 versus 11.53 +/- 7.85 micromol FFA released/ml/h, P < 0.05) whereas plasma cholesteryl ester transfer protein (CETP) activity was significantly increased (8.15 +/- 1.81 versus 5.54 +/- 1.86 pmol/microl/h, P < 0.001). Both GH and IGF-I were significantly associated with HL, LPL and CETP activities. Multivariate analysis on this relatively small sample size showed that in normal subjects, triglyceride and HL activity were the major determinants of LDL-III. In contrast, GH and HDL were the main determinants in acromegaly, accounting for 32 and 24% in the variability of LDL-III respectively. In conclusion, GH excess has a direct effect on LDL subfraction distribution.
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PMID:LDL subfractions in acromegaly: relation to growth hormone and insulin-like growth factor-I. 906 18

Secondary hyperlipidemia is common and occurs frequently in patients with endocrine disease such as hy- pothyroidism, Cushing's syndrome, and acromegaly, metabolic disease such as diabetes mellitus, renal dis- ease such as nephrotic syndrome and chronic renal failure, liver disease such as obstructive liver disease, and as a side-effect of glucocorticoids and estrogens. The underlying cause of high serum lipid levels will often be missed if it is not actively sought. We describe. the causes and abnormal lipid laboratory values of sec- ondary hyperlipidemia in endocrine disease patients such as those with hypothyroidism, Cushing's syndrome, and acromegaly. Hypothyroidism is associated with elevated serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), and normal or elevated high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG), respectively. The lipid abnormalities are due to the reductions in hepatic LDL receptor function and hepatic TG lipase (HTGL) activity. Cushing's syndrome is associated with elevated serum TC, LDL-C, and TG and elevated or normal HDL-C. The lipid abnormalities are due to the glucocorticoid- induced increase in very low-density lipoprotein (VLDL) and elevation in lipoprotein lipase (LPL) activity. Acromegaly is associated with normal serum TC, reduced LDL-C and HDL-C, and elevated TG. The lipid abnormalities are due to the growth hormone-induced reductions in LPL and HTGL activity and increase in hepatic LDL receptors. When we examine hyperlipidemic patients, it is important to diagnose the true name of the disease, usually in consideration of the possibility of the cause of secondary hyperlipidemia. [Review].
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PMID:[Causes and Abnormal Lipid Laboratory Values of Secondary Hyperlipidemia: Endocrine Disease]. 3069 60